LOSS OF THYMIC FUNCTION PROMOTES EAE RELAPSE IN ANTI-CD52-TREATED MICE

Loss of thymic function promotes EAE relapse in anti-CD52-treated mice

Loss of thymic function promotes EAE relapse in anti-CD52-treated mice

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Anti-CD52 treatment creates a long-lasting CD4 T cell lymphopenia and reduces multiple orange zinger tomato sclerosis (MS) relapses in humans.In contrast, anti-CD52 therapy at disease onset more fully suppresses experimental autoimmune encephalomyelitis (EAE) in mice, and T cell repopulation is rapid.To test whether prolonged T cell lymphopenia promotes relapses, we thymectomized mice prior to EAE induction and anti-CD52 treatment.Thymectomy greatly reduced the number of recent thymic click here emigrant T cells and was associated with a prolonged reduction in CD4 T cells in peripheral blood.

Two-thirds of thymectomized C57BL/6 mice had an EAE relapse post anti-CD52 treatment, while no surgery and sham surgery euthymic controls remained relapse-free.These data demonstrate that thymus function can alter the effectiveness of anti-CD52 treatment.

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