Chemokine Receptors
Abstract Leukocyte infiltration of the lung is a characteristic feature of allergic asthma and it is thought that these cells are selectively recruited by chemokines. Extensive research has confirmed that chemokine receptors are expressed on the main cell types involved in asthma, including eosinoph...
Ausführliche Beschreibung
Autor*in: |
Lloyd, Clare M. [verfasserIn] |
---|
Format: |
E-Artikel |
---|---|
Sprache: |
Englisch |
Erschienen: |
2006 |
---|
Schlagwörter: |
---|
Anmerkung: |
© adis data information BV 2006 |
---|
Übergeordnetes Werk: |
Enthalten in: American Journal of Respiratory Medicine - Springer International Publishing, 2002, 5(2006), 3 vom: Juni, Seite 159-166 |
---|---|
Übergeordnetes Werk: |
volume:5 ; year:2006 ; number:3 ; month:06 ; pages:159-166 |
Links: |
---|
DOI / URN: |
10.2165/00151829-200605030-00002 |
---|
Katalog-ID: |
SPR035355484 |
---|
LEADER | 01000caa a22002652 4500 | ||
---|---|---|---|
001 | SPR035355484 | ||
003 | DE-627 | ||
005 | 20230519225942.0 | ||
007 | cr uuu---uuuuu | ||
008 | 201007s2006 xx |||||o 00| ||eng c | ||
024 | 7 | |a 10.2165/00151829-200605030-00002 |2 doi | |
035 | |a (DE-627)SPR035355484 | ||
035 | |a (SPR)00151829-200605030-00002-e | ||
040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
041 | |a eng | ||
100 | 1 | |a Lloyd, Clare M. |e verfasserin |4 aut | |
245 | 1 | 0 | |a Chemokine Receptors |
264 | 1 | |c 2006 | |
336 | |a Text |b txt |2 rdacontent | ||
337 | |a Computermedien |b c |2 rdamedia | ||
338 | |a Online-Ressource |b cr |2 rdacarrier | ||
500 | |a © adis data information BV 2006 | ||
520 | |a Abstract Leukocyte infiltration of the lung is a characteristic feature of allergic asthma and it is thought that these cells are selectively recruited by chemokines. Extensive research has confirmed that chemokine receptors are expressed on the main cell types involved in asthma, including eosinophils, T helper type 2 cells, mast cells and even neutrophils. Moreover, animal experiments have outlined a functional role for these receptors and their ligands. Chemokines signal via seven-transmembrane spanning G-protein coupled receptors, which are favored targets of the pharmaceutical industry due to the possibility of designing small-molecule inhibitors. In fact, this family represents the first group of cytokines where small-molecule inhibitors have been designed. However, the search for efficient antagonists of chemokine/chemokine receptors has not been easy; a particular feature of the chemokine system is the number of molecules with overlapping functions and binding specificities, as well as the difficulty in reconciling the in vivo biologic functional validation of chemokines in rodent models with the development of antagonists which bind the human receptor, because of the lack of species cross-reactivity. The chemokines and their receptors that are active during allergic reactions are reviewed. Possible points of interaction that may be a target for development of new therapies, as well as the progress to date in developing inhibitors of key chemokine receptors for asthma therapy, are also discussed. | ||
650 | 4 | |a Asthma |7 (dpeaa)DE-He213 | |
650 | 4 | |a Respiratory Syncytial Virus |7 (dpeaa)DE-He213 | |
650 | 4 | |a Allergic Rhinitis |7 (dpeaa)DE-He213 | |
650 | 4 | |a Chemokine Receptor |7 (dpeaa)DE-He213 | |
650 | 4 | |a Respiratory Syncytial Virus Infection |7 (dpeaa)DE-He213 | |
700 | 1 | |a Brown, Zarin |4 aut | |
773 | 0 | 8 | |i Enthalten in |t American Journal of Respiratory Medicine |d Springer International Publishing, 2002 |g 5(2006), 3 vom: Juni, Seite 159-166 |w (DE-627)SPR035353236 |7 nnns |
773 | 1 | 8 | |g volume:5 |g year:2006 |g number:3 |g month:06 |g pages:159-166 |
856 | 4 | 0 | |u https://dx.doi.org/10.2165/00151829-200605030-00002 |z lizenzpflichtig |3 Volltext |
912 | |a GBV_USEFLAG_A | ||
912 | |a SYSFLAG_A | ||
912 | |a GBV_SPRINGER | ||
912 | |a SSG-OLC-PHA | ||
951 | |a AR | ||
952 | |d 5 |j 2006 |e 3 |c 06 |h 159-166 |
author_variant |
c m l cm cml z b zb |
---|---|
matchkey_str |
lloydclarembrownzarin:2006----:hmknrc |
hierarchy_sort_str |
2006 |
publishDate |
2006 |
allfields |
10.2165/00151829-200605030-00002 doi (DE-627)SPR035355484 (SPR)00151829-200605030-00002-e DE-627 ger DE-627 rakwb eng Lloyd, Clare M. verfasserin aut Chemokine Receptors 2006 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © adis data information BV 2006 Abstract Leukocyte infiltration of the lung is a characteristic feature of allergic asthma and it is thought that these cells are selectively recruited by chemokines. Extensive research has confirmed that chemokine receptors are expressed on the main cell types involved in asthma, including eosinophils, T helper type 2 cells, mast cells and even neutrophils. Moreover, animal experiments have outlined a functional role for these receptors and their ligands. Chemokines signal via seven-transmembrane spanning G-protein coupled receptors, which are favored targets of the pharmaceutical industry due to the possibility of designing small-molecule inhibitors. In fact, this family represents the first group of cytokines where small-molecule inhibitors have been designed. However, the search for efficient antagonists of chemokine/chemokine receptors has not been easy; a particular feature of the chemokine system is the number of molecules with overlapping functions and binding specificities, as well as the difficulty in reconciling the in vivo biologic functional validation of chemokines in rodent models with the development of antagonists which bind the human receptor, because of the lack of species cross-reactivity. The chemokines and their receptors that are active during allergic reactions are reviewed. Possible points of interaction that may be a target for development of new therapies, as well as the progress to date in developing inhibitors of key chemokine receptors for asthma therapy, are also discussed. Asthma (dpeaa)DE-He213 Respiratory Syncytial Virus (dpeaa)DE-He213 Allergic Rhinitis (dpeaa)DE-He213 Chemokine Receptor (dpeaa)DE-He213 Respiratory Syncytial Virus Infection (dpeaa)DE-He213 Brown, Zarin aut Enthalten in American Journal of Respiratory Medicine Springer International Publishing, 2002 5(2006), 3 vom: Juni, Seite 159-166 (DE-627)SPR035353236 nnns volume:5 year:2006 number:3 month:06 pages:159-166 https://dx.doi.org/10.2165/00151829-200605030-00002 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA AR 5 2006 3 06 159-166 |
spelling |
10.2165/00151829-200605030-00002 doi (DE-627)SPR035355484 (SPR)00151829-200605030-00002-e DE-627 ger DE-627 rakwb eng Lloyd, Clare M. verfasserin aut Chemokine Receptors 2006 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © adis data information BV 2006 Abstract Leukocyte infiltration of the lung is a characteristic feature of allergic asthma and it is thought that these cells are selectively recruited by chemokines. Extensive research has confirmed that chemokine receptors are expressed on the main cell types involved in asthma, including eosinophils, T helper type 2 cells, mast cells and even neutrophils. Moreover, animal experiments have outlined a functional role for these receptors and their ligands. Chemokines signal via seven-transmembrane spanning G-protein coupled receptors, which are favored targets of the pharmaceutical industry due to the possibility of designing small-molecule inhibitors. In fact, this family represents the first group of cytokines where small-molecule inhibitors have been designed. However, the search for efficient antagonists of chemokine/chemokine receptors has not been easy; a particular feature of the chemokine system is the number of molecules with overlapping functions and binding specificities, as well as the difficulty in reconciling the in vivo biologic functional validation of chemokines in rodent models with the development of antagonists which bind the human receptor, because of the lack of species cross-reactivity. The chemokines and their receptors that are active during allergic reactions are reviewed. Possible points of interaction that may be a target for development of new therapies, as well as the progress to date in developing inhibitors of key chemokine receptors for asthma therapy, are also discussed. Asthma (dpeaa)DE-He213 Respiratory Syncytial Virus (dpeaa)DE-He213 Allergic Rhinitis (dpeaa)DE-He213 Chemokine Receptor (dpeaa)DE-He213 Respiratory Syncytial Virus Infection (dpeaa)DE-He213 Brown, Zarin aut Enthalten in American Journal of Respiratory Medicine Springer International Publishing, 2002 5(2006), 3 vom: Juni, Seite 159-166 (DE-627)SPR035353236 nnns volume:5 year:2006 number:3 month:06 pages:159-166 https://dx.doi.org/10.2165/00151829-200605030-00002 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA AR 5 2006 3 06 159-166 |
allfields_unstemmed |
10.2165/00151829-200605030-00002 doi (DE-627)SPR035355484 (SPR)00151829-200605030-00002-e DE-627 ger DE-627 rakwb eng Lloyd, Clare M. verfasserin aut Chemokine Receptors 2006 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © adis data information BV 2006 Abstract Leukocyte infiltration of the lung is a characteristic feature of allergic asthma and it is thought that these cells are selectively recruited by chemokines. Extensive research has confirmed that chemokine receptors are expressed on the main cell types involved in asthma, including eosinophils, T helper type 2 cells, mast cells and even neutrophils. Moreover, animal experiments have outlined a functional role for these receptors and their ligands. Chemokines signal via seven-transmembrane spanning G-protein coupled receptors, which are favored targets of the pharmaceutical industry due to the possibility of designing small-molecule inhibitors. In fact, this family represents the first group of cytokines where small-molecule inhibitors have been designed. However, the search for efficient antagonists of chemokine/chemokine receptors has not been easy; a particular feature of the chemokine system is the number of molecules with overlapping functions and binding specificities, as well as the difficulty in reconciling the in vivo biologic functional validation of chemokines in rodent models with the development of antagonists which bind the human receptor, because of the lack of species cross-reactivity. The chemokines and their receptors that are active during allergic reactions are reviewed. Possible points of interaction that may be a target for development of new therapies, as well as the progress to date in developing inhibitors of key chemokine receptors for asthma therapy, are also discussed. Asthma (dpeaa)DE-He213 Respiratory Syncytial Virus (dpeaa)DE-He213 Allergic Rhinitis (dpeaa)DE-He213 Chemokine Receptor (dpeaa)DE-He213 Respiratory Syncytial Virus Infection (dpeaa)DE-He213 Brown, Zarin aut Enthalten in American Journal of Respiratory Medicine Springer International Publishing, 2002 5(2006), 3 vom: Juni, Seite 159-166 (DE-627)SPR035353236 nnns volume:5 year:2006 number:3 month:06 pages:159-166 https://dx.doi.org/10.2165/00151829-200605030-00002 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA AR 5 2006 3 06 159-166 |
allfieldsGer |
10.2165/00151829-200605030-00002 doi (DE-627)SPR035355484 (SPR)00151829-200605030-00002-e DE-627 ger DE-627 rakwb eng Lloyd, Clare M. verfasserin aut Chemokine Receptors 2006 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © adis data information BV 2006 Abstract Leukocyte infiltration of the lung is a characteristic feature of allergic asthma and it is thought that these cells are selectively recruited by chemokines. Extensive research has confirmed that chemokine receptors are expressed on the main cell types involved in asthma, including eosinophils, T helper type 2 cells, mast cells and even neutrophils. Moreover, animal experiments have outlined a functional role for these receptors and their ligands. Chemokines signal via seven-transmembrane spanning G-protein coupled receptors, which are favored targets of the pharmaceutical industry due to the possibility of designing small-molecule inhibitors. In fact, this family represents the first group of cytokines where small-molecule inhibitors have been designed. However, the search for efficient antagonists of chemokine/chemokine receptors has not been easy; a particular feature of the chemokine system is the number of molecules with overlapping functions and binding specificities, as well as the difficulty in reconciling the in vivo biologic functional validation of chemokines in rodent models with the development of antagonists which bind the human receptor, because of the lack of species cross-reactivity. The chemokines and their receptors that are active during allergic reactions are reviewed. Possible points of interaction that may be a target for development of new therapies, as well as the progress to date in developing inhibitors of key chemokine receptors for asthma therapy, are also discussed. Asthma (dpeaa)DE-He213 Respiratory Syncytial Virus (dpeaa)DE-He213 Allergic Rhinitis (dpeaa)DE-He213 Chemokine Receptor (dpeaa)DE-He213 Respiratory Syncytial Virus Infection (dpeaa)DE-He213 Brown, Zarin aut Enthalten in American Journal of Respiratory Medicine Springer International Publishing, 2002 5(2006), 3 vom: Juni, Seite 159-166 (DE-627)SPR035353236 nnns volume:5 year:2006 number:3 month:06 pages:159-166 https://dx.doi.org/10.2165/00151829-200605030-00002 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA AR 5 2006 3 06 159-166 |
allfieldsSound |
10.2165/00151829-200605030-00002 doi (DE-627)SPR035355484 (SPR)00151829-200605030-00002-e DE-627 ger DE-627 rakwb eng Lloyd, Clare M. verfasserin aut Chemokine Receptors 2006 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © adis data information BV 2006 Abstract Leukocyte infiltration of the lung is a characteristic feature of allergic asthma and it is thought that these cells are selectively recruited by chemokines. Extensive research has confirmed that chemokine receptors are expressed on the main cell types involved in asthma, including eosinophils, T helper type 2 cells, mast cells and even neutrophils. Moreover, animal experiments have outlined a functional role for these receptors and their ligands. Chemokines signal via seven-transmembrane spanning G-protein coupled receptors, which are favored targets of the pharmaceutical industry due to the possibility of designing small-molecule inhibitors. In fact, this family represents the first group of cytokines where small-molecule inhibitors have been designed. However, the search for efficient antagonists of chemokine/chemokine receptors has not been easy; a particular feature of the chemokine system is the number of molecules with overlapping functions and binding specificities, as well as the difficulty in reconciling the in vivo biologic functional validation of chemokines in rodent models with the development of antagonists which bind the human receptor, because of the lack of species cross-reactivity. The chemokines and their receptors that are active during allergic reactions are reviewed. Possible points of interaction that may be a target for development of new therapies, as well as the progress to date in developing inhibitors of key chemokine receptors for asthma therapy, are also discussed. Asthma (dpeaa)DE-He213 Respiratory Syncytial Virus (dpeaa)DE-He213 Allergic Rhinitis (dpeaa)DE-He213 Chemokine Receptor (dpeaa)DE-He213 Respiratory Syncytial Virus Infection (dpeaa)DE-He213 Brown, Zarin aut Enthalten in American Journal of Respiratory Medicine Springer International Publishing, 2002 5(2006), 3 vom: Juni, Seite 159-166 (DE-627)SPR035353236 nnns volume:5 year:2006 number:3 month:06 pages:159-166 https://dx.doi.org/10.2165/00151829-200605030-00002 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA AR 5 2006 3 06 159-166 |
language |
English |
source |
Enthalten in American Journal of Respiratory Medicine 5(2006), 3 vom: Juni, Seite 159-166 volume:5 year:2006 number:3 month:06 pages:159-166 |
sourceStr |
Enthalten in American Journal of Respiratory Medicine 5(2006), 3 vom: Juni, Seite 159-166 volume:5 year:2006 number:3 month:06 pages:159-166 |
format_phy_str_mv |
Article |
institution |
findex.gbv.de |
topic_facet |
Asthma Respiratory Syncytial Virus Allergic Rhinitis Chemokine Receptor Respiratory Syncytial Virus Infection |
isfreeaccess_bool |
false |
container_title |
American Journal of Respiratory Medicine |
authorswithroles_txt_mv |
Lloyd, Clare M. @@aut@@ Brown, Zarin @@aut@@ |
publishDateDaySort_date |
2006-06-01T00:00:00Z |
hierarchy_top_id |
SPR035353236 |
id |
SPR035355484 |
language_de |
englisch |
fullrecord |
<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">SPR035355484</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230519225942.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">201007s2006 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.2165/00151829-200605030-00002</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)SPR035355484</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(SPR)00151829-200605030-00002-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">Lloyd, Clare M.</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Chemokine Receptors</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2006</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">© adis data information BV 2006</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Abstract Leukocyte infiltration of the lung is a characteristic feature of allergic asthma and it is thought that these cells are selectively recruited by chemokines. Extensive research has confirmed that chemokine receptors are expressed on the main cell types involved in asthma, including eosinophils, T helper type 2 cells, mast cells and even neutrophils. Moreover, animal experiments have outlined a functional role for these receptors and their ligands. Chemokines signal via seven-transmembrane spanning G-protein coupled receptors, which are favored targets of the pharmaceutical industry due to the possibility of designing small-molecule inhibitors. In fact, this family represents the first group of cytokines where small-molecule inhibitors have been designed. However, the search for efficient antagonists of chemokine/chemokine receptors has not been easy; a particular feature of the chemokine system is the number of molecules with overlapping functions and binding specificities, as well as the difficulty in reconciling the in vivo biologic functional validation of chemokines in rodent models with the development of antagonists which bind the human receptor, because of the lack of species cross-reactivity. The chemokines and their receptors that are active during allergic reactions are reviewed. Possible points of interaction that may be a target for development of new therapies, as well as the progress to date in developing inhibitors of key chemokine receptors for asthma therapy, are also discussed.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Asthma</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Respiratory Syncytial Virus</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Allergic Rhinitis</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Chemokine Receptor</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Respiratory Syncytial Virus Infection</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Brown, Zarin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="t">American Journal of Respiratory Medicine</subfield><subfield code="d">Springer International Publishing, 2002</subfield><subfield code="g">5(2006), 3 vom: Juni, Seite 159-166</subfield><subfield code="w">(DE-627)SPR035353236</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:5</subfield><subfield code="g">year:2006</subfield><subfield code="g">number:3</subfield><subfield code="g">month:06</subfield><subfield code="g">pages:159-166</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://dx.doi.org/10.2165/00151829-200605030-00002</subfield><subfield code="z">lizenzpflichtig</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_A</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_A</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_SPRINGER</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-PHA</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">5</subfield><subfield code="j">2006</subfield><subfield code="e">3</subfield><subfield code="c">06</subfield><subfield code="h">159-166</subfield></datafield></record></collection>
|
author |
Lloyd, Clare M. |
spellingShingle |
Lloyd, Clare M. misc Asthma misc Respiratory Syncytial Virus misc Allergic Rhinitis misc Chemokine Receptor misc Respiratory Syncytial Virus Infection Chemokine Receptors |
authorStr |
Lloyd, Clare M. |
ppnlink_with_tag_str_mv |
@@773@@(DE-627)SPR035353236 |
format |
electronic Article |
delete_txt_mv |
keep |
author_role |
aut aut |
collection |
springer |
remote_str |
true |
illustrated |
Not Illustrated |
topic_title |
Chemokine Receptors Asthma (dpeaa)DE-He213 Respiratory Syncytial Virus (dpeaa)DE-He213 Allergic Rhinitis (dpeaa)DE-He213 Chemokine Receptor (dpeaa)DE-He213 Respiratory Syncytial Virus Infection (dpeaa)DE-He213 |
topic |
misc Asthma misc Respiratory Syncytial Virus misc Allergic Rhinitis misc Chemokine Receptor misc Respiratory Syncytial Virus Infection |
topic_unstemmed |
misc Asthma misc Respiratory Syncytial Virus misc Allergic Rhinitis misc Chemokine Receptor misc Respiratory Syncytial Virus Infection |
topic_browse |
misc Asthma misc Respiratory Syncytial Virus misc Allergic Rhinitis misc Chemokine Receptor misc Respiratory Syncytial Virus Infection |
format_facet |
Elektronische Aufsätze Aufsätze Elektronische Ressource |
format_main_str_mv |
Text Zeitschrift/Artikel |
carriertype_str_mv |
cr |
hierarchy_parent_title |
American Journal of Respiratory Medicine |
hierarchy_parent_id |
SPR035353236 |
hierarchy_top_title |
American Journal of Respiratory Medicine |
isfreeaccess_txt |
false |
familylinks_str_mv |
(DE-627)SPR035353236 |
title |
Chemokine Receptors |
ctrlnum |
(DE-627)SPR035355484 (SPR)00151829-200605030-00002-e |
title_full |
Chemokine Receptors |
author_sort |
Lloyd, Clare M. |
journal |
American Journal of Respiratory Medicine |
journalStr |
American Journal of Respiratory Medicine |
lang_code |
eng |
isOA_bool |
false |
recordtype |
marc |
publishDateSort |
2006 |
contenttype_str_mv |
txt |
container_start_page |
159 |
author_browse |
Lloyd, Clare M. Brown, Zarin |
container_volume |
5 |
format_se |
Elektronische Aufsätze |
author-letter |
Lloyd, Clare M. |
doi_str_mv |
10.2165/00151829-200605030-00002 |
title_sort |
chemokine receptors |
title_auth |
Chemokine Receptors |
abstract |
Abstract Leukocyte infiltration of the lung is a characteristic feature of allergic asthma and it is thought that these cells are selectively recruited by chemokines. Extensive research has confirmed that chemokine receptors are expressed on the main cell types involved in asthma, including eosinophils, T helper type 2 cells, mast cells and even neutrophils. Moreover, animal experiments have outlined a functional role for these receptors and their ligands. Chemokines signal via seven-transmembrane spanning G-protein coupled receptors, which are favored targets of the pharmaceutical industry due to the possibility of designing small-molecule inhibitors. In fact, this family represents the first group of cytokines where small-molecule inhibitors have been designed. However, the search for efficient antagonists of chemokine/chemokine receptors has not been easy; a particular feature of the chemokine system is the number of molecules with overlapping functions and binding specificities, as well as the difficulty in reconciling the in vivo biologic functional validation of chemokines in rodent models with the development of antagonists which bind the human receptor, because of the lack of species cross-reactivity. The chemokines and their receptors that are active during allergic reactions are reviewed. Possible points of interaction that may be a target for development of new therapies, as well as the progress to date in developing inhibitors of key chemokine receptors for asthma therapy, are also discussed. © adis data information BV 2006 |
abstractGer |
Abstract Leukocyte infiltration of the lung is a characteristic feature of allergic asthma and it is thought that these cells are selectively recruited by chemokines. Extensive research has confirmed that chemokine receptors are expressed on the main cell types involved in asthma, including eosinophils, T helper type 2 cells, mast cells and even neutrophils. Moreover, animal experiments have outlined a functional role for these receptors and their ligands. Chemokines signal via seven-transmembrane spanning G-protein coupled receptors, which are favored targets of the pharmaceutical industry due to the possibility of designing small-molecule inhibitors. In fact, this family represents the first group of cytokines where small-molecule inhibitors have been designed. However, the search for efficient antagonists of chemokine/chemokine receptors has not been easy; a particular feature of the chemokine system is the number of molecules with overlapping functions and binding specificities, as well as the difficulty in reconciling the in vivo biologic functional validation of chemokines in rodent models with the development of antagonists which bind the human receptor, because of the lack of species cross-reactivity. The chemokines and their receptors that are active during allergic reactions are reviewed. Possible points of interaction that may be a target for development of new therapies, as well as the progress to date in developing inhibitors of key chemokine receptors for asthma therapy, are also discussed. © adis data information BV 2006 |
abstract_unstemmed |
Abstract Leukocyte infiltration of the lung is a characteristic feature of allergic asthma and it is thought that these cells are selectively recruited by chemokines. Extensive research has confirmed that chemokine receptors are expressed on the main cell types involved in asthma, including eosinophils, T helper type 2 cells, mast cells and even neutrophils. Moreover, animal experiments have outlined a functional role for these receptors and their ligands. Chemokines signal via seven-transmembrane spanning G-protein coupled receptors, which are favored targets of the pharmaceutical industry due to the possibility of designing small-molecule inhibitors. In fact, this family represents the first group of cytokines where small-molecule inhibitors have been designed. However, the search for efficient antagonists of chemokine/chemokine receptors has not been easy; a particular feature of the chemokine system is the number of molecules with overlapping functions and binding specificities, as well as the difficulty in reconciling the in vivo biologic functional validation of chemokines in rodent models with the development of antagonists which bind the human receptor, because of the lack of species cross-reactivity. The chemokines and their receptors that are active during allergic reactions are reviewed. Possible points of interaction that may be a target for development of new therapies, as well as the progress to date in developing inhibitors of key chemokine receptors for asthma therapy, are also discussed. © adis data information BV 2006 |
collection_details |
GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA |
container_issue |
3 |
title_short |
Chemokine Receptors |
url |
https://dx.doi.org/10.2165/00151829-200605030-00002 |
remote_bool |
true |
author2 |
Brown, Zarin |
author2Str |
Brown, Zarin |
ppnlink |
SPR035353236 |
mediatype_str_mv |
c |
isOA_txt |
false |
hochschulschrift_bool |
false |
doi_str |
10.2165/00151829-200605030-00002 |
up_date |
2024-07-03T14:13:42.012Z |
_version_ |
1803567520300400640 |
fullrecord_marcxml |
<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">SPR035355484</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230519225942.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">201007s2006 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.2165/00151829-200605030-00002</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)SPR035355484</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(SPR)00151829-200605030-00002-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">Lloyd, Clare M.</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Chemokine Receptors</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2006</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">© adis data information BV 2006</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Abstract Leukocyte infiltration of the lung is a characteristic feature of allergic asthma and it is thought that these cells are selectively recruited by chemokines. Extensive research has confirmed that chemokine receptors are expressed on the main cell types involved in asthma, including eosinophils, T helper type 2 cells, mast cells and even neutrophils. Moreover, animal experiments have outlined a functional role for these receptors and their ligands. Chemokines signal via seven-transmembrane spanning G-protein coupled receptors, which are favored targets of the pharmaceutical industry due to the possibility of designing small-molecule inhibitors. In fact, this family represents the first group of cytokines where small-molecule inhibitors have been designed. However, the search for efficient antagonists of chemokine/chemokine receptors has not been easy; a particular feature of the chemokine system is the number of molecules with overlapping functions and binding specificities, as well as the difficulty in reconciling the in vivo biologic functional validation of chemokines in rodent models with the development of antagonists which bind the human receptor, because of the lack of species cross-reactivity. The chemokines and their receptors that are active during allergic reactions are reviewed. Possible points of interaction that may be a target for development of new therapies, as well as the progress to date in developing inhibitors of key chemokine receptors for asthma therapy, are also discussed.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Asthma</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Respiratory Syncytial Virus</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Allergic Rhinitis</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Chemokine Receptor</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Respiratory Syncytial Virus Infection</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Brown, Zarin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="t">American Journal of Respiratory Medicine</subfield><subfield code="d">Springer International Publishing, 2002</subfield><subfield code="g">5(2006), 3 vom: Juni, Seite 159-166</subfield><subfield code="w">(DE-627)SPR035353236</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:5</subfield><subfield code="g">year:2006</subfield><subfield code="g">number:3</subfield><subfield code="g">month:06</subfield><subfield code="g">pages:159-166</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://dx.doi.org/10.2165/00151829-200605030-00002</subfield><subfield code="z">lizenzpflichtig</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_A</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_A</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_SPRINGER</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-PHA</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">5</subfield><subfield code="j">2006</subfield><subfield code="e">3</subfield><subfield code="c">06</subfield><subfield code="h">159-166</subfield></datafield></record></collection>
|
score |
7.400728 |