Requirement of CD30 expression on CD4 T cells in the pathogenesis of experimental autoimmune encephalomyelitis

- MOG35-55 peptide-induced EAE is ameliorated in CD30 knockout mice.
- Antigen-specific Th1 and Th17 cells are significantly reduced in CD30 knockout mice.
- CD30 signaling on CD4 T cells induces the encephalitogenic CD4 T cells.

CD30, a member of the tumor necrosis factor receptor superfamily, is expressed preferentially by effector or memory helper T cells. Here we show that experimental autoimmune encephalomyelitis (EAE) is ameliorated with markedly reduced induction of antigen-specific Th1 and Th17 cells in CD30 knockout mice. Passive EAE indicated that CD30 on non-hematopoietic parenchymal cell is not required and mixed bone marrow chimera experiments revealed that CD30 signaling on CD4 T cells amplified the development of antigen-specific and encephalitogenic CD4 T cells. Thus, CD30 expression on CD4 T cells is critically involved in the pathogenesis of central nervous system autoimmunity.

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