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Thymic stromal lymphopoietin deficiency attenuates experimental autoimmune encephalomyelitis.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Eckhardt, J. Döbbeler, M. König, C. Kuczera, K. Kuhnt, C. Ostalecki, C. Zinser, E. Mak, T. W. Steinkasserer, A. Lechmann, M.
Description	Author Affiliation: Eckhardt J ( Department of Immune Modulation at the Department of Dermatology.); Döbbeler M ( Department of Immune Modulation at the Department of Dermatology.); König C ( Department of Immune Modulation at the Department of Dermatology.); Kuczera K ( Department of Immune Modulation at the Department of Dermatology.); Kuhnt C ( Department of Immune Modulation at the Department of Dermatology.); Ostalecki C ( Department of Dermatology, University Hospital Erlangen, Erlangen, Germany.); Zinser E ( Department of Immune Modulation at the Department of Dermatology.); Mak TW ( The Campbell Family Institute for Breast Cancer Research at Princess Margaret Hospital, University Health Network, Toronto, Ontario, Canada.); Steinkasserer A ( Department of Immune Modulation at the Department of Dermatology.); Lechmann M ( Department of Immune Modulation at the Department of Dermatology.)
Abstract	In the present study we examined the role of thymic stromal lymphopoietin (TSLP) in experimental autoimmune encephalomyelitis (EAE). Here, we report that TSLP knock-out (KO) mice display a delayed onset of disease and an attenuated form of EAE. This delayed onset was accompanied by a reduced number of encephalitogenic T helper type 1 (Th1) cells in the central nervous system (CNS) of TSLP KO mice. In addition, CD4(+) and CD8(+) T cells from CNS of TSLP KO mice show a reduced activation status in comparison to wild-type mice. It is noteworthy that we could also show that lymph node cells from TSLP KO mice expanded less efficiently and that interleukin (IL)-6-, interferon (IFN)-Î³ and tumour necrosis factor (TNF)- levels were reduced. Furthermore, CD3(+) T cells isolated in the preclinical phase from myelin oligodendrocyte glycoprotein peptide 35-55 (MOG(35-55))-immunized TSLP KO mice showed a reduced response after secondary exposure to MOG(35-55), indicating that differentiation of naive T cells into MOG(35-55)-specific effector and memory T cells was impaired in KO mice. The addition of recombinant TSLP enhanced T cell proliferation during MOG(35-55) restimulation, showing that T cells also respond directly to TSLP. In summary, these data demonstrate that expression of, and immune activation by, TSLP contributes significantly to the immunopathology of EAE.
File Format	HTM / HTML
ISSN	00099104
e-ISSN	13652249
DOI	10.1111/cei.12621
Journal	Clinical & Experimental Immunology
Issue Number	1
Volume Number	181
Language	English
Publisher	Wiley-Blackwell
Publisher Date	2015-07-01
Publisher Place	Great Britain (UK)
Access Restriction	Open
Subject Keyword	Discipline Immunology Cd8-positive T-lymphocytes Immunology Cytokines Encephalomyelitis, Autoimmune, Experimental Myelin-oligodendrocyte Glycoprotein Th1 Cells Animals Bone Marrow Cells Cell Proliferation Cells, Cultured Central Nervous System Deficiency Genetics Pathology Inflammation Interferon-gamma Metabolism Interleukin-6 Lymphocyte Activation Mice Mice, Inbred Balb C Mice, Inbred C57bl Mice, Knockout Peptide Fragments Cytology Tumor Necrosis Factor-alpha Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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