دورية أكاديمية
أعرض في EDS

TCR-independent functions of Th17 cells mediated by the synergistic actions of cytokines of the IL-12 and IL-1 families.

التفاصيل البيبلوغرافية
العنوان: TCR-independent functions of Th17 cells mediated by the synergistic actions of cytokines of the IL-12 and IL-1 families.
المؤلفون: Lee YK; Department of Pathology, University of Alabama at Birmingham, Birmingham, AL, United States of America.; Soonchunhyang Institute of Medi-Bioscience (SIMS), Soonchunhyang University, Cheonan-si, Korea., Landuyt AE; Department of Pathology, University of Alabama at Birmingham, Birmingham, AL, United States of America., Lobionda S; Soonchunhyang Institute of Medi-Bioscience (SIMS), Soonchunhyang University, Cheonan-si, Korea., Sittipo P; Soonchunhyang Institute of Medi-Bioscience (SIMS), Soonchunhyang University, Cheonan-si, Korea., Zhao Q; Department of Medicine, University of Alabama at Birmingham, Birmingham, AL, United States of America., Maynard CL; Department of Pathology, University of Alabama at Birmingham, Birmingham, AL, United States of America.
المصدر: PloS one [PLoS One] 2017 Oct 12; Vol. 12 (10), pp. e0186351. Date of Electronic Publication: 2017 Oct 12 (Print Publication: 2017).
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Public Library of Science Country of Publication: United States NLM ID: 101285081 Publication Model: eCollection Cited Medium: Internet ISSN: 1932-6203 (Electronic) Linking ISSN: 19326203 NLM ISO Abbreviation: PLoS One Subsets: MEDLINE
أسماء مطبوعة: Original Publication: San Francisco, CA : Public Library of Science
مواضيع طبية MeSH: Interleukin-1/*metabolism , Interleukin-12/*metabolism , Receptors, Antigen, T-Cell/*metabolism , Th17 Cells/*metabolism, Animals ; CD4-Positive T-Lymphocytes/cytology ; Cell Differentiation/drug effects ; Cells, Cultured ; Interleukin-1beta/metabolism ; Interleukin-6/pharmacology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Transgenic ; RNA Interference ; Receptors, Antigen, T-Cell/genetics ; STAT3 Transcription Factor/antagonists & inhibitors ; STAT3 Transcription Factor/genetics ; STAT3 Transcription Factor/metabolism ; Signal Transduction/drug effects ; Th1 Cells/cytology ; Th1 Cells/immunology ; Th1 Cells/metabolism ; Th17 Cells/cytology ; Th17 Cells/drug effects ; Transforming Growth Factor beta/pharmacology ; Up-Regulation/drug effects
مستخلص: The development of Th17 cells is accompanied by the acquisition of responsiveness to both IL-12 and IL-23, cytokines with established roles in the development and/or function of Th1 and Th17 cells, respectively. IL-12 signaling promotes antigen-dependent Th1 differentiation but, in combination with IL-18, allows the antigen-independent perpetuation of Th1 responses. On the other hand, while IL-23 is dispensable for initial commitment to the Th17 lineage, it promotes the pathogenic function of the Th17 cells. In this study, we have examined the overlap between Th1 and Th17 cells in their responsiveness to common pro-inflammatory cytokines and how this affects the antigen-independent cytokine responses of Th17 cells. We found that in addition to the IL-1 receptor, developing Th17 cells also up-regulate the IL-18 receptor. Consequently, in the presence of IL-1β or IL-18, and in the absence of TCR activation, Th17 cells produce Th17 lineage cytokines in a STAT3-dependent manner when stimulated with IL-23, and IFN© via a STAT4-dependent mechanism when stimulated with IL-12. Thus, building on previous findings of antigen-induced plasticity of Th17 cells, our results indicate that this potential of Th17 cells extends to their cytokine-dependent antigen-independent responses. Collectively, our data suggest a model whereby signaling via either IL-1β or IL-18 allows for bystander responses of Th17 cells to pathogens or pathogen products that differentially activate innate cell production of IL-12 or IL-23.
References: J Exp Med. 2006 Jul 10;203(7):1685-91. (PMID: 16818675)
Trends Immunol. 2006 Jan;27(1):17-23. (PMID: 16290228)
J Immunol. 2008 Nov 1;181(9):5948-55. (PMID: 18941183)
Nat Immunol. 2007 Dec;8(12):1390-7. (PMID: 17994024)
J Immunol. 2007 Oct 1;179(7):4313-7. (PMID: 17878325)
J Immunol. 2001 Jan 15;166(2):1097-105. (PMID: 11145690)
J Leukoc Biol. 2007 May;81(5):1258-68. (PMID: 17307864)
J Immunol. 2007 Aug 1;179(3):1423-6. (PMID: 17641006)
Cell. 2006 Sep 22;126(6):1121-33. (PMID: 16990136)
Nat Immunol. 2007 Sep;8(9):942-9. (PMID: 17676045)
J Biol Chem. 2007 Mar 30;282(13):9358-63. (PMID: 17277312)
Proc Natl Acad Sci U S A. 2009 Aug 11;106(32):13463-8. (PMID: 19666510)
Immunity. 2009 Nov 20;31(5):787-98. (PMID: 19879162)
Nat Immunol. 2007 Sep;8(9):958-66. (PMID: 17676043)
Eur J Immunol. 1999 Feb;29(2):548-55. (PMID: 10064070)
Nat Immunol. 2009 Mar;10(3):314-24. (PMID: 19182808)
Eur J Immunol. 2008 Oct;38(10):2654-64. (PMID: 18825747)
Immunity. 2010 May 28;32(5):616-27. (PMID: 20471290)
Res Immunol. 1997 Jul-Aug;148(6):413-6. (PMID: 9443580)
Nat Immunol. 2007 Sep;8(9):967-74. (PMID: 17581537)
Nat Immunol. 2002 Jun;3(6):549-57. (PMID: 12006974)
Nat Immunol. 2007 Sep;8(9):950-7. (PMID: 17676044)
J Exp Med. 2012 Feb 13;209(2):251-8. (PMID: 22291094)
Curr Top Microbiol Immunol. 1999;238:13-26. (PMID: 10087648)
Proc Natl Acad Sci U S A. 2007 Jul 17;104(29):12099-104. (PMID: 17623780)
J Immunol. 2014 Feb 15;192(4):1449-58. (PMID: 24431229)
Immunity. 2009 Jan 16;30(1):92-107. (PMID: 19119024)
Nature. 2007 Feb 8;445(7128):648-51. (PMID: 17187052)
Immunity. 1997 Oct;7(4):571-81. (PMID: 9354477)
Cell. 2000 Mar 17;100(6):655-69. (PMID: 10761931)
Immunity. 2006 Jun;24(6):677-88. (PMID: 16782025)
Immunity. 2007 Mar;26(3):371-81. (PMID: 17363300)
Immunity. 2008 Jan;28(1):29-39. (PMID: 18164222)
Immunity. 2008 Jul 18;29(1):44-56. (PMID: 18585065)
J Immunol. 2008 Oct 1;181(7):5120-7. (PMID: 18802116)
Nat Rev Immunol. 2010 Feb;10(2):103-10. (PMID: 20081870)
Arthritis Rheum. 2008 Nov;58(11):3461-70. (PMID: 18975337)
Nature. 2007 Jul 26;448(7152):480-3. (PMID: 17581589)
Cell Host Microbe. 2008 Oct 16;4(4):337-49. (PMID: 18854238)
Annu Rev Immunol. 2007;25:821-52. (PMID: 17201677)
معلومات مُعتمدة: P30 CA013148 United States CA NCI NIH HHS
المشرفين على المادة: 0 (Interleukin-1)
0 (Interleukin-1beta)
0 (Interleukin-6)
0 (Receptors, Antigen, T-Cell)
0 (STAT3 Transcription Factor)
0 (Transforming Growth Factor beta)
187348-17-0 (Interleukin-12)
تواريخ الأحداث: Date Created: 20171013 Date Completed: 20171024 Latest Revision: 20210414
رمز التحديث: 20240628
مُعرف محوري في PubMed: PMC5638524
DOI: 10.1371/journal.pone.0186351
PMID: 29023599
قاعدة البيانات: MEDLINE
الوصف
تدمد:1932-6203
DOI:10.1371/journal.pone.0186351