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Interleukin-7 receptor alpha contributes to experimental autoimmune encephalomyelitis (148.24)
Journal article   Peer reviewed

Interleukin-7 receptor alpha contributes to experimental autoimmune encephalomyelitis (148.24)

Jessica Jopek Ashbaugh, Roberta Brambilla, Thomas Malek and John Bethea
The Journal of immunology (1950), v 186(1_Supplement), pp 148-148.24
01 Apr 2011
DOI: https://doi.org/10.4049/jimmunol.186.Supp.148.24

Abstract

Abstract Multiple sclerosis (MS) is a neurodegenerative disease characterized by extensive inflammation, demyelination, and axonal damage. The interleukin-7 receptor alpha (IL7Rα) chain is an essential subunit for the signaling receptors of both interleukin-7 (IL7) and thymic stromal lymphopoietin (TSLP), which are involved in lymphocyte development, function, and homeostasis. Recently a mutation in the IL7Rα chain locus has been identified as a risk factor for MS. We show that mice with IL7Rα expression limited to thymic tissue (IL7RTgIL7R-/-) display a less severe form of experimental autoimmune encephalomyelitis (EAE), an animal model for MS. However, TSLPR-/- mice showed no protection from disease. Furthermore, anti-IL7Rα treatment in wild type (WT) mice after disease onset significantly decreased EAE severity and lymphocyte infiltration into the CNS, which was accompanied by a relative increase in resident microglia. Additionally, Rag-/- chimeric mice grafted with IL7RTgIL7R-/- or WT bone marrow cells displayed equivalent disease severity, implying that IL7Rα on a non-hematopoietic cell population contributes to EAE. Taken together, our data shows that systemic blockade of IL7Rα reduces EAE severity, and therefore serves as an optimal target for MS therapies.

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