Autoimmune arthritis induces paired immunoglobulin‐like receptor B expression on CD4+ T cells from SKG mice |
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| Authors: | Kathrin Rothe Nora Raulien Gabriele Köhler Matthias Pierer Dagmar Quandt Ulf Wagner |
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| Affiliation: | 1. University of Leipzig, Department of Internal Medicine, Division of Rheumatology, Leipzig, Germany;2. Klinikum of Fulda, Institute of Pathology, Fulda, Germany |
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| Abstract: | The chronic, destructive autoimmune arthritis in SKG mice, which closely resembles human rheumatoid arthritis, is the result of self‐reactive T cells escaping thymic deletion. Since the inhibitory receptor LIR‐1 is up‐regulated on auto‐reactive T cells in human rheumatoid arthritis, the role of its murine ortholog PIR‐B was investigated. Peripheral CD4+ T cells from SKG mice were found to frequently express PIR‐B, and this population produces more frequently IL‐17 upon in vitro stimulation compared to PIR‐B? cells. A much larger fraction of PIR‐B+ T cells, however, was found to secret no IL‐17, but IFN‐γ. With regards to the clinical course of the disease, high frequencies of PIR‐B+ CD4+ T cells were found to be associated with a milder course of arthritis, suggesting that the net effect of PIR‐B expression is suppression of autoreactive T cells. Our results indicate that overexpression of PIR‐B on IL‐17‐producing SKG CD4+ T cells might represent an effective counter‐regulatory mechanism against the destructive potential of those cells. More importantly, a major population of PIR‐B+ T cells in SKG mice appears to play an inhibitory role by way of their IFN‐γ production, since high frequencies of those cells ameliorate the disease. |
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| Keywords: | Arthritis CD4+ T cells Inhibitory receptors PIR‐B SKG |
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