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Thy1(+) Sca1(+) innate lymphoid cells infiltrate the CNS during autoimmune inflammation, but do not contribute to disease development


Mair, Florian; Becher, Burkhard (2013). Thy1(+) Sca1(+) innate lymphoid cells infiltrate the CNS during autoimmune inflammation, but do not contribute to disease development. European Journal of Immunology:online.

Abstract

IL-23 is absolutely crucial for the development of T-cell driven autoimmune disease in mice. Even though IL-23 is widely held to be involved in the stabilization of IL-17-secreting T cells, naïve T cells lack the IL-23 receptor. Thus, the primary cellular target of IL-23 in the context of autoimmunity is a subject of some debate. Innate lymphoid cells (ILCs) are a recently discovered family of lymphocytes being involved in early host defense, particularly at mucosal epithelial surfaces. Given the fact that RORγt-dependent ILCs (group 3 ILCs) constitutively express the IL-23-receptor, and that they have been implicated in intestinal autoimmunity, we hypothesized that ILCs could contribute to the early development of autoimmune neuroinflammation. Through systematic analysis, we detected a sizable population of Thy1(+) Sca1(+) ILCs in the inflamed CNS tissue. CNS-infiltrating ILCs were characterized by expression of the IL-7-receptor and production of proinflammatory IL-17 and IFN-γ. Furthermore, genetic fate-mapping revealed their dependence on the transcription factor RORγt. However, upon specific in vivo ablation of this cell population, we found that they do not influence the course of the disease.

Abstract

IL-23 is absolutely crucial for the development of T-cell driven autoimmune disease in mice. Even though IL-23 is widely held to be involved in the stabilization of IL-17-secreting T cells, naïve T cells lack the IL-23 receptor. Thus, the primary cellular target of IL-23 in the context of autoimmunity is a subject of some debate. Innate lymphoid cells (ILCs) are a recently discovered family of lymphocytes being involved in early host defense, particularly at mucosal epithelial surfaces. Given the fact that RORγt-dependent ILCs (group 3 ILCs) constitutively express the IL-23-receptor, and that they have been implicated in intestinal autoimmunity, we hypothesized that ILCs could contribute to the early development of autoimmune neuroinflammation. Through systematic analysis, we detected a sizable population of Thy1(+) Sca1(+) ILCs in the inflamed CNS tissue. CNS-infiltrating ILCs were characterized by expression of the IL-7-receptor and production of proinflammatory IL-17 and IFN-γ. Furthermore, genetic fate-mapping revealed their dependence on the transcription factor RORγt. However, upon specific in vivo ablation of this cell population, we found that they do not influence the course of the disease.

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Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > Institute of Experimental Immunology
Dewey Decimal Classification:570 Life sciences; biology
610 Medicine & health
Language:English
Date:2013
Deposited On:16 Dec 2013 10:05
Last Modified:08 Dec 2017 01:00
Publisher:Wiley-VCH Verlag Berlin
ISSN:0014-2980
Publisher DOI:https://doi.org/10.1002/eji.201343653
PubMed ID:24105463

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