A Paradoxical Effect of Systemic IL-23 in EAE – Limitation of Autoimmune Inflammatory Demyelination

T. Touil, N. Chu, U. Bohlmann, P. Bargsten, L. Yonghai, Denise Fitzgerald, G. Zhang, B. Becher, A.M. Rostami, B. Gran

Research output: Contribution to journalArticlepeer-review

Abstract

The heterodimeric cytokine IL-23 plays a non-redundant function in the development of cell-mediated, organspecific autoimmune diseases such as experimental autoimmune encephalomyelitis (EAE). To further characterize the mechanisms of action of IL-23 in autoimmune inflammation, we administered IL-23 systemically at different time points during both relapsing and chronic EAE. Surprisingly, we found suppression of disease in all treatment protocols. We observed a reduction in the number of activated macrophages and microglia in the CNS, while T cell infiltration was not significantly affected. Disease suppression correlated with reduced expansion of myelin-reactive T cells, loss of T-bet expression, loss of lymphoid structures, and increased production of IL-6 and IL-4. Here we describe an unexpected function of exogenous IL-23 in limiting the scope and extent of organ-specific autoimmunity.
Original languageEnglish
Pages (from-to)141-150
Number of pages10
JournalOpen Autoimmunity Journal
Volume2
DOIs
Publication statusPublished - 2010

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