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Intracellular JNK, p38 MAPK and NF-kappaB regulate IL-25 induced release of cytokines and chemokines from costimulated T helper lymphocytes.
Immunol Lett. 2007 Oct 15; 112(2):82-91.IL

Abstract

Novel Th2 cytokine IL-25 has been shown to be elevated in allergic inflammation. We investigated the intracellular mechanisms regulating IL-25-induced Th2 cytokines and chemokines from human Th lymphocytes upon costimulation by anti-CD3 and anti-CD28 antibodies. Cytokines, chemokines, and phosphorylated p38 mitogen activated protein kinases (MAPK), c-Jun amino-terminal kinase (JNK) and extracellular signal-regulated protein kinase were analyzed by bead-based array using flow cytometry. Nuclear factor (NF)-kappaB and total MAPK were assessed by electrophoretic mobility shift assay and Western blot, respectively. IL-25 could synergistically induce the release of Th2 cytokines IL-4, IL-5 and IL-10, inflammatory cytokine IL-6, Th1 related chemokines CXCL9 and CXCL10, and chemokine CCL5 from anti-CD3 and anti-CD28 antibodies costimulated Th cells, especially memory Th cells. Costimulation could also upregulate the cell surface expression of IL-25 receptor on Th cells. Costimulation with or without IL-25 treatment could activate JNK, p38 MAPK and NF-kappaB. The upregulation of costimulation-induced IL-25 receptors and release of cytokines and chemokines from IL-25 treated costimulated Th cells were differentially regulated by intracellular JNK, p38 MAPK and NF-kappaB activity. Therefore, the optimal activation of Th cells by IL-25 for the release of Th2 cytokines and chemokines requires the CD3 and CD28 mediated costimulation of Th cells via the upregulation of IL-25 receptors and the activation of intracellular signaling pathways. This mechanistic study shows that IL-25 and CD28 costimulation can play pathophysiological roles by inducing inflammation and hyperresponsiveness through the production of both Th2 cytokines and chemokines from memory Th cells.

Authors+Show Affiliations

Department of Chemical Pathology, The Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, Hong Kong, China.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

17719653

Citation

Wong, Chun Kwok, et al. "Intracellular JNK, P38 MAPK and NF-kappaB Regulate IL-25 Induced Release of Cytokines and Chemokines From Costimulated T Helper Lymphocytes." Immunology Letters, vol. 112, no. 2, 2007, pp. 82-91.
Wong CK, Li PW, Lam CW. Intracellular JNK, p38 MAPK and NF-kappaB regulate IL-25 induced release of cytokines and chemokines from costimulated T helper lymphocytes. Immunol Lett. 2007;112(2):82-91.
Wong, C. K., Li, P. W., & Lam, C. W. (2007). Intracellular JNK, p38 MAPK and NF-kappaB regulate IL-25 induced release of cytokines and chemokines from costimulated T helper lymphocytes. Immunology Letters, 112(2), 82-91.
Wong CK, Li PW, Lam CW. Intracellular JNK, P38 MAPK and NF-kappaB Regulate IL-25 Induced Release of Cytokines and Chemokines From Costimulated T Helper Lymphocytes. Immunol Lett. 2007 Oct 15;112(2):82-91. PubMed PMID: 17719653.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Intracellular JNK, p38 MAPK and NF-kappaB regulate IL-25 induced release of cytokines and chemokines from costimulated T helper lymphocytes. AU - Wong,Chun Kwok, AU - Li,Pok Wai, AU - Lam,Christopher Wai Kei, Y1 - 2007/08/01/ PY - 2007/03/16/received PY - 2007/07/09/revised PY - 2007/07/09/accepted PY - 2007/8/28/pubmed PY - 2008/2/28/medline PY - 2007/8/28/entrez SP - 82 EP - 91 JF - Immunology letters JO - Immunol Lett VL - 112 IS - 2 N2 - Novel Th2 cytokine IL-25 has been shown to be elevated in allergic inflammation. We investigated the intracellular mechanisms regulating IL-25-induced Th2 cytokines and chemokines from human Th lymphocytes upon costimulation by anti-CD3 and anti-CD28 antibodies. Cytokines, chemokines, and phosphorylated p38 mitogen activated protein kinases (MAPK), c-Jun amino-terminal kinase (JNK) and extracellular signal-regulated protein kinase were analyzed by bead-based array using flow cytometry. Nuclear factor (NF)-kappaB and total MAPK were assessed by electrophoretic mobility shift assay and Western blot, respectively. IL-25 could synergistically induce the release of Th2 cytokines IL-4, IL-5 and IL-10, inflammatory cytokine IL-6, Th1 related chemokines CXCL9 and CXCL10, and chemokine CCL5 from anti-CD3 and anti-CD28 antibodies costimulated Th cells, especially memory Th cells. Costimulation could also upregulate the cell surface expression of IL-25 receptor on Th cells. Costimulation with or without IL-25 treatment could activate JNK, p38 MAPK and NF-kappaB. The upregulation of costimulation-induced IL-25 receptors and release of cytokines and chemokines from IL-25 treated costimulated Th cells were differentially regulated by intracellular JNK, p38 MAPK and NF-kappaB activity. Therefore, the optimal activation of Th cells by IL-25 for the release of Th2 cytokines and chemokines requires the CD3 and CD28 mediated costimulation of Th cells via the upregulation of IL-25 receptors and the activation of intracellular signaling pathways. This mechanistic study shows that IL-25 and CD28 costimulation can play pathophysiological roles by inducing inflammation and hyperresponsiveness through the production of both Th2 cytokines and chemokines from memory Th cells. SN - 0165-2478 UR - https://www.unboundmedicine.com/medline/citation/17719653/Intracellular_JNK_p38_MAPK_and_NF_kappaB_regulate_IL_25_induced_release_of_cytokines_and_chemokines_from_costimulated_T_helper_lymphocytes_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0165-2478(07)00149-6 DB - PRIME DP - Unbound Medicine ER -