Experimental autoimmune encephalomyelitis (EAE) is an inflammatory autoimmune disease of the central nervous system which serves as a model for the human disease multiple sclerosis. We demonstrate here that encephalitogenic T cells, transduced with a retroviral gene, construct to express interleukin 4, and can delay the onset and reduce the severity of EAE when adoptively transferred to myelin basic protein–immunized mice. Thus, T lymphocytes transduced with retroviral vectors can deliver “regulatory cytokines” in a site-specific manner and may represent a viable therapeutic strategy for the treatment of autoimmune disease.
Atherosclerosis is a chronic inflammatory disease of the artery wall. Atherosclerotic lesions contain monocytes, macrophages, smooth muscle cells and T lymphocytes. Here, we review the role of T-lymphocyte subsets in atherosclerosis. Among CD4⁺T cells, T(h)1 cells are pro-atherogenic, T(reg) cells are athero-protective and the role of T(h)2 and T(h)17 cells remains unclear. The role of follicular helper T cells in atherosclerosis remains unknown, as is the role of CD8⁺T cells. NKT cells bind glycolipid antigens and exert a pro-atherogenic role. The antigen specificity of T-cell responses in atherosclerosis is poorly understood. In order to enable antigen-specific prevention or therapy, a better understanding of these mechanisms is needed.
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