A variant of the CXCL11 gene may influence susceptibility to contact allergy, particularly in polysensitized patients
BACKGROUND: Hereditary factors may influence individual susceptibility to contact allergy. OBJECTIVES: To investigate genetic variants with impacts on early inflammatory reactions and T cell functions that possibly increase the risk of contact allergy. PATIENTS AND METHODS: Three hundred and seventy...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Westphal, Götz Alexander [verfasserIn] Schäkel, Knut [verfasserIn] |
|---|
| Format: |
E-Artikel |
|---|---|
| Sprache: |
Englisch |
| Erschienen: |
28 April 2016 |
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| Schlagwörter: |
Genetic Predisposition to Disease |
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| Anmerkung: |
Gesehen am 07.12.2017 |
|---|---|
| Umfang: |
5 |
| Übergeordnetes Werk: |
Enthalten in: Contact dermatitis - Oxford [u.a.] : Wiley-Blackwell, 1975, 75(2016), 5, Seite 303-307 |
|---|---|
| Übergeordnetes Werk: |
volume:75 ; year:2016 ; number:5 ; pages:303-307 ; extent:5 |
| DOI / URN: |
10.1111/cod.12623 |
|---|
| Katalog-ID: |
1566160235 |
|---|
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| 100 | 1 | |a Westphal, Götz Alexander |e verfasserin |0 (DE-588)1022870297 |0 (DE-627)717321266 |0 (DE-576)366135260 |4 aut | |
| 245 | 1 | 2 | |a A variant of the CXCL11 gene may influence susceptibility to contact allergy, particularly in polysensitized patients |c Götz A. Westphal, Hans-Peter Rihs, Antje Schaffranek, Thomas Zeiler, Thomas Werfel, Annice Heratizadeh, Heinrich Dickel, Elke Weisshaar, Andrea Bauer, Sibylle Schliemann, Kristian Reich, Kristine Breuer, Claudia Schröder-Kraft, Margitta Worm, Sonja Molin, Richard Brans, Knut Schäkel, Hilmar Schwantes, Claudia Pföhler, Christiane Szliska, Burkhard Kreft, Harald Löffler, Jürgen Bünger, Thomas Brüning, Johannes Geier andAxel Schnuch |
| 264 | 1 | |c 28 April 2016 | |
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| 500 | |a Gesehen am 07.12.2017 | ||
| 520 | |a BACKGROUND: Hereditary factors may influence individual susceptibility to contact allergy. OBJECTIVES: To investigate genetic variants with impacts on early inflammatory reactions and T cell functions that possibly increase the risk of contact allergy. PATIENTS AND METHODS: Three hundred and seventy two patients undergoing patch testing were recruited from the Information Network of Departments of Dermatology (IVDK). Of these, 133 were monosensitized and 239 were polysensitized, defined as reacting to three or more unrelated sensitizers. Within the polysensitized individuals, a subgroup with at least one particularly strong patch test reaction (strong reactors; n = 194) was considered. Three hundred and forty-seven blood bank donors served as controls. Fifteen genetic variants in 13 genes were analysed. RESULTS: The homozygous variant CXCL11 AA genotype (rs6817952) was significantly more frequent among polysensitized patients (10 of 239 = 4.2%; p = 0.0048; odds ratio 7.49; 95%CI: 1.7-36.1) than among monosensitized patients (2.2%) and in the control group (0.6%). None of the remaining genetic variants investigated were characterized by similarly strong associations. However, the significance was lost after correction for multiple comparisons. CONCLUSIONS: The homozygous variant CXCL11 genotype is associated with an increased risk of contact allergy. To confirm this exploratory finding, further independent studies are needed. | ||
| 650 | 4 | |a Aged | |
| 650 | 4 | |a Female | |
| 650 | 4 | |a Humans | |
| 650 | 4 | |a Male | |
| 650 | 4 | |a Middle Aged | |
| 650 | 4 | |a Adult | |
| 650 | 4 | |a Cytokines | |
| 650 | 4 | |a Young Adult | |
| 650 | 4 | |a Adolescent | |
| 650 | 4 | |a Case-Control Studies | |
| 650 | 4 | |a Chemokine CXCL11 | |
| 650 | 4 | |a contact allergy | |
| 650 | 4 | |a CXCL11 | |
| 650 | 4 | |a Dermatitis, Allergic Contact | |
| 650 | 4 | |a Genetic Predisposition to Disease | |
| 650 | 4 | |a Homozygote | |
| 650 | 4 | |a Odds Ratio | |
| 650 | 4 | |a Patch Tests | |
| 650 | 4 | |a Polymorphism, Single Nucleotide | |
| 650 | 4 | |a polysensitization | |
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| 912 | |a GBV_ILN_20 | ||
| 912 | |a GBV_ILN_22 | ||
| 912 | |a GBV_ILN_23 | ||
| 912 | |a GBV_ILN_24 | ||
| 912 | |a GBV_ILN_31 | ||
| 912 | |a GBV_ILN_32 | ||
| 912 | |a GBV_ILN_39 | ||
| 912 | |a GBV_ILN_40 | ||
| 912 | |a GBV_ILN_60 | ||
| 912 | |a GBV_ILN_62 | ||
| 912 | |a GBV_ILN_63 | ||
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| 912 | |a GBV_ILN_120 | ||
| 912 | |a GBV_ILN_138 | ||
| 912 | |a GBV_ILN_150 | ||
| 912 | |a GBV_ILN_151 | ||
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| 912 | |a GBV_ILN_171 | ||
| 912 | |a GBV_ILN_187 | ||
| 912 | |a GBV_ILN_206 | ||
| 912 | |a GBV_ILN_213 | ||
| 912 | |a GBV_ILN_224 | ||
| 912 | |a GBV_ILN_230 | ||
| 912 | |a GBV_ILN_266 | ||
| 912 | |a GBV_ILN_285 | ||
| 912 | |a GBV_ILN_293 | ||
| 912 | |a GBV_ILN_370 | ||
| 912 | |a GBV_ILN_602 | ||
| 912 | |a GBV_ILN_636 | ||
| 912 | |a GBV_ILN_647 | ||
| 912 | |a GBV_ILN_702 | ||
| 912 | |a GBV_ILN_2001 | ||
| 912 | |a GBV_ILN_2003 | ||
| 912 | |a GBV_ILN_2004 | ||
| 912 | |a GBV_ILN_2005 | ||
| 912 | |a GBV_ILN_2006 | ||
| 912 | |a GBV_ILN_2007 | ||
| 912 | |a GBV_ILN_2008 | ||
| 912 | |a GBV_ILN_2009 | ||
| 912 | |a GBV_ILN_2010 | ||
| 912 | |a GBV_ILN_2011 | ||
| 912 | |a GBV_ILN_2014 | ||
| 912 | |a GBV_ILN_2015 | ||
| 912 | |a GBV_ILN_2018 | ||
| 912 | |a GBV_ILN_2020 | ||
| 912 | |a GBV_ILN_2021 | ||
| 912 | |a GBV_ILN_2025 | ||
| 912 | |a GBV_ILN_2026 | ||
| 912 | |a GBV_ILN_2027 | ||
| 912 | |a GBV_ILN_2031 | ||
| 912 | |a GBV_ILN_2034 | ||
| 912 | |a GBV_ILN_2037 | ||
| 912 | |a GBV_ILN_2038 | ||
| 912 | |a GBV_ILN_2039 | ||
| 912 | |a GBV_ILN_2044 | ||
| 912 | |a GBV_ILN_2048 | ||
| 912 | |a GBV_ILN_2049 | ||
| 912 | |a GBV_ILN_2050 | ||
| 912 | |a GBV_ILN_2055 | ||
| 912 | |a GBV_ILN_2056 | ||
| 912 | |a GBV_ILN_2057 | ||
| 912 | |a GBV_ILN_2059 | ||
| 912 | |a GBV_ILN_2061 | ||
| 912 | |a GBV_ILN_2064 | ||
| 912 | |a GBV_ILN_2068 | ||
| 912 | |a GBV_ILN_2088 | ||
| 912 | |a GBV_ILN_2093 | ||
| 912 | |a GBV_ILN_2106 | ||
| 912 | |a GBV_ILN_2108 | ||
| 912 | |a GBV_ILN_2110 | ||
| 912 | |a GBV_ILN_2111 | ||
| 912 | |a GBV_ILN_2112 | ||
| 912 | |a GBV_ILN_2113 | ||
| 912 | |a GBV_ILN_2118 | ||
| 912 | |a GBV_ILN_2119 | ||
| 912 | |a GBV_ILN_2122 | ||
| 912 | |a GBV_ILN_2129 | ||
| 912 | |a GBV_ILN_2143 | ||
| 912 | |a GBV_ILN_2144 | ||
| 912 | |a GBV_ILN_2147 | ||
| 912 | |a GBV_ILN_2148 | ||
| 912 | |a GBV_ILN_2152 | ||
| 912 | |a GBV_ILN_2153 | ||
| 912 | |a GBV_ILN_2188 | ||
| 912 | |a GBV_ILN_2190 | ||
| 912 | |a GBV_ILN_2232 | ||
| 912 | |a GBV_ILN_2336 | ||
| 912 | |a GBV_ILN_2470 | ||
| 912 | |a GBV_ILN_2472 | ||
| 912 | |a GBV_ILN_2507 | ||
| 912 | |a GBV_ILN_2522 | ||
| 912 | |a GBV_ILN_2548 | ||
| 912 | |a GBV_ILN_4012 | ||
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28 April 2016 |
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10.1111/cod.12623 doi (DE-627)1566160235 (DE-576)496160230 (DE-599)BSZ496160230 (OCoLC)1340983223 DE-627 ger DE-627 rda eng Westphal, Götz Alexander verfasserin (DE-588)1022870297 (DE-627)717321266 (DE-576)366135260 aut A variant of the CXCL11 gene may influence susceptibility to contact allergy, particularly in polysensitized patients Götz A. Westphal, Hans-Peter Rihs, Antje Schaffranek, Thomas Zeiler, Thomas Werfel, Annice Heratizadeh, Heinrich Dickel, Elke Weisshaar, Andrea Bauer, Sibylle Schliemann, Kristian Reich, Kristine Breuer, Claudia Schröder-Kraft, Margitta Worm, Sonja Molin, Richard Brans, Knut Schäkel, Hilmar Schwantes, Claudia Pföhler, Christiane Szliska, Burkhard Kreft, Harald Löffler, Jürgen Bünger, Thomas Brüning, Johannes Geier andAxel Schnuch 28 April 2016 5 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Gesehen am 07.12.2017 BACKGROUND: Hereditary factors may influence individual susceptibility to contact allergy. OBJECTIVES: To investigate genetic variants with impacts on early inflammatory reactions and T cell functions that possibly increase the risk of contact allergy. PATIENTS AND METHODS: Three hundred and seventy two patients undergoing patch testing were recruited from the Information Network of Departments of Dermatology (IVDK). Of these, 133 were monosensitized and 239 were polysensitized, defined as reacting to three or more unrelated sensitizers. Within the polysensitized individuals, a subgroup with at least one particularly strong patch test reaction (strong reactors; n = 194) was considered. Three hundred and forty-seven blood bank donors served as controls. Fifteen genetic variants in 13 genes were analysed. RESULTS: The homozygous variant CXCL11 AA genotype (rs6817952) was significantly more frequent among polysensitized patients (10 of 239 = 4.2%; p = 0.0048; odds ratio 7.49; 95%CI: 1.7-36.1) than among monosensitized patients (2.2%) and in the control group (0.6%). None of the remaining genetic variants investigated were characterized by similarly strong associations. However, the significance was lost after correction for multiple comparisons. CONCLUSIONS: The homozygous variant CXCL11 genotype is associated with an increased risk of contact allergy. To confirm this exploratory finding, further independent studies are needed. Aged Female Humans Male Middle Aged Adult Cytokines Young Adult Adolescent Case-Control Studies Chemokine CXCL11 contact allergy CXCL11 Dermatitis, Allergic Contact Genetic Predisposition to Disease Homozygote Odds Ratio Patch Tests Polymorphism, Single Nucleotide polysensitization Schäkel, Knut verfasserin (DE-588)1032757418 (DE-627)739272896 (DE-576)251064476 aut Enthalten in Contact dermatitis Oxford [u.a.] : Wiley-Blackwell, 1975 75(2016), 5, Seite 303-307 Online-Ressource (DE-627)32448464X (DE-600)2027120-7 (DE-576)093888872 1600-0536 nnns volume:75 year:2016 number:5 pages:303-307 extent:5 GBV_USEFLAG_U GBV_ILN_2013 ISIL_DE-16-250 SYSFLAG_1 GBV_KXP SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_266 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_647 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 75 2016 5 303-307 5 2013 01 DE-16-250 2989520481 00 --%%-- --%%-- --%%-- --%%-- l01 07-12-17 2013 01 DE-16-250 00 s hd2016 2013 01 DE-16-250 01 s (DE-627)1410508463 wissenschaftlicher Artikel (Zeitschrift) 2013 01 DE-16-250 02 s per_26 2013 01 DE-16-250 03 s s_5 2013 01 DE-16-250 04 p (DE-627)1450269095 Schäkel, Knut 2013 01 DE-16-250 04 k (DE-627)1416741372 Universitäts-Hautklinik 2013 01 DE-16-250 04 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 04 s pos_17 |
| spelling |
10.1111/cod.12623 doi (DE-627)1566160235 (DE-576)496160230 (DE-599)BSZ496160230 (OCoLC)1340983223 DE-627 ger DE-627 rda eng Westphal, Götz Alexander verfasserin (DE-588)1022870297 (DE-627)717321266 (DE-576)366135260 aut A variant of the CXCL11 gene may influence susceptibility to contact allergy, particularly in polysensitized patients Götz A. Westphal, Hans-Peter Rihs, Antje Schaffranek, Thomas Zeiler, Thomas Werfel, Annice Heratizadeh, Heinrich Dickel, Elke Weisshaar, Andrea Bauer, Sibylle Schliemann, Kristian Reich, Kristine Breuer, Claudia Schröder-Kraft, Margitta Worm, Sonja Molin, Richard Brans, Knut Schäkel, Hilmar Schwantes, Claudia Pföhler, Christiane Szliska, Burkhard Kreft, Harald Löffler, Jürgen Bünger, Thomas Brüning, Johannes Geier andAxel Schnuch 28 April 2016 5 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Gesehen am 07.12.2017 BACKGROUND: Hereditary factors may influence individual susceptibility to contact allergy. OBJECTIVES: To investigate genetic variants with impacts on early inflammatory reactions and T cell functions that possibly increase the risk of contact allergy. PATIENTS AND METHODS: Three hundred and seventy two patients undergoing patch testing were recruited from the Information Network of Departments of Dermatology (IVDK). Of these, 133 were monosensitized and 239 were polysensitized, defined as reacting to three or more unrelated sensitizers. Within the polysensitized individuals, a subgroup with at least one particularly strong patch test reaction (strong reactors; n = 194) was considered. Three hundred and forty-seven blood bank donors served as controls. Fifteen genetic variants in 13 genes were analysed. RESULTS: The homozygous variant CXCL11 AA genotype (rs6817952) was significantly more frequent among polysensitized patients (10 of 239 = 4.2%; p = 0.0048; odds ratio 7.49; 95%CI: 1.7-36.1) than among monosensitized patients (2.2%) and in the control group (0.6%). None of the remaining genetic variants investigated were characterized by similarly strong associations. However, the significance was lost after correction for multiple comparisons. CONCLUSIONS: The homozygous variant CXCL11 genotype is associated with an increased risk of contact allergy. To confirm this exploratory finding, further independent studies are needed. Aged Female Humans Male Middle Aged Adult Cytokines Young Adult Adolescent Case-Control Studies Chemokine CXCL11 contact allergy CXCL11 Dermatitis, Allergic Contact Genetic Predisposition to Disease Homozygote Odds Ratio Patch Tests Polymorphism, Single Nucleotide polysensitization Schäkel, Knut verfasserin (DE-588)1032757418 (DE-627)739272896 (DE-576)251064476 aut Enthalten in Contact dermatitis Oxford [u.a.] : Wiley-Blackwell, 1975 75(2016), 5, Seite 303-307 Online-Ressource (DE-627)32448464X (DE-600)2027120-7 (DE-576)093888872 1600-0536 nnns volume:75 year:2016 number:5 pages:303-307 extent:5 GBV_USEFLAG_U GBV_ILN_2013 ISIL_DE-16-250 SYSFLAG_1 GBV_KXP SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_266 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_647 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 75 2016 5 303-307 5 2013 01 DE-16-250 2989520481 00 --%%-- --%%-- --%%-- --%%-- l01 07-12-17 2013 01 DE-16-250 00 s hd2016 2013 01 DE-16-250 01 s (DE-627)1410508463 wissenschaftlicher Artikel (Zeitschrift) 2013 01 DE-16-250 02 s per_26 2013 01 DE-16-250 03 s s_5 2013 01 DE-16-250 04 p (DE-627)1450269095 Schäkel, Knut 2013 01 DE-16-250 04 k (DE-627)1416741372 Universitäts-Hautklinik 2013 01 DE-16-250 04 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 04 s pos_17 |
| allfields_unstemmed |
10.1111/cod.12623 doi (DE-627)1566160235 (DE-576)496160230 (DE-599)BSZ496160230 (OCoLC)1340983223 DE-627 ger DE-627 rda eng Westphal, Götz Alexander verfasserin (DE-588)1022870297 (DE-627)717321266 (DE-576)366135260 aut A variant of the CXCL11 gene may influence susceptibility to contact allergy, particularly in polysensitized patients Götz A. Westphal, Hans-Peter Rihs, Antje Schaffranek, Thomas Zeiler, Thomas Werfel, Annice Heratizadeh, Heinrich Dickel, Elke Weisshaar, Andrea Bauer, Sibylle Schliemann, Kristian Reich, Kristine Breuer, Claudia Schröder-Kraft, Margitta Worm, Sonja Molin, Richard Brans, Knut Schäkel, Hilmar Schwantes, Claudia Pföhler, Christiane Szliska, Burkhard Kreft, Harald Löffler, Jürgen Bünger, Thomas Brüning, Johannes Geier andAxel Schnuch 28 April 2016 5 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Gesehen am 07.12.2017 BACKGROUND: Hereditary factors may influence individual susceptibility to contact allergy. OBJECTIVES: To investigate genetic variants with impacts on early inflammatory reactions and T cell functions that possibly increase the risk of contact allergy. PATIENTS AND METHODS: Three hundred and seventy two patients undergoing patch testing were recruited from the Information Network of Departments of Dermatology (IVDK). Of these, 133 were monosensitized and 239 were polysensitized, defined as reacting to three or more unrelated sensitizers. Within the polysensitized individuals, a subgroup with at least one particularly strong patch test reaction (strong reactors; n = 194) was considered. Three hundred and forty-seven blood bank donors served as controls. Fifteen genetic variants in 13 genes were analysed. RESULTS: The homozygous variant CXCL11 AA genotype (rs6817952) was significantly more frequent among polysensitized patients (10 of 239 = 4.2%; p = 0.0048; odds ratio 7.49; 95%CI: 1.7-36.1) than among monosensitized patients (2.2%) and in the control group (0.6%). None of the remaining genetic variants investigated were characterized by similarly strong associations. However, the significance was lost after correction for multiple comparisons. CONCLUSIONS: The homozygous variant CXCL11 genotype is associated with an increased risk of contact allergy. To confirm this exploratory finding, further independent studies are needed. Aged Female Humans Male Middle Aged Adult Cytokines Young Adult Adolescent Case-Control Studies Chemokine CXCL11 contact allergy CXCL11 Dermatitis, Allergic Contact Genetic Predisposition to Disease Homozygote Odds Ratio Patch Tests Polymorphism, Single Nucleotide polysensitization Schäkel, Knut verfasserin (DE-588)1032757418 (DE-627)739272896 (DE-576)251064476 aut Enthalten in Contact dermatitis Oxford [u.a.] : Wiley-Blackwell, 1975 75(2016), 5, Seite 303-307 Online-Ressource (DE-627)32448464X (DE-600)2027120-7 (DE-576)093888872 1600-0536 nnns volume:75 year:2016 number:5 pages:303-307 extent:5 GBV_USEFLAG_U GBV_ILN_2013 ISIL_DE-16-250 SYSFLAG_1 GBV_KXP SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_266 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_647 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 75 2016 5 303-307 5 2013 01 DE-16-250 2989520481 00 --%%-- --%%-- --%%-- --%%-- l01 07-12-17 2013 01 DE-16-250 00 s hd2016 2013 01 DE-16-250 01 s (DE-627)1410508463 wissenschaftlicher Artikel (Zeitschrift) 2013 01 DE-16-250 02 s per_26 2013 01 DE-16-250 03 s s_5 2013 01 DE-16-250 04 p (DE-627)1450269095 Schäkel, Knut 2013 01 DE-16-250 04 k (DE-627)1416741372 Universitäts-Hautklinik 2013 01 DE-16-250 04 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 04 s pos_17 |
| allfieldsGer |
10.1111/cod.12623 doi (DE-627)1566160235 (DE-576)496160230 (DE-599)BSZ496160230 (OCoLC)1340983223 DE-627 ger DE-627 rda eng Westphal, Götz Alexander verfasserin (DE-588)1022870297 (DE-627)717321266 (DE-576)366135260 aut A variant of the CXCL11 gene may influence susceptibility to contact allergy, particularly in polysensitized patients Götz A. Westphal, Hans-Peter Rihs, Antje Schaffranek, Thomas Zeiler, Thomas Werfel, Annice Heratizadeh, Heinrich Dickel, Elke Weisshaar, Andrea Bauer, Sibylle Schliemann, Kristian Reich, Kristine Breuer, Claudia Schröder-Kraft, Margitta Worm, Sonja Molin, Richard Brans, Knut Schäkel, Hilmar Schwantes, Claudia Pföhler, Christiane Szliska, Burkhard Kreft, Harald Löffler, Jürgen Bünger, Thomas Brüning, Johannes Geier andAxel Schnuch 28 April 2016 5 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Gesehen am 07.12.2017 BACKGROUND: Hereditary factors may influence individual susceptibility to contact allergy. OBJECTIVES: To investigate genetic variants with impacts on early inflammatory reactions and T cell functions that possibly increase the risk of contact allergy. PATIENTS AND METHODS: Three hundred and seventy two patients undergoing patch testing were recruited from the Information Network of Departments of Dermatology (IVDK). Of these, 133 were monosensitized and 239 were polysensitized, defined as reacting to three or more unrelated sensitizers. Within the polysensitized individuals, a subgroup with at least one particularly strong patch test reaction (strong reactors; n = 194) was considered. Three hundred and forty-seven blood bank donors served as controls. Fifteen genetic variants in 13 genes were analysed. RESULTS: The homozygous variant CXCL11 AA genotype (rs6817952) was significantly more frequent among polysensitized patients (10 of 239 = 4.2%; p = 0.0048; odds ratio 7.49; 95%CI: 1.7-36.1) than among monosensitized patients (2.2%) and in the control group (0.6%). None of the remaining genetic variants investigated were characterized by similarly strong associations. However, the significance was lost after correction for multiple comparisons. CONCLUSIONS: The homozygous variant CXCL11 genotype is associated with an increased risk of contact allergy. To confirm this exploratory finding, further independent studies are needed. Aged Female Humans Male Middle Aged Adult Cytokines Young Adult Adolescent Case-Control Studies Chemokine CXCL11 contact allergy CXCL11 Dermatitis, Allergic Contact Genetic Predisposition to Disease Homozygote Odds Ratio Patch Tests Polymorphism, Single Nucleotide polysensitization Schäkel, Knut verfasserin (DE-588)1032757418 (DE-627)739272896 (DE-576)251064476 aut Enthalten in Contact dermatitis Oxford [u.a.] : Wiley-Blackwell, 1975 75(2016), 5, Seite 303-307 Online-Ressource (DE-627)32448464X (DE-600)2027120-7 (DE-576)093888872 1600-0536 nnns volume:75 year:2016 number:5 pages:303-307 extent:5 GBV_USEFLAG_U GBV_ILN_2013 ISIL_DE-16-250 SYSFLAG_1 GBV_KXP SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_266 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_647 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 75 2016 5 303-307 5 2013 01 DE-16-250 2989520481 00 --%%-- --%%-- --%%-- --%%-- l01 07-12-17 2013 01 DE-16-250 00 s hd2016 2013 01 DE-16-250 01 s (DE-627)1410508463 wissenschaftlicher Artikel (Zeitschrift) 2013 01 DE-16-250 02 s per_26 2013 01 DE-16-250 03 s s_5 2013 01 DE-16-250 04 p (DE-627)1450269095 Schäkel, Knut 2013 01 DE-16-250 04 k (DE-627)1416741372 Universitäts-Hautklinik 2013 01 DE-16-250 04 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 04 s pos_17 |
| allfieldsSound |
10.1111/cod.12623 doi (DE-627)1566160235 (DE-576)496160230 (DE-599)BSZ496160230 (OCoLC)1340983223 DE-627 ger DE-627 rda eng Westphal, Götz Alexander verfasserin (DE-588)1022870297 (DE-627)717321266 (DE-576)366135260 aut A variant of the CXCL11 gene may influence susceptibility to contact allergy, particularly in polysensitized patients Götz A. Westphal, Hans-Peter Rihs, Antje Schaffranek, Thomas Zeiler, Thomas Werfel, Annice Heratizadeh, Heinrich Dickel, Elke Weisshaar, Andrea Bauer, Sibylle Schliemann, Kristian Reich, Kristine Breuer, Claudia Schröder-Kraft, Margitta Worm, Sonja Molin, Richard Brans, Knut Schäkel, Hilmar Schwantes, Claudia Pföhler, Christiane Szliska, Burkhard Kreft, Harald Löffler, Jürgen Bünger, Thomas Brüning, Johannes Geier andAxel Schnuch 28 April 2016 5 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Gesehen am 07.12.2017 BACKGROUND: Hereditary factors may influence individual susceptibility to contact allergy. OBJECTIVES: To investigate genetic variants with impacts on early inflammatory reactions and T cell functions that possibly increase the risk of contact allergy. PATIENTS AND METHODS: Three hundred and seventy two patients undergoing patch testing were recruited from the Information Network of Departments of Dermatology (IVDK). Of these, 133 were monosensitized and 239 were polysensitized, defined as reacting to three or more unrelated sensitizers. Within the polysensitized individuals, a subgroup with at least one particularly strong patch test reaction (strong reactors; n = 194) was considered. Three hundred and forty-seven blood bank donors served as controls. Fifteen genetic variants in 13 genes were analysed. RESULTS: The homozygous variant CXCL11 AA genotype (rs6817952) was significantly more frequent among polysensitized patients (10 of 239 = 4.2%; p = 0.0048; odds ratio 7.49; 95%CI: 1.7-36.1) than among monosensitized patients (2.2%) and in the control group (0.6%). None of the remaining genetic variants investigated were characterized by similarly strong associations. However, the significance was lost after correction for multiple comparisons. CONCLUSIONS: The homozygous variant CXCL11 genotype is associated with an increased risk of contact allergy. To confirm this exploratory finding, further independent studies are needed. Aged Female Humans Male Middle Aged Adult Cytokines Young Adult Adolescent Case-Control Studies Chemokine CXCL11 contact allergy CXCL11 Dermatitis, Allergic Contact Genetic Predisposition to Disease Homozygote Odds Ratio Patch Tests Polymorphism, Single Nucleotide polysensitization Schäkel, Knut verfasserin (DE-588)1032757418 (DE-627)739272896 (DE-576)251064476 aut Enthalten in Contact dermatitis Oxford [u.a.] : Wiley-Blackwell, 1975 75(2016), 5, Seite 303-307 Online-Ressource (DE-627)32448464X (DE-600)2027120-7 (DE-576)093888872 1600-0536 nnns volume:75 year:2016 number:5 pages:303-307 extent:5 GBV_USEFLAG_U GBV_ILN_2013 ISIL_DE-16-250 SYSFLAG_1 GBV_KXP SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_266 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_647 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 75 2016 5 303-307 5 2013 01 DE-16-250 2989520481 00 --%%-- --%%-- --%%-- --%%-- l01 07-12-17 2013 01 DE-16-250 00 s hd2016 2013 01 DE-16-250 01 s (DE-627)1410508463 wissenschaftlicher Artikel (Zeitschrift) 2013 01 DE-16-250 02 s per_26 2013 01 DE-16-250 03 s s_5 2013 01 DE-16-250 04 p (DE-627)1450269095 Schäkel, Knut 2013 01 DE-16-250 04 k (DE-627)1416741372 Universitäts-Hautklinik 2013 01 DE-16-250 04 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 04 s pos_17 |
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Aged Female Humans Male Middle Aged Adult Cytokines Young Adult Adolescent Case-Control Studies Chemokine CXCL11 contact allergy CXCL11 Dermatitis, Allergic Contact Genetic Predisposition to Disease Homozygote Odds Ratio Patch Tests Polymorphism, Single Nucleotide polysensitization |
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| container_title |
Contact dermatitis |
| authorswithroles_txt_mv |
Westphal, Götz Alexander @@aut@@ Schäkel, Knut @@aut@@ |
| publishDateDaySort_date |
2016-01-01T00:00:00Z |
| hierarchy_top_id |
32448464X |
| id |
1566160235 |
| language_de |
englisch |
| fullrecord |
<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a2200265 4500</leader><controlfield tag="001">1566160235</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230426064422.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">171207s2016 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1111/cod.12623</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)1566160235</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-576)496160230</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-599)BSZ496160230</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(OCoLC)1340983223</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rda</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Westphal, Götz Alexander</subfield><subfield code="e">verfasserin</subfield><subfield code="0">(DE-588)1022870297</subfield><subfield code="0">(DE-627)717321266</subfield><subfield code="0">(DE-576)366135260</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="2"><subfield code="a">A variant of the CXCL11 gene may influence susceptibility to contact allergy, particularly in polysensitized patients</subfield><subfield code="c">Götz A. Westphal, Hans-Peter Rihs, Antje Schaffranek, Thomas Zeiler, Thomas Werfel, Annice Heratizadeh, Heinrich Dickel, Elke Weisshaar, Andrea Bauer, Sibylle Schliemann, Kristian Reich, Kristine Breuer, Claudia Schröder-Kraft, Margitta Worm, Sonja Molin, Richard Brans, Knut Schäkel, Hilmar Schwantes, Claudia Pföhler, Christiane Szliska, Burkhard Kreft, Harald Löffler, Jürgen Bünger, Thomas Brüning, Johannes Geier andAxel Schnuch</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">28 April 2016</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">5</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="500" ind1=" " ind2=" "><subfield code="a">Gesehen am 07.12.2017</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">BACKGROUND: Hereditary factors may influence individual susceptibility to contact allergy. OBJECTIVES: To investigate genetic variants with impacts on early inflammatory reactions and T cell functions that possibly increase the risk of contact allergy. PATIENTS AND METHODS: Three hundred and seventy two patients undergoing patch testing were recruited from the Information Network of Departments of Dermatology (IVDK). Of these, 133 were monosensitized and 239 were polysensitized, defined as reacting to three or more unrelated sensitizers. Within the polysensitized individuals, a subgroup with at least one particularly strong patch test reaction (strong reactors; n = 194) was considered. Three hundred and forty-seven blood bank donors served as controls. Fifteen genetic variants in 13 genes were analysed. RESULTS: The homozygous variant CXCL11 AA genotype (rs6817952) was significantly more frequent among polysensitized patients (10 of 239 = 4.2%; p = 0.0048; odds ratio 7.49; 95%CI: 1.7-36.1) than among monosensitized patients (2.2%) and in the control group (0.6%). None of the remaining genetic variants investigated were characterized by similarly strong associations. However, the significance was lost after correction for multiple comparisons. CONCLUSIONS: The homozygous variant CXCL11 genotype is associated with an increased risk of contact allergy. To confirm this exploratory finding, further independent studies are needed.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Aged</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Female</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Humans</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Male</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Middle Aged</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Adult</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Cytokines</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Young Adult</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Adolescent</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Case-Control 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A variant of the CXCL11 gene may influence susceptibility to contact allergy, particularly in polysensitized patients Götz A. Westphal, Hans-Peter Rihs, Antje Schaffranek, Thomas Zeiler, Thomas Werfel, Annice Heratizadeh, Heinrich Dickel, Elke Weisshaar, Andrea Bauer, Sibylle Schliemann, Kristian Reich, Kristine Breuer, Claudia Schröder-Kraft, Margitta Worm, Sonja Molin, Richard Brans, Knut Schäkel, Hilmar Schwantes, Claudia Pföhler, Christiane Szliska, Burkhard Kreft, Harald Löffler, Jürgen Bünger, Thomas Brüning, Johannes Geier andAxel Schnuch |
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A variant of the CXCL11 gene may influence susceptibility to contact allergy, particularly in polysensitized patients |
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BACKGROUND: Hereditary factors may influence individual susceptibility to contact allergy. OBJECTIVES: To investigate genetic variants with impacts on early inflammatory reactions and T cell functions that possibly increase the risk of contact allergy. PATIENTS AND METHODS: Three hundred and seventy two patients undergoing patch testing were recruited from the Information Network of Departments of Dermatology (IVDK). Of these, 133 were monosensitized and 239 were polysensitized, defined as reacting to three or more unrelated sensitizers. Within the polysensitized individuals, a subgroup with at least one particularly strong patch test reaction (strong reactors; n = 194) was considered. Three hundred and forty-seven blood bank donors served as controls. Fifteen genetic variants in 13 genes were analysed. RESULTS: The homozygous variant CXCL11 AA genotype (rs6817952) was significantly more frequent among polysensitized patients (10 of 239 = 4.2%; p = 0.0048; odds ratio 7.49; 95%CI: 1.7-36.1) than among monosensitized patients (2.2%) and in the control group (0.6%). None of the remaining genetic variants investigated were characterized by similarly strong associations. However, the significance was lost after correction for multiple comparisons. CONCLUSIONS: The homozygous variant CXCL11 genotype is associated with an increased risk of contact allergy. To confirm this exploratory finding, further independent studies are needed. Gesehen am 07.12.2017 |
| abstractGer |
BACKGROUND: Hereditary factors may influence individual susceptibility to contact allergy. OBJECTIVES: To investigate genetic variants with impacts on early inflammatory reactions and T cell functions that possibly increase the risk of contact allergy. PATIENTS AND METHODS: Three hundred and seventy two patients undergoing patch testing were recruited from the Information Network of Departments of Dermatology (IVDK). Of these, 133 were monosensitized and 239 were polysensitized, defined as reacting to three or more unrelated sensitizers. Within the polysensitized individuals, a subgroup with at least one particularly strong patch test reaction (strong reactors; n = 194) was considered. Three hundred and forty-seven blood bank donors served as controls. Fifteen genetic variants in 13 genes were analysed. RESULTS: The homozygous variant CXCL11 AA genotype (rs6817952) was significantly more frequent among polysensitized patients (10 of 239 = 4.2%; p = 0.0048; odds ratio 7.49; 95%CI: 1.7-36.1) than among monosensitized patients (2.2%) and in the control group (0.6%). None of the remaining genetic variants investigated were characterized by similarly strong associations. However, the significance was lost after correction for multiple comparisons. CONCLUSIONS: The homozygous variant CXCL11 genotype is associated with an increased risk of contact allergy. To confirm this exploratory finding, further independent studies are needed. Gesehen am 07.12.2017 |
| abstract_unstemmed |
BACKGROUND: Hereditary factors may influence individual susceptibility to contact allergy. OBJECTIVES: To investigate genetic variants with impacts on early inflammatory reactions and T cell functions that possibly increase the risk of contact allergy. PATIENTS AND METHODS: Three hundred and seventy two patients undergoing patch testing were recruited from the Information Network of Departments of Dermatology (IVDK). Of these, 133 were monosensitized and 239 were polysensitized, defined as reacting to three or more unrelated sensitizers. Within the polysensitized individuals, a subgroup with at least one particularly strong patch test reaction (strong reactors; n = 194) was considered. Three hundred and forty-seven blood bank donors served as controls. Fifteen genetic variants in 13 genes were analysed. RESULTS: The homozygous variant CXCL11 AA genotype (rs6817952) was significantly more frequent among polysensitized patients (10 of 239 = 4.2%; p = 0.0048; odds ratio 7.49; 95%CI: 1.7-36.1) than among monosensitized patients (2.2%) and in the control group (0.6%). None of the remaining genetic variants investigated were characterized by similarly strong associations. However, the significance was lost after correction for multiple comparisons. CONCLUSIONS: The homozygous variant CXCL11 genotype is associated with an increased risk of contact allergy. To confirm this exploratory finding, further independent studies are needed. Gesehen am 07.12.2017 |
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