Abstract
Interactions between mouse lymphoid cell populations across major histocompatibility complex (MHC) differences activate a variety of alloreactive T cells differing in their functional characteristics, cell surface phenotype and molecular specificity. Early studies indicated that class I (i.e., H-2K/D) or class II (i.e., Ia) MHC antigens could stimulate Lyt-1−, 2+ cytolytic or Lyt-1+2− helper/amplifier allospecific T cell populations, respectively (1). However, in recent years such an absolute functional dichotomy of the H-2 complex has been challenged by several lines of evidence. First, class I antigens could in some instances cause strong T cell proliferation, and second, generation of effector cytolytic T cell (CTL) was documented during allogeneic interactions across I-region disparities (2). Class II antigens — besides their crucial role in immunoregulation — may thus function as transplantation antigens controlling skin graft rejection in vivo and cell mediated lympholysis in vitro (3–7). Studies based on genetic evidence, cold target inhibition and blocking of cytolysis by anti- la alloantisera have demonstrated that both I-A and I-E can serve as targets for class II specific CTL populations (8–10). In addition, the latter were shown to differ from class I specific CTL by their Lyt-l+2−or low cell surface phenotype and hence might represent a distinct subset of alloreactive T cells (11).
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Pierres, A. et al. (1982). Cytolytic T Cell Clones against H-2I Region Products: An Analysis Using Monoclonal Antibodies against Ia, Lyt-2 and P94, 180 Cell Surface Antigens. In: Clark, W.R., Golstein, P. (eds) Mechanisms of Cell-Mediated Cytotoxicity. Advances in Experimental Medicine and Biology, vol 146. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-8959-0_30
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DOI: https://doi.org/10.1007/978-1-4684-8959-0_30
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