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致病性 TH17 细胞的诱导和分子特征。

Induction and molecular signature of pathogenic TH17 cells.

机构信息

Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.

出版信息

Nat Immunol. 2012 Oct;13(10):991-9. doi: 10.1038/ni.2416. Epub 2012 Sep 9.

DOI:10.1038/ni.2416
PMID:22961052
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3459594/
Abstract

Interleukin 17 (IL-17)-producing helper T cells (T(H)17 cells) are often present at the sites of tissue inflammation in autoimmune diseases, which has led to the conclusion that T(H)17 cells are main drivers of autoimmune tissue injury. However, not all T(H)17 cells are pathogenic; in fact, T(H)17 cells generated with transforming growth factor-β1 (TGF-β1) and IL-6 produce IL-17 but do not readily induce autoimmune disease without further exposure to IL-23. Here we found that the production of TGF-β3 by developing T(H)17 cells was dependent on IL-23, which together with IL-6 induced very pathogenic T(H)17 cells. Moreover, TGF-β3-induced T(H)17 cells were functionally and molecularly distinct from TGF-β1-induced T(H)17 cells and had a molecular signature that defined pathogenic effector T(H)17 cells in autoimmune disease.

摘要

白细胞介素 17（IL-17）-产生辅助性 T 细胞（T(H)17 细胞）通常存在于自身免疫性疾病的组织炎症部位，这导致了 T(H)17 细胞是自身免疫性组织损伤的主要驱动因素的结论。然而，并非所有的 T(H)17 细胞都是致病性的；事实上，用转化生长因子-β1（TGF-β1）和 IL-6 产生的 T(H)17 细胞产生 IL-17，但如果没有进一步暴露于 IL-23，它们不易诱发自身免疫性疾病。在这里，我们发现，发育中的 T(H)17 细胞产生 TGF-β3 依赖于 IL-23，IL-23 与 IL-6 一起诱导非常致病性的 T(H)17 细胞。此外，TGF-β3 诱导的 T(H)17 细胞在功能和分子上与 TGF-β1 诱导的 T(H)17 细胞不同，并且具有分子特征，定义了自身免疫性疾病中的致病性效应 T(H)17 细胞。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7661/3459594/f404674568c2/nihms398264f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7661/3459594/481f1162d0ff/nihms398264f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7661/3459594/370a22301ed2/nihms398264f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7661/3459594/1428ddffb407/nihms398264f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7661/3459594/ee80ccc451d4/nihms398264f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7661/3459594/f404674568c2/nihms398264f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7661/3459594/481f1162d0ff/nihms398264f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7661/3459594/370a22301ed2/nihms398264f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7661/3459594/1428ddffb407/nihms398264f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7661/3459594/ee80ccc451d4/nihms398264f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7661/3459594/f404674568c2/nihms398264f5.jpg

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本文引用的文献

[1]
Pathogen-induced human TH17 cells produce IFN-γ or IL-10 and are regulated by IL-1β.

Nature. 2012-4-26

[2]
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Nature. 2011-7-17

[3]
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Nat Immunol. 2011-4-24

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The encephalitogenicity of T(H)17 cells is dependent on IL-1- and IL-23-induced production of the cytokine GM-CSF.

Nat Immunol. 2011-4-24

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Nat Immunol. 2011-1-30

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Nature. 2010-10-21

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Nat Immunol. 2010-8-1

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Nat Med. 2010-1-10

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J Immunol. 2009-12-1

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