Abstract
The protective activity of anti-Listeria-immune T cells assayed in an adoptive transfer system is H-2 restricted. As shown in the present studies, the demonstration of the restriction is directly dependent on the dose and the relative protective activity of spleen cells. In addition, some H-2-unrestricted protection is conferred predominantly by other than immunoglobulin-negative spleen cells. Thus, the activity of Listeria-immune T cells appears to be "absolutely" restricted and is in this respect comparable to in vivo T-cell-mediated anti-viral protection. The predominant genetic region of H-2 coding for the structures which are mainly involved in this restriction in T-cell immunity to this prototype intracellular bacterium is the I region. The specificity ofListeria-immune T cells is determined by the H-2 haplotype of the donor. Thus, F1 hybrids seem to possess at least two separable sets of T cells, each specific for one parental haplotype. As is true in the virus model, the results cannot distinguish between an altered-self or a dual recognition model of T-cell recognition to explain H-2 restriction. They are, however, compatible with the idea that I-coded cell surface structures may serve as receptors for cell-specific differentiation signals, which trigger direct or lymphokine-mediated activation of macrophages to manifest increased bactericidal capacity. The interesting parallels in selfmarker recognition by T cells in the virus and intracellular bacterium systems, respectively, appear to be reasonably explained by the different types of signals transmitted by T cells to various target cells via the distinctly different selfmarkers employed (i.e., K or D vs. I). © American Society for Clinical Pathology.
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CITATION STYLE
Zinkernagel, R. M., Althage, A., Adler, B., Blanden, R. V., Davidson, W. F., Kees, U., … Shreffler, D. C. (1977). H-2 restriction of cell-mediated immunity to an intracellular bacterium: Effector T cells are specific for listeria antigen in association with H-2I region-coded self-markers*. Journal of Experimental Medicine, 145(5), 1353–1367. https://doi.org/10.1084/jem.145.5.1353
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