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Originalarbeiten, Bücher, Buchkapitel und Übersichtsartikel von Prof. Marcus Maurer
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Mast Cell Promotion of T Cell–Driven Antigen-Induced Arthritis Despite Being Dispensable for Antibody-Induced Arthritis in Which T Cells Are Bypassed
Filename | 222. Schubert et al., MC prom. arthr., Arthr.andRheumat. 2015.pdf |
Filesize | 974,69 kB |
Version | o.222 |
Date added | Juli 30, 2020 |
Downloaded | 0 times |
Category | Original Work |
Tags | Arthritis, mast cell |
Authors | Schubert, N., Dudeck, J., Liu, P., Karutz, A., Speier, S., Maurer, M. Tuckermann, J., and Dudeck, A. |
Citation | Schubert, N., Dudeck, J., Liu, P., Karutz, A., Speier, S., Maurer, M. Tuckermann, J., and Dudeck, A.+: Mast cell promotion of T cell-driven antigen-induced arthritis despite being dispensable for antibody-induced arthritis in which T cells are bypassed. Arthritis Rheumatol. 2015: 67; 903-913. |
Corresponding authors | Dudeck, A. |
DocNum | O.222 |
DocType | |
Edition; Page | 67; 903-913 |
IF | 6.00 |
Publisher | Arthritis Rheumatol. |
ReleaseDate | 2015 |
Objective: The function of mast cells (MCs) in autoimmune disorders has been a subject of controversy recently. MC-deficient KitW/W-v mice were found to be resistant to K/BxN serum–transfer arthritis, whereas KitW-sh/W-sh mice and a genetic model of MC deficiency independent of the Kit mutation were found to be fully susceptible. This debate might lead to the assumption that MCs are dispensable in autoimmunity in general.Thus, the purpose of this study was to examine the relevance of MCs to arthritis using a genetic model of inducible MC deficiency without compromised Kit signaling.
Methods: We compared MC functions in K/BxN serum–induced arthritis and in collagen-induced arthritis (CIA) in a mouse model of inducible MC deficiency by analyzing joint inflammation, parameters of cartilage degradation and bone erosion, and the autoreactive adaptive immune response.
Results:We observed a redundant role of MCs inK/BxN serum–induced arthritis, where joint inflammation is triggered by cartilage-bound immune complexes independently of T cells. In contrast, we found MCs to be critically relevant in CIA, which is provoked by two arms of autoimmune attack: autoreactive antibodies and effector T cells. In addition to diminished joint inflammation in the absence of MCs, we found a dramatic loss of T cell expansion upon immunization,accompanied by reduced T cell cytokine responses.
Conclusion: In this analysis of an arthritis model in which the cellular arm of adaptive immunity was not bypassed, we identified MCs as important promoters of T cell–conditioned autoimmune disorders and, consequently, as potential therapeutic targets in rheumatoid arthritis.
(Last update: 12.2023)
Number of original publications in peer-reviewed journals: | 580 |
Number of reviews in peer-reviewed journals: | 210 |
Number of publications (original work and reviews) in peer-reviewed journals: | 790 |
Cumulative IF for original publications in peer-reviewed journals: | 4196.39 |
Cumulative IF for reviews in peer-reviewed journals: | 1409.32 |
Cumulative IF of publications (original work & reviews) in peer-reviewed journals: | 5605.71 |
Total number of citations: 36,836, h-index: 99 (Web of Science December 2023) | 36836 |
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