IL-25 and IL-25 Receptor Expression on Eosinophils from Subjects with Allergic Asthma
Background: Allergic asthma is an inflammatory airway disease in which Th2 cytokines play an important role. Epithelial-derived interleukin (IL)-25 has been suggested to be important in the maintenance of Th2-type responses. The effects of IL-25 are mediated by the IL-25 receptor, composed of two su...
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| Published in | International archives of allergy and immunology Vol. 163; no. 1; pp. 5 - 10 |
|---|---|
| Main Authors | , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Basel, Switzerland
S. Karger AG
01.01.2014
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| Subjects | |
| Online Access | Get full text |
| ISSN | 1018-2438 1423-0097 1423-0097 |
| DOI | 10.1159/000355331 |
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| Abstract | Background: Allergic asthma is an inflammatory airway disease in which Th2 cytokines play an important role. Epithelial-derived interleukin (IL)-25 has been suggested to be important in the maintenance of Th2-type responses. The effects of IL-25 are mediated by the IL-25 receptor, composed of two subunits, IL-17RA and IL-17RB. Eosinophils are effector cells in allergic asthma. The role of IL-25 in eosinophil function is unknown. This study examined the expression of IL-25 and its receptor on eosinophils in allergic asthmatics compared to atopic nonasthmatics and normal controls. Methods: The expression of IL-25, IL-17RA and IL-17RB on eosinophils, and levels of plasma IL-25 were measured in 14 normal control subjects, 15 atopic nonasthmatics and 14 mild allergic asthmatics. Results: The expression of IL-17RB on eosinophils was significantly higher in allergic asthmatics (43.08%, range 33.96-59.98%) than in atopic nonasthmatics (11.98%, range 6.33-27.11%, p = 0.002) and normal controls (17.70%, range 10.97-38.9%, p = 0.01). IL-17RA expression was also significantly higher in the allergic asthmatic group. No differences were observed in the intracellular expression of IL-25. The concentration of IL-25 in plasma was significantly increased in the allergic asthmatics (145 ng/ml, range 64-290 ng/ml) when compared to the normal controls (21 ng/ml, range 0-116 ng/ml, p = 0.012), but not compared to atopic nonasthmatics. There was a significant negative correlation between FEV 1 % predicted and the IL-25 level in the plasma (r = -0.443, p = 0.003). Conclusions: The increased IL-25 levels in plasma and the expression of IL-17RA and IL-17RB on eosinophils in allergic asthma patients suggests that IL-25 may activate eosinophils during allergic inflammation. |
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| AbstractList | Allergic asthma is an inflammatory airway disease in which Th2 cytokines play an important role. Epithelial-derived interleukin (IL)-25 has been suggested to be important in the maintenance of Th2-type responses. The effects of IL-25 are mediated by the IL-25 receptor, composed of two subunits, IL-17RA and IL-17RB. Eosinophils are effector cells in allergic asthma. The role of IL-25 in eosinophil function is unknown. This study examined the expression of IL-25 and its receptor on eosinophils in allergic asthmatics compared to atopic nonasthmatics and normal controls.
The expression of IL-25, IL-17RA and IL-17RB on eosinophils, and levels of plasma IL-25 were measured in 14 normal control subjects, 15 atopic nonasthmatics and 14 mild allergic asthmatics.
The expression of IL-17RB on eosinophils was significantly higher in allergic asthmatics (43.08%, range 33.96-59.98%) than in atopic nonasthmatics (11.98%, range 6.33-27.11%, p = 0.002) and normal controls (17.70%, range 10.97-38.9%, p = 0.01). IL-17RA expression was also significantly higher in the allergic asthmatic group. No differences were observed in the intracellular expression of IL-25. The concentration of IL-25 in plasma was significantly increased in the allergic asthmatics (145 ng/ml, range 64-290 ng/ml) when compared to the normal controls (21 ng/ml, range 0-116 ng/ml, p = 0.012), but not compared to atopic nonasthmatics. There was a significant negative correlation between FEV1 % predicted and the IL-25 level in the plasma (r = -0.443, p = 0.003).
The increased IL-25 levels in plasma and the expression of IL-17RA and IL-17RB on eosinophils in allergic asthma patients suggests that IL-25 may activate eosinophils during allergic inflammation. Background: Allergic asthma is an inflammatory airway disease in which Th2 cytokines play an important role. Epithelial-derived interleukin (IL)-25 has been suggested to be important in the maintenance of Th2-type responses. The effects of IL-25 are mediated by the IL-25 receptor, composed of two subunits, IL-17RA and IL-17RB. Eosinophils are effector cells in allergic asthma. The role of IL-25 in eosinophil function is unknown. This study examined the expression of IL-25 and its receptor on eosinophils in allergic asthmatics compared to atopic nonasthmatics and normal controls. Methods: The expression of IL-25, IL-17RA and IL-17RB on eosinophils, and levels of plasma IL-25 were measured in 14 normal control subjects, 15 atopic nonasthmatics and 14 mild allergic asthmatics. Results: The expression of IL-17RB on eosinophils was significantly higher in allergic asthmatics (43.08%, range 33.96-59.98%) than in atopic nonasthmatics (11.98%, range 6.33-27.11%, p = 0.002) and normal controls (17.70%, range 10.97-38.9%, p = 0.01). IL-17RA expression was also significantly higher in the allergic asthmatic group. No differences were observed in the intracellular expression of IL-25. The concentration of IL-25 in plasma was significantly increased in the allergic asthmatics (145 ng/ml, range 64-290 ng/ml) when compared to the normal controls (21 ng/ml, range 0-116 ng/ml, p = 0.012), but not compared to atopic nonasthmatics. There was a significant negative correlation between FEV1 % predicted and the IL-25 level in the plasma (r = -0.443, p = 0.003). Conclusions: The increased IL-25 levels in plasma and the expression of IL-17RA and IL-17RB on eosinophils in allergic asthma patients suggests that IL-25 may activate eosinophils during allergic inflammation. copyright 2013 S. Karger AG, Basel Background: Allergic asthma is an inflammatory airway disease in which Th2 cytokines play an important role. Epithelial-derived interleukin (IL)-25 has been suggested to be important in the maintenance of Th2-type responses. The effects of IL-25 are mediated by the IL-25 receptor, composed of two subunits, IL-17RA and IL-17RB. Eosinophils are effector cells in allergic asthma. The role of IL-25 in eosinophil function is unknown. This study examined the expression of IL-25 and its receptor on eosinophils in allergic asthmatics compared to atopic nonasthmatics and normal controls. Methods: The expression of IL-25, IL-17RA and IL-17RB on eosinophils, and levels of plasma IL-25 were measured in 14 normal control subjects, 15 atopic nonasthmatics and 14 mild allergic asthmatics. Results: The expression of IL-17RB on eosinophils was significantly higher in allergic asthmatics (43.08%, range 33.96-59.98%) than in atopic nonasthmatics (11.98%, range 6.33-27.11%, p = 0.002) and normal controls (17.70%, range 10.97-38.9%, p = 0.01). IL-17RA expression was also significantly higher in the allergic asthmatic group. No differences were observed in the intracellular expression of IL-25. The concentration of IL-25 in plasma was significantly increased in the allergic asthmatics (145 ng/ml, range 64-290 ng/ml) when compared to the normal controls (21 ng/ml, range 0-116 ng/ml, p = 0.012), but not compared to atopic nonasthmatics. There was a significant negative correlation between FEV 1 % predicted and the IL-25 level in the plasma (r = -0.443, p = 0.003). Conclusions: The increased IL-25 levels in plasma and the expression of IL-17RA and IL-17RB on eosinophils in allergic asthma patients suggests that IL-25 may activate eosinophils during allergic inflammation. Background: Allergic asthma is an inflammatory airway disease in which Th2 cytokines play an important role. Epithelial-derived interleukin (IL)-25 has been suggested to be important in the maintenance of Th2-type responses. The effects of IL-25 are mediated by the IL-25 receptor, composed of two subunits, IL-17RA and IL-17RB. Eosinophils are effector cells in allergic asthma. The role of IL-25 in eosinophil function is unknown. This study examined the expression of IL-25 and its receptor on eosinophils in allergic asthmatics compared to atopic nonasthmatics and normal controls. Methods: The expression of IL-25, IL-17RA and IL-17RB on eosinophils, and levels of plasma IL-25 were measured in 14 normal control subjects, 15 atopic nonasthmatics and 14 mild allergic asthmatics. Results: The expression of IL-17RB on eosinophils was significantly higher in allergic asthmatics (43.08%, range 33.96-59.98%) than in atopic nonasthmatics (11.98%, range 6.33-27.11%, p = 0.002) and normal controls (17.70%, range 10.97-38.9%, p = 0.01). IL-17RA expression was also significantly higher in the allergic asthmatic group. No differences were observed in the intracellular expression of IL-25. The concentration of IL-25 in plasma was significantly increased in the allergic asthmatics (145 ng/ml, range 64-290 ng/ml) when compared to the normal controls (21 ng/ml, range 0-116 ng/ml, p = 0.012), but not compared to atopic nonasthmatics. There was a significant negative correlation between FEV1 % predicted and the IL-25 level in the plasma (r = -0.443, p = 0.003). Conclusions: The increased IL-25 levels in plasma and the expression of IL-17RA and IL-17RB on eosinophils in allergic asthma patients suggests that IL-25 may activate eosinophils during allergic inflammation. Allergic asthma is an inflammatory airway disease in which Th2 cytokines play an important role. Epithelial-derived interleukin (IL)-25 has been suggested to be important in the maintenance of Th2-type responses. The effects of IL-25 are mediated by the IL-25 receptor, composed of two subunits, IL-17RA and IL-17RB. Eosinophils are effector cells in allergic asthma. The role of IL-25 in eosinophil function is unknown. This study examined the expression of IL-25 and its receptor on eosinophils in allergic asthmatics compared to atopic nonasthmatics and normal controls.BACKGROUNDAllergic asthma is an inflammatory airway disease in which Th2 cytokines play an important role. Epithelial-derived interleukin (IL)-25 has been suggested to be important in the maintenance of Th2-type responses. The effects of IL-25 are mediated by the IL-25 receptor, composed of two subunits, IL-17RA and IL-17RB. Eosinophils are effector cells in allergic asthma. The role of IL-25 in eosinophil function is unknown. This study examined the expression of IL-25 and its receptor on eosinophils in allergic asthmatics compared to atopic nonasthmatics and normal controls.The expression of IL-25, IL-17RA and IL-17RB on eosinophils, and levels of plasma IL-25 were measured in 14 normal control subjects, 15 atopic nonasthmatics and 14 mild allergic asthmatics.METHODSThe expression of IL-25, IL-17RA and IL-17RB on eosinophils, and levels of plasma IL-25 were measured in 14 normal control subjects, 15 atopic nonasthmatics and 14 mild allergic asthmatics.The expression of IL-17RB on eosinophils was significantly higher in allergic asthmatics (43.08%, range 33.96-59.98%) than in atopic nonasthmatics (11.98%, range 6.33-27.11%, p = 0.002) and normal controls (17.70%, range 10.97-38.9%, p = 0.01). IL-17RA expression was also significantly higher in the allergic asthmatic group. No differences were observed in the intracellular expression of IL-25. The concentration of IL-25 in plasma was significantly increased in the allergic asthmatics (145 ng/ml, range 64-290 ng/ml) when compared to the normal controls (21 ng/ml, range 0-116 ng/ml, p = 0.012), but not compared to atopic nonasthmatics. There was a significant negative correlation between FEV1 % predicted and the IL-25 level in the plasma (r = -0.443, p = 0.003).RESULTSThe expression of IL-17RB on eosinophils was significantly higher in allergic asthmatics (43.08%, range 33.96-59.98%) than in atopic nonasthmatics (11.98%, range 6.33-27.11%, p = 0.002) and normal controls (17.70%, range 10.97-38.9%, p = 0.01). IL-17RA expression was also significantly higher in the allergic asthmatic group. No differences were observed in the intracellular expression of IL-25. The concentration of IL-25 in plasma was significantly increased in the allergic asthmatics (145 ng/ml, range 64-290 ng/ml) when compared to the normal controls (21 ng/ml, range 0-116 ng/ml, p = 0.012), but not compared to atopic nonasthmatics. There was a significant negative correlation between FEV1 % predicted and the IL-25 level in the plasma (r = -0.443, p = 0.003).The increased IL-25 levels in plasma and the expression of IL-17RA and IL-17RB on eosinophils in allergic asthma patients suggests that IL-25 may activate eosinophils during allergic inflammation.CONCLUSIONSThe increased IL-25 levels in plasma and the expression of IL-17RA and IL-17RB on eosinophils in allergic asthma patients suggests that IL-25 may activate eosinophils during allergic inflammation. Background: Allergic asthma is an inflammatory airway disease in which Th2 cytokines play an important role. Epithelial-derived interleukin (IL)-25 has been suggested to be important in the maintenance of Th2-type responses. The effects of IL-25 are mediated by the IL-25 receptor, composed of two subunits, IL-17RA and IL-17RB. Eosinophils are effector cells in allergic asthma. The role of IL-25 in eosinophil function is unknown. This study examined the expression of IL-25 and its receptor on eosinophils in allergic asthmatics compared to atopic nonasthmatics and normal controls. Methods: The expression of IL-25, IL-17RA and IL-17RB on eosinophils, and levels of plasma IL-25 were measured in 14 normal control subjects, 15 atopic nonasthmatics and 14 mild allergic asthmatics. Results: The expression of IL-17RB on eosinophils was significantly higher in allergic asthmatics (43.08%, range 33.96-59.98%) than in atopic nonasthmatics (11.98%, range 6.33-27.11%, p = 0.002) and normal controls (17.70%, range 10.97-38.9%, p = 0.01). IL-17RA expression was also significantly higher in the allergic asthmatic group. No differences were observed in the intracellular expression of IL-25. The concentration of IL-25 in plasma was significantly increased in the allergic asthmatics (145 ng/ml, range 64-290 ng/ml) when compared to the normal controls (21 ng/ml, range 0-116 ng/ml, p = 0.012), but not compared to atopic nonasthmatics. There was a significant negative correlation between FEV1 % predicted and the IL-25 level in the plasma (r = -0.443, p = 0.003). Conclusions: The increased IL-25 levels in plasma and the expression of IL-17RA and IL-17RB on eosinophils in allergic asthma patients suggests that IL-25 may activate eosinophils during allergic inflammation. © 2013 S. Karger AG, Basel [PUBLICATION ABSTRACT] |
| Author | O'Byrne, Paul M. Howie, Karen Tang, Wei Smith, Steven G. Beaudin, Sue Dua, Benny Gauvreau, Gail |
| Author_xml | – sequence: 1 givenname: Wei surname: Tang fullname: Tang, Wei – sequence: 2 givenname: Steven G. surname: Smith fullname: Smith, Steven G. – sequence: 3 givenname: Sue surname: Beaudin fullname: Beaudin, Sue – sequence: 4 givenname: Benny surname: Dua fullname: Dua, Benny – sequence: 5 givenname: Karen surname: Howie fullname: Howie, Karen – sequence: 6 givenname: Gail surname: Gauvreau fullname: Gauvreau, Gail – sequence: 7 givenname: Paul M. surname: O'Byrne fullname: O'Byrne, Paul M. email: obyrnep@mcmaster.ca |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/24247484$$D View this record in MEDLINE/PubMed |
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| Keywords | Interleukin 17 family Allergic inflammation Asthma Eosinophils |
| Language | English |
| License | Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. https://www.karger.com/Services/SiteLicenses 2013 S. Karger AG, Basel. |
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| References | Gaffen SL: Structure and signalling in the IL-17 receptor superfamily. Nat Rev Immunol 2009;9:556-567.1957502810.1038/nri2586 Dolgachev V, Petersen BC, Budelsky AL, Berlin AA, Lukacs NW: Pulmonary IL-17E (IL-25) production and IL-17RB+ myeloid cell-derived Th2 cytokine production are dependent upon stem cell factor-induced responses during chronic allergic pulmonary disease. J Immunol 2009;183:5705-5715.1982863610.4049/jimmunol.0901666 Hurst SD, Muchamuel T, Gorman DM, et al: New IL-17 family members promote Th1 or Th2 responses in the lung: in vivo function of the novel cytokine IL-25. J Immunol 2002;169:443-453.12077275 Cheung PF, Wong CK, Ip WK, Lam CW: IL-25 regulates the expression of adhesion molecules on eosinophils: mechanism of eosinophilia in allergic inflammation. Allergy 2006;61:878-885.1679258810.1111/j.1398-9995.2006.01102.x Kim MR, Manoukian R, Yeh R, et al: Transgenic overexpression of human IL-17E results in eosinophilia, B-lymphocyte hyperplasia, and altered antibody production. Blood 2002;100:2330-2340.1223914010.1182/blood-2002-01-0012 Angkasekwinai P, Park H, Wang YH, et al: Interleukin 25 promotes the initiation of proallergic type 2 responses. J Exp Med 2007;204:1509-1517.1756281410.1084/jem.20061675 Corrigan CJ, Wang W, Meng Q, et al: Allergen-induced expression of IL-25 and IL-25 receptor in atopic asthmatic airways and late-phase cutaneous responses. J Allergy Clin Immunol 2011;128:116-124.2157071910.1016/j.jaci.2011.03.043 Terrier B, Biéche I, Maisonobe T, et al: Interleukin-25: a cytokine linking eosinophils and adaptive immunity in Churg-Strauss syndrome. Blood 2010;116:4523-4531.2072946810.1182/blood-2010-02-267542 Barlow JL, McKenzie AN: IL-25: a key requirement for the regulation of type-2 immunity. Biofactors 2009;35:178-182.1944944610.1002/biof.24 Humbles AA, Lloyd CM, McMillan SJ, et al: A critical role for eosinophils in allergic airways remodeling. Science 2004;305:1776-1779.1537526810.1126/science.1100283 Fort MM, Cheung J, Yen D, et al: IL-25 induces IL-4, IL-5, and IL-13 and Th2-associated pathologies in vivo. Immunity 2001:15:985-995.1175481910.1016/S1074-7613(01)00243-6 Zhao Y, Yang J, Gao YD, et al: Th17 immunity in patients with allergic asthma. Int Arch Allergy Immunol 2010;151:297-307.1984412910.1159/000250438 Wang YH, Liu YJ: Thymic stromal lymphopoietin, OX40-ligand, and interleukin-25 in allergic responses. Clin Exp Allergy 2009;39:798-806.1940090810.1111/j.1365-2222.2009.03241.x Chang SH, Dong C: Signaling of interleukin-17 family cytokines in immunity and inflammation. Cellular Signalling 2011;23:1069-1075.2113087210.1016/j.cellsig.2010.11.022 Saenz SA, Taylor BC, Artis D: Welcome to the neighborhood: epithelial cell-derived cytokines license innate and adaptive immune responses at mucosal sites. Immunol Rev 2008;226:172-190.1916142410.1111/j.1600-065X.2008.00713.x Wang YH, Angkasekwinai P, Lu N, et al: IL-25 augments type 2 immune responses by enhancing the expansion and functions of TSLP-DC-activated Th2 memory cells. J Exp Med 2007;204:1837-1847.1763595510.1084/jem.20070406 Ballantyne SJ, Barlow JL, Jolin HE, et al: Blocking IL-25 prevents airway hyperresponsiveness in allergic asthma. J Allergy Clin Immunol 2007;120:1324-1331.1788929010.1016/j.jaci.2007.07.051 Dong C: Regulation and pro-inflammatory function of interleukin-17 family cytokines. Immunol Rev 2008;226:80-86.1916141710.1111/j.1600-065X.2008.00709.x Wong CK, Cheung PF, Ip WK, Lam CW: Interleukin-25-induced chemokines and interleukin-6 release from eosinophils is mediated by p38 mitogen-activated protein kinase, c-Jun N-terminal kinase, and nuclear factor-kappaB. Am J Respir Cell Mol Biol 2005;33:186-194.1586079510.1165/rcmb.2005-0034OC Rickel EA, Siegel LA, Yoon BR, et al: Identification of functional roles for both IL-17RB and IL-17RA in mediating IL-25-induced activities. J Immunol 2008;181:4299-4310.18768888 Lee J, Ho WH, Maruoka M, et al: IL-17E, a novel proinflammatory ligand for the IL-17 receptor homolog IL-17Rh1. J Biol Chem 2001;276:1660-1664.1105859710.1074/jbc.M008289200 ref13 ref12 ref15 ref14 ref11 ref10 ref2 ref1 ref17 ref16 ref19 ref18 ref8 ref7 ref9 ref4 ref3 ref6 ref5 |
| References_xml | – reference: Chang SH, Dong C: Signaling of interleukin-17 family cytokines in immunity and inflammation. Cellular Signalling 2011;23:1069-1075.2113087210.1016/j.cellsig.2010.11.022 – reference: Wong CK, Cheung PF, Ip WK, Lam CW: Interleukin-25-induced chemokines and interleukin-6 release from eosinophils is mediated by p38 mitogen-activated protein kinase, c-Jun N-terminal kinase, and nuclear factor-kappaB. Am J Respir Cell Mol Biol 2005;33:186-194.1586079510.1165/rcmb.2005-0034OC – reference: Corrigan CJ, Wang W, Meng Q, et al: Allergen-induced expression of IL-25 and IL-25 receptor in atopic asthmatic airways and late-phase cutaneous responses. J Allergy Clin Immunol 2011;128:116-124.2157071910.1016/j.jaci.2011.03.043 – reference: Ballantyne SJ, Barlow JL, Jolin HE, et al: Blocking IL-25 prevents airway hyperresponsiveness in allergic asthma. J Allergy Clin Immunol 2007;120:1324-1331.1788929010.1016/j.jaci.2007.07.051 – reference: Saenz SA, Taylor BC, Artis D: Welcome to the neighborhood: epithelial cell-derived cytokines license innate and adaptive immune responses at mucosal sites. Immunol Rev 2008;226:172-190.1916142410.1111/j.1600-065X.2008.00713.x – reference: Dong C: Regulation and pro-inflammatory function of interleukin-17 family cytokines. Immunol Rev 2008;226:80-86.1916141710.1111/j.1600-065X.2008.00709.x – reference: Zhao Y, Yang J, Gao YD, et al: Th17 immunity in patients with allergic asthma. Int Arch Allergy Immunol 2010;151:297-307.1984412910.1159/000250438 – reference: Humbles AA, Lloyd CM, McMillan SJ, et al: A critical role for eosinophils in allergic airways remodeling. Science 2004;305:1776-1779.1537526810.1126/science.1100283 – reference: Barlow JL, McKenzie AN: IL-25: a key requirement for the regulation of type-2 immunity. Biofactors 2009;35:178-182.1944944610.1002/biof.24 – reference: Angkasekwinai P, Park H, Wang YH, et al: Interleukin 25 promotes the initiation of proallergic type 2 responses. J Exp Med 2007;204:1509-1517.1756281410.1084/jem.20061675 – reference: Cheung PF, Wong CK, Ip WK, Lam CW: IL-25 regulates the expression of adhesion molecules on eosinophils: mechanism of eosinophilia in allergic inflammation. Allergy 2006;61:878-885.1679258810.1111/j.1398-9995.2006.01102.x – reference: Kim MR, Manoukian R, Yeh R, et al: Transgenic overexpression of human IL-17E results in eosinophilia, B-lymphocyte hyperplasia, and altered antibody production. Blood 2002;100:2330-2340.1223914010.1182/blood-2002-01-0012 – reference: Dolgachev V, Petersen BC, Budelsky AL, Berlin AA, Lukacs NW: Pulmonary IL-17E (IL-25) production and IL-17RB+ myeloid cell-derived Th2 cytokine production are dependent upon stem cell factor-induced responses during chronic allergic pulmonary disease. J Immunol 2009;183:5705-5715.1982863610.4049/jimmunol.0901666 – reference: Hurst SD, Muchamuel T, Gorman DM, et al: New IL-17 family members promote Th1 or Th2 responses in the lung: in vivo function of the novel cytokine IL-25. J Immunol 2002;169:443-453.12077275 – reference: Lee J, Ho WH, Maruoka M, et al: IL-17E, a novel proinflammatory ligand for the IL-17 receptor homolog IL-17Rh1. J Biol Chem 2001;276:1660-1664.1105859710.1074/jbc.M008289200 – reference: Wang YH, Liu YJ: Thymic stromal lymphopoietin, OX40-ligand, and interleukin-25 in allergic responses. Clin Exp Allergy 2009;39:798-806.1940090810.1111/j.1365-2222.2009.03241.x – reference: Terrier B, Biéche I, Maisonobe T, et al: Interleukin-25: a cytokine linking eosinophils and adaptive immunity in Churg-Strauss syndrome. Blood 2010;116:4523-4531.2072946810.1182/blood-2010-02-267542 – reference: Fort MM, Cheung J, Yen D, et al: IL-25 induces IL-4, IL-5, and IL-13 and Th2-associated pathologies in vivo. Immunity 2001:15:985-995.1175481910.1016/S1074-7613(01)00243-6 – reference: Wang YH, Angkasekwinai P, Lu N, et al: IL-25 augments type 2 immune responses by enhancing the expansion and functions of TSLP-DC-activated Th2 memory cells. J Exp Med 2007;204:1837-1847.1763595510.1084/jem.20070406 – reference: Rickel EA, Siegel LA, Yoon BR, et al: Identification of functional roles for both IL-17RB and IL-17RA in mediating IL-25-induced activities. J Immunol 2008;181:4299-4310.18768888 – reference: Gaffen SL: Structure and signalling in the IL-17 receptor superfamily. Nat Rev Immunol 2009;9:556-567.1957502810.1038/nri2586 – ident: ref8 doi: 10.1111/j.1600-065X.2008.00713.x – ident: ref3 doi: 10.1016/S1074-7613(01)00243-6 – ident: ref19 doi: 10.1159/000250438 – ident: ref11 doi: 10.1038/nri2586 – ident: ref17 doi: 10.1002/biof.24 – ident: ref2 doi: 10.1111/j.1600-065X.2008.00709.x – ident: ref16 doi: 10.1084/jem.20070406 – ident: ref10 doi: 10.1074/jbc.M008289200 – ident: ref12 doi: 10.1111/j.1398-9995.2006.01102.x – ident: ref14 doi: 10.1182/blood-2010-02-267542 – ident: ref9 doi: 10.1016/j.cellsig.2010.11.022 – ident: ref15 doi: 10.4049/jimmunol.0901666 – ident: ref1 doi: 10.1126/science.1100283 – ident: ref18 doi: 10.1016/j.jaci.2011.03.043 – ident: ref13 doi: 10.1165/rcmb.2005-0034OC – ident: ref6 doi: 10.1084/jem.20061675 – ident: ref7 doi: 10.1111/j.1365-2222.2009.03241.x – ident: ref4 doi: 10.1182/blood-2002-01-0012 – ident: ref5 doi: 10.1016/j.jaci.2007.07.051 |
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| Snippet | Background: Allergic asthma is an inflammatory airway disease in which Th2 cytokines play an important role. Epithelial-derived interleukin (IL)-25 has been... Allergic asthma is an inflammatory airway disease in which Th2 cytokines play an important role. Epithelial-derived interleukin (IL)-25 has been suggested to... |
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| SubjectTerms | Adult Allergies Asthma Asthma - genetics Asthma - immunology Asthma - metabolism Asthma - pathology Case-Control Studies Eosinophils - immunology Eosinophils - metabolism Eosinophils - pathology Female Gene Expression Humans Hypersensitivity, Immediate - genetics Hypersensitivity, Immediate - immunology Hypersensitivity, Immediate - metabolism Hypersensitivity, Immediate - pathology Interleukin-17 - blood Interleukin-17 - genetics Interleukin-17 - immunology Leukocyte Count Male Middle Aged Neurons Neutrophil Activation Original Paper Protein Subunits - genetics Protein Subunits - immunology Protein Subunits - metabolism Receptors, Interleukin-17 - genetics Receptors, Interleukin-17 - immunology Receptors, Interleukin-17 - metabolism |
| Title | IL-25 and IL-25 Receptor Expression on Eosinophils from Subjects with Allergic Asthma |
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