Atopic Dermatitis and Type 2 Immune Deviation
Purpose of the review To summarize recent topics on type 2 signatures in atopic dermatitis (AD). Recent findings Therapeutic success of anti-IL-4 receptor antibody dupilumab does suggest that type 2 cytokines IL-4 and IL-13 have pivotal roles in the pathogenesis of AD. Lesional skin of AD expresses...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Furue, Masutaka [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2019 |
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| Schlagwörter: |
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| Anmerkung: |
© Springer Nature Switzerland AG 2019 |
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| Übergeordnetes Werk: |
Enthalten in: Current treatment options in allergy - Cham : Springer Internat. Publ., 2014, 6(2019), 3 vom: 09. Juli, Seite 200-210 |
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| Übergeordnetes Werk: |
volume:6 ; year:2019 ; number:3 ; day:09 ; month:07 ; pages:200-210 |
| Links: |
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| DOI / URN: |
10.1007/s40521-019-00219-w |
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| Katalog-ID: |
SPR036620300 |
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| 245 | 1 | 0 | |a Atopic Dermatitis and Type 2 Immune Deviation |
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| 520 | |a Purpose of the review To summarize recent topics on type 2 signatures in atopic dermatitis (AD). Recent findings Therapeutic success of anti-IL-4 receptor antibody dupilumab does suggest that type 2 cytokines IL-4 and IL-13 have pivotal roles in the pathogenesis of AD. Lesional skin of AD expresses increased levels of IL-4 and IL-13. In parallel, type 2 chemokines such as CCL17, CCL22, and CCL26 are overexpressed in AD, and these chemokines recruit type 2 T cells and eosinophils. IL-4 and IL-13 downregulate the expression of filaggrin and exacerbate epidermal barrier dysfunction. Keratinocytes in barrier-disrupted epidermis produce thymic stromal lymphopoietin, IL-25 and IL-33, which enhance the type 2 immune response. IL-31, released from type 2 T cells, is an essential pruritogenic cytokine. IL-4 and IL-13 amplify the IL-31-mediated neuronal signal. Summary Type 2 cytokines IL-4 and IL-13 are profoundly associated with three cardinal features of AD: barrier dysfunction, skin inflammation, and chronic pruritus. These findings explain the high efficacy of dupilumab in the treatment of AD. | ||
| 650 | 4 | |a Atopic dermatitis |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Dupilumab |7 (dpeaa)DE-He213 | |
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| 700 | 1 | |a Tsuji, Gaku |4 aut | |
| 700 | 1 | |a Kido-Nakahara, Makiko |4 aut | |
| 700 | 1 | |a Nakahara, Takeshi |4 aut | |
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10.1007/s40521-019-00219-w doi (DE-627)SPR036620300 (SPR)s40521-019-00219-w-e DE-627 ger DE-627 rakwb eng Furue, Masutaka verfasserin aut Atopic Dermatitis and Type 2 Immune Deviation 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer Nature Switzerland AG 2019 Purpose of the review To summarize recent topics on type 2 signatures in atopic dermatitis (AD). Recent findings Therapeutic success of anti-IL-4 receptor antibody dupilumab does suggest that type 2 cytokines IL-4 and IL-13 have pivotal roles in the pathogenesis of AD. Lesional skin of AD expresses increased levels of IL-4 and IL-13. In parallel, type 2 chemokines such as CCL17, CCL22, and CCL26 are overexpressed in AD, and these chemokines recruit type 2 T cells and eosinophils. IL-4 and IL-13 downregulate the expression of filaggrin and exacerbate epidermal barrier dysfunction. Keratinocytes in barrier-disrupted epidermis produce thymic stromal lymphopoietin, IL-25 and IL-33, which enhance the type 2 immune response. IL-31, released from type 2 T cells, is an essential pruritogenic cytokine. IL-4 and IL-13 amplify the IL-31-mediated neuronal signal. Summary Type 2 cytokines IL-4 and IL-13 are profoundly associated with three cardinal features of AD: barrier dysfunction, skin inflammation, and chronic pruritus. These findings explain the high efficacy of dupilumab in the treatment of AD. Atopic dermatitis (dpeaa)DE-He213 Dupilumab (dpeaa)DE-He213 Type 2 immune deviation (dpeaa)DE-He213 Ulzii, Dugarmaa aut Vu, Yen Hai aut Tsuji, Gaku aut Kido-Nakahara, Makiko aut Nakahara, Takeshi aut Enthalten in Current treatment options in allergy Cham : Springer Internat. Publ., 2014 6(2019), 3 vom: 09. Juli, Seite 200-210 (DE-627)780378458 (DE-600)2760308-8 2196-3053 nnns volume:6 year:2019 number:3 day:09 month:07 pages:200-210 https://dx.doi.org/10.1007/s40521-019-00219-w lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER 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_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 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_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_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 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_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 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 6 2019 3 09 07 200-210 |
| spelling |
10.1007/s40521-019-00219-w doi (DE-627)SPR036620300 (SPR)s40521-019-00219-w-e DE-627 ger DE-627 rakwb eng Furue, Masutaka verfasserin aut Atopic Dermatitis and Type 2 Immune Deviation 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer Nature Switzerland AG 2019 Purpose of the review To summarize recent topics on type 2 signatures in atopic dermatitis (AD). Recent findings Therapeutic success of anti-IL-4 receptor antibody dupilumab does suggest that type 2 cytokines IL-4 and IL-13 have pivotal roles in the pathogenesis of AD. Lesional skin of AD expresses increased levels of IL-4 and IL-13. In parallel, type 2 chemokines such as CCL17, CCL22, and CCL26 are overexpressed in AD, and these chemokines recruit type 2 T cells and eosinophils. IL-4 and IL-13 downregulate the expression of filaggrin and exacerbate epidermal barrier dysfunction. Keratinocytes in barrier-disrupted epidermis produce thymic stromal lymphopoietin, IL-25 and IL-33, which enhance the type 2 immune response. IL-31, released from type 2 T cells, is an essential pruritogenic cytokine. IL-4 and IL-13 amplify the IL-31-mediated neuronal signal. Summary Type 2 cytokines IL-4 and IL-13 are profoundly associated with three cardinal features of AD: barrier dysfunction, skin inflammation, and chronic pruritus. These findings explain the high efficacy of dupilumab in the treatment of AD. Atopic dermatitis (dpeaa)DE-He213 Dupilumab (dpeaa)DE-He213 Type 2 immune deviation (dpeaa)DE-He213 Ulzii, Dugarmaa aut Vu, Yen Hai aut Tsuji, Gaku aut Kido-Nakahara, Makiko aut Nakahara, Takeshi aut Enthalten in Current treatment options in allergy Cham : Springer Internat. Publ., 2014 6(2019), 3 vom: 09. Juli, Seite 200-210 (DE-627)780378458 (DE-600)2760308-8 2196-3053 nnns volume:6 year:2019 number:3 day:09 month:07 pages:200-210 https://dx.doi.org/10.1007/s40521-019-00219-w lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER 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_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 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_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_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 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_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 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 6 2019 3 09 07 200-210 |
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10.1007/s40521-019-00219-w doi (DE-627)SPR036620300 (SPR)s40521-019-00219-w-e DE-627 ger DE-627 rakwb eng Furue, Masutaka verfasserin aut Atopic Dermatitis and Type 2 Immune Deviation 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer Nature Switzerland AG 2019 Purpose of the review To summarize recent topics on type 2 signatures in atopic dermatitis (AD). Recent findings Therapeutic success of anti-IL-4 receptor antibody dupilumab does suggest that type 2 cytokines IL-4 and IL-13 have pivotal roles in the pathogenesis of AD. Lesional skin of AD expresses increased levels of IL-4 and IL-13. In parallel, type 2 chemokines such as CCL17, CCL22, and CCL26 are overexpressed in AD, and these chemokines recruit type 2 T cells and eosinophils. IL-4 and IL-13 downregulate the expression of filaggrin and exacerbate epidermal barrier dysfunction. Keratinocytes in barrier-disrupted epidermis produce thymic stromal lymphopoietin, IL-25 and IL-33, which enhance the type 2 immune response. IL-31, released from type 2 T cells, is an essential pruritogenic cytokine. IL-4 and IL-13 amplify the IL-31-mediated neuronal signal. Summary Type 2 cytokines IL-4 and IL-13 are profoundly associated with three cardinal features of AD: barrier dysfunction, skin inflammation, and chronic pruritus. These findings explain the high efficacy of dupilumab in the treatment of AD. Atopic dermatitis (dpeaa)DE-He213 Dupilumab (dpeaa)DE-He213 Type 2 immune deviation (dpeaa)DE-He213 Ulzii, Dugarmaa aut Vu, Yen Hai aut Tsuji, Gaku aut Kido-Nakahara, Makiko aut Nakahara, Takeshi aut Enthalten in Current treatment options in allergy Cham : Springer Internat. Publ., 2014 6(2019), 3 vom: 09. Juli, Seite 200-210 (DE-627)780378458 (DE-600)2760308-8 2196-3053 nnns volume:6 year:2019 number:3 day:09 month:07 pages:200-210 https://dx.doi.org/10.1007/s40521-019-00219-w lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER 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_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 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_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_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 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_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 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 6 2019 3 09 07 200-210 |
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10.1007/s40521-019-00219-w doi (DE-627)SPR036620300 (SPR)s40521-019-00219-w-e DE-627 ger DE-627 rakwb eng Furue, Masutaka verfasserin aut Atopic Dermatitis and Type 2 Immune Deviation 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer Nature Switzerland AG 2019 Purpose of the review To summarize recent topics on type 2 signatures in atopic dermatitis (AD). Recent findings Therapeutic success of anti-IL-4 receptor antibody dupilumab does suggest that type 2 cytokines IL-4 and IL-13 have pivotal roles in the pathogenesis of AD. Lesional skin of AD expresses increased levels of IL-4 and IL-13. In parallel, type 2 chemokines such as CCL17, CCL22, and CCL26 are overexpressed in AD, and these chemokines recruit type 2 T cells and eosinophils. IL-4 and IL-13 downregulate the expression of filaggrin and exacerbate epidermal barrier dysfunction. Keratinocytes in barrier-disrupted epidermis produce thymic stromal lymphopoietin, IL-25 and IL-33, which enhance the type 2 immune response. IL-31, released from type 2 T cells, is an essential pruritogenic cytokine. IL-4 and IL-13 amplify the IL-31-mediated neuronal signal. Summary Type 2 cytokines IL-4 and IL-13 are profoundly associated with three cardinal features of AD: barrier dysfunction, skin inflammation, and chronic pruritus. These findings explain the high efficacy of dupilumab in the treatment of AD. Atopic dermatitis (dpeaa)DE-He213 Dupilumab (dpeaa)DE-He213 Type 2 immune deviation (dpeaa)DE-He213 Ulzii, Dugarmaa aut Vu, Yen Hai aut Tsuji, Gaku aut Kido-Nakahara, Makiko aut Nakahara, Takeshi aut Enthalten in Current treatment options in allergy Cham : Springer Internat. Publ., 2014 6(2019), 3 vom: 09. Juli, Seite 200-210 (DE-627)780378458 (DE-600)2760308-8 2196-3053 nnns volume:6 year:2019 number:3 day:09 month:07 pages:200-210 https://dx.doi.org/10.1007/s40521-019-00219-w lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER 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_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 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_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_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 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_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 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 6 2019 3 09 07 200-210 |
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10.1007/s40521-019-00219-w doi (DE-627)SPR036620300 (SPR)s40521-019-00219-w-e DE-627 ger DE-627 rakwb eng Furue, Masutaka verfasserin aut Atopic Dermatitis and Type 2 Immune Deviation 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer Nature Switzerland AG 2019 Purpose of the review To summarize recent topics on type 2 signatures in atopic dermatitis (AD). Recent findings Therapeutic success of anti-IL-4 receptor antibody dupilumab does suggest that type 2 cytokines IL-4 and IL-13 have pivotal roles in the pathogenesis of AD. Lesional skin of AD expresses increased levels of IL-4 and IL-13. In parallel, type 2 chemokines such as CCL17, CCL22, and CCL26 are overexpressed in AD, and these chemokines recruit type 2 T cells and eosinophils. IL-4 and IL-13 downregulate the expression of filaggrin and exacerbate epidermal barrier dysfunction. Keratinocytes in barrier-disrupted epidermis produce thymic stromal lymphopoietin, IL-25 and IL-33, which enhance the type 2 immune response. IL-31, released from type 2 T cells, is an essential pruritogenic cytokine. IL-4 and IL-13 amplify the IL-31-mediated neuronal signal. Summary Type 2 cytokines IL-4 and IL-13 are profoundly associated with three cardinal features of AD: barrier dysfunction, skin inflammation, and chronic pruritus. These findings explain the high efficacy of dupilumab in the treatment of AD. Atopic dermatitis (dpeaa)DE-He213 Dupilumab (dpeaa)DE-He213 Type 2 immune deviation (dpeaa)DE-He213 Ulzii, Dugarmaa aut Vu, Yen Hai aut Tsuji, Gaku aut Kido-Nakahara, Makiko aut Nakahara, Takeshi aut Enthalten in Current treatment options in allergy Cham : Springer Internat. Publ., 2014 6(2019), 3 vom: 09. Juli, Seite 200-210 (DE-627)780378458 (DE-600)2760308-8 2196-3053 nnns volume:6 year:2019 number:3 day:09 month:07 pages:200-210 https://dx.doi.org/10.1007/s40521-019-00219-w lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER 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_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 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_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_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 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_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 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 6 2019 3 09 07 200-210 |
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English |
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Enthalten in Current treatment options in allergy 6(2019), 3 vom: 09. Juli, Seite 200-210 volume:6 year:2019 number:3 day:09 month:07 pages:200-210 |
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Enthalten in Current treatment options in allergy 6(2019), 3 vom: 09. Juli, Seite 200-210 volume:6 year:2019 number:3 day:09 month:07 pages:200-210 |
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Atopic dermatitis Dupilumab Type 2 immune deviation |
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Current treatment options in allergy |
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Furue, Masutaka @@aut@@ Ulzii, Dugarmaa @@aut@@ Vu, Yen Hai @@aut@@ Tsuji, Gaku @@aut@@ Kido-Nakahara, Makiko @@aut@@ Nakahara, Takeshi @@aut@@ |
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2019-07-09T00:00:00Z |
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780378458 |
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<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">SPR036620300</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230519072534.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">201007s2019 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1007/s40521-019-00219-w</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)SPR036620300</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(SPR)s40521-019-00219-w-e</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">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Furue, Masutaka</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Atopic Dermatitis and Type 2 Immune Deviation</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2019</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">© Springer Nature Switzerland AG 2019</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Purpose of the review To summarize recent topics on type 2 signatures in atopic dermatitis (AD). 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Furue, Masutaka |
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Atopic Dermatitis and Type 2 Immune Deviation Atopic dermatitis (dpeaa)DE-He213 Dupilumab (dpeaa)DE-He213 Type 2 immune deviation (dpeaa)DE-He213 |
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Furue, Masutaka Ulzii, Dugarmaa Vu, Yen Hai Tsuji, Gaku Kido-Nakahara, Makiko Nakahara, Takeshi |
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atopic dermatitis and type 2 immune deviation |
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Atopic Dermatitis and Type 2 Immune Deviation |
| abstract |
Purpose of the review To summarize recent topics on type 2 signatures in atopic dermatitis (AD). Recent findings Therapeutic success of anti-IL-4 receptor antibody dupilumab does suggest that type 2 cytokines IL-4 and IL-13 have pivotal roles in the pathogenesis of AD. Lesional skin of AD expresses increased levels of IL-4 and IL-13. In parallel, type 2 chemokines such as CCL17, CCL22, and CCL26 are overexpressed in AD, and these chemokines recruit type 2 T cells and eosinophils. IL-4 and IL-13 downregulate the expression of filaggrin and exacerbate epidermal barrier dysfunction. Keratinocytes in barrier-disrupted epidermis produce thymic stromal lymphopoietin, IL-25 and IL-33, which enhance the type 2 immune response. IL-31, released from type 2 T cells, is an essential pruritogenic cytokine. IL-4 and IL-13 amplify the IL-31-mediated neuronal signal. Summary Type 2 cytokines IL-4 and IL-13 are profoundly associated with three cardinal features of AD: barrier dysfunction, skin inflammation, and chronic pruritus. These findings explain the high efficacy of dupilumab in the treatment of AD. © Springer Nature Switzerland AG 2019 |
| abstractGer |
Purpose of the review To summarize recent topics on type 2 signatures in atopic dermatitis (AD). Recent findings Therapeutic success of anti-IL-4 receptor antibody dupilumab does suggest that type 2 cytokines IL-4 and IL-13 have pivotal roles in the pathogenesis of AD. Lesional skin of AD expresses increased levels of IL-4 and IL-13. In parallel, type 2 chemokines such as CCL17, CCL22, and CCL26 are overexpressed in AD, and these chemokines recruit type 2 T cells and eosinophils. IL-4 and IL-13 downregulate the expression of filaggrin and exacerbate epidermal barrier dysfunction. Keratinocytes in barrier-disrupted epidermis produce thymic stromal lymphopoietin, IL-25 and IL-33, which enhance the type 2 immune response. IL-31, released from type 2 T cells, is an essential pruritogenic cytokine. IL-4 and IL-13 amplify the IL-31-mediated neuronal signal. Summary Type 2 cytokines IL-4 and IL-13 are profoundly associated with three cardinal features of AD: barrier dysfunction, skin inflammation, and chronic pruritus. These findings explain the high efficacy of dupilumab in the treatment of AD. © Springer Nature Switzerland AG 2019 |
| abstract_unstemmed |
Purpose of the review To summarize recent topics on type 2 signatures in atopic dermatitis (AD). Recent findings Therapeutic success of anti-IL-4 receptor antibody dupilumab does suggest that type 2 cytokines IL-4 and IL-13 have pivotal roles in the pathogenesis of AD. Lesional skin of AD expresses increased levels of IL-4 and IL-13. In parallel, type 2 chemokines such as CCL17, CCL22, and CCL26 are overexpressed in AD, and these chemokines recruit type 2 T cells and eosinophils. IL-4 and IL-13 downregulate the expression of filaggrin and exacerbate epidermal barrier dysfunction. Keratinocytes in barrier-disrupted epidermis produce thymic stromal lymphopoietin, IL-25 and IL-33, which enhance the type 2 immune response. IL-31, released from type 2 T cells, is an essential pruritogenic cytokine. IL-4 and IL-13 amplify the IL-31-mediated neuronal signal. Summary Type 2 cytokines IL-4 and IL-13 are profoundly associated with three cardinal features of AD: barrier dysfunction, skin inflammation, and chronic pruritus. These findings explain the high efficacy of dupilumab in the treatment of AD. © Springer Nature Switzerland AG 2019 |
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Atopic Dermatitis and Type 2 Immune Deviation |
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Ulzii, Dugarmaa Vu, Yen Hai Tsuji, Gaku Kido-Nakahara, Makiko Nakahara, Takeshi |
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| score |
7.401532 |