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Antigen-specific inhibition of the IL-2-driven proliferation of myelin basic protein-reactive, human T cells
J Burns1, L J Krasner, K Littlefield
1Department of Neurology, Veterans Administration Medical Center, Salt Lake City, Utah.
This report examines the antigen-specific inhibition of the IL-2-driven proliferation of autoantigen-reactive, human T cells. Human, myelin basic protein (MBP)-reactive CD4+ cell lines and clones were isolated and maintained in culture by use of IL-2 and periodic antigen stimulation. When freshly isolated antigen-presenting cells (APC) were present, MBP induced proliferation of MBP-reactive T cell populations. However, under different culture conditions, MBP reduced the IL-2-driven proliferation of some MBP-reactive T cell populations. The inhibition of IL-2-driven proliferation did not appear to require CD8+ or OKM 1+ cells since these were not detected when inhibition studies were performed at least 9 days after the last restimulation by irradiated APC and MBP. Supraoptimal concentrations of MBP were not required for inhibition of proliferation. Some heterogeneity of response was apparent since MBP inhibited the IL-2-driven proliferation of some T cell clones while for others MBP had either no effect or produced slight enhancement of proliferation. These results demonstrate an antigen-specific, in vitro immune mechanism that reduces the IL-2-dependent proliferation of autoantigen-reactive, human T cells.
This report examines the antigen-specific inhibition of the IL-2-driven proliferation of autoantigen-reactive, human T cells. Human, myelin basic protein (MBP)-reactive CD4+ cell lines and clones were isolated and maintained in culture by use of IL-2 and periodic antigen stimulation. When freshly isolated antigen-presenting cells (APC) were present, MBP induced proliferation of MBP-reactive T cell populations. However, under different culture conditions, MBP reduced the IL-2-driven proliferation of some MBP-reactive T cell populations. The inhibition of IL-2-driven proliferation did not appear to require CD8+ or OKM 1+ cells since these were not detected when inhibition studies were performed at least 9 days after the last restimulation by irradiated APC and MBP. Supraoptimal concentrations of MBP were not required for inhibition of proliferation. Some heterogeneity of response was apparent since MBP inhibited the IL-2-driven proliferation of some T cell clones while for others MBP had either no effect or produced slight enhancement of proliferation. These results demonstrate an antigen-specific, in vitro immune mechanism that reduces the IL-2-dependent proliferation of autoantigen-reactive, human T cells.