Major histocompatibility complex, effect

Wedekind, C., Walker, M. and Little, T.J. (2005) The course of malaria in mice major histocompatibility complex (MHC) effects, but no general MHC heterozygosity advantage in single-strain infections. Genetics 170, 1427-1430. 

Ironically, SE or TSST-1 concentrations that cause T-cell proliferation do not always correlate with receptor affinity. For instance, SEE binds HLA-DR with 100-fold lower affinity relative to the very similarly structured SEA however, SEE stimulates T-cell proliferation to equivalent levels as SEA. The dose-response curves for cytokine and chemokine production in vitro by staphylococcal superantigen-stimulated cells are also very similar despite differences in affmity/specificity for major histocompatibility complex class II and T-cell receptor V/3 molecules. Overall, these observations suggest that the biological effects of staphylococcal superantigens are induced at rather low, nonsaturating occupancy rates not readily classified by typical biokinetics. 

SEA (Leu-48-Gly) and SEB (Phe-44-Ser) mutants unable to bind major histocompatibility complex class II remain emetic but lack T-cell mitogenic effects. " A disulfide loop in SEs, which is absent in the non-enterotoxic TSST-1, may be responsible for the emetic activity of SEs but that too remains controversial. Carboxymethylation of histidines on SEA or SEB generates superantigenic molecules devoid of enter-otoxicity or skin reactivity. This chemically modified SEB also inhibits, perhaps in a competitive fashion, the... 

LPS can be directly mitogenic for T cells [130], but the antitumoral activity of lymphocytes depends on antigen recognition by their TCR in the context of the major histocompatibility complex (MHC) class I or n. Though LPS enhance it, T lymphocyte activity requires APC [131]. The effect of LPS on T lymphocytes has been shown to depend on monocytes independent of MHC, but to be due to the secretion of costimulatory signals and IL-12 in humans [132]. In vivo, LPS induces principally the proliferation of CD8+ T lymphocytes, but also that of CD4+ T and B lymphocytes through the activation of APC and secretion of IFN 0(7(3 in C57BL/6 mice [133],... 

Figure 32.7. Mechanism underlying UVR-induced immune suppression. Uroconic acid, membrane lipids, and DNA are molecular targets. Langerhans cells and keratinocytes are the cellular targets. Mediators produced by skin cells have both local and systemic effects. Abbreviations MHC, major histocompatibility complex ICAM, intracellular adhesion molecule UCA, urocanic acid IL, interleukin PGE, prostaglandin E.

Zhu J, Bengtsson BO, Mix E, Thorell LH, Olsson T, Link H (1994) Effect of monoamine reuptake inhibiting antidepressants on major histocompatibility complex expression on macrophages in normal rats and rats with experimental allergic neuritis (EAN). Immuno-pharmacology 27 225-244. 

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