Major histocompatibility, class

Silverman, T., Rein, A., Orrison, B., Langloss, J., Bratthauer, G., Miyazaki, J., andOzato, K. (1988) Establishment of cell lines from somite stage mouse anbryos and expression of major histocompatibility class I genes in these cells. J. Immunol. 140,4378-4387. 

Schmidt, A.M. and Stern, D.M. (2001) Receptor for AGE (RAGE) is a gene within the major histocompatibility class III region implications for host response mechanisms in homeostasis and chronic disease. Front. Biosci. 6, D1151-D1160. 

Frohman EM, Vayuvegula B, Gupta S, van den Noort S (1988) Norepinephrine inhibits gamma-interferon-induced major histocompatibility class II (la) antigen expression on cultured astrocytes via beta-2-adrenergic signal transduction mechanisms. Proc. Natl. AcadSci. USA 85 1292-1296. 

Streptococcus pyogenes and Staphylococcus aureus secrete a number of enterotoxins and pyrogenic exotoxins, respectively. These toxins are known as superantigens, since they simultaneously form complexes with the major histocompatibility class II (MHC-II) molecules and T-cell receptors (TCRs) enabling them to activate a number of T-cell lymphocytes. Thus, superantigens stimulate up to... 

Neumann H, Misgeld T, Matsumuro K, Wekerle H (1998) Neuro-trophins inhibit major histocompatibility class II inducibility of microglia Involvement of the p75 neurotrophin receptor. Proc Natl Acad Sci USA 95 5779-5784. 

Fusion proteins have been constructed from peptide epitopes from influenza A antigens and the binding and translocation domains of Pseudomonas exotoxin A (Donelly ef al., 1993). When target cells were incubated with these fusion proteins, and subsequently exposed to cytotoxic T lymphocytes (CTLs) specific for the relevant epitopes, a CTL mediate lysis of the target cells was observed. These experiments suggest that the translocation machinery supplied by protein toxins may be useful tools for bringing peptides into cells for presentation via the major histocompatibility class I (MHC I) system. It should be noted that no direct evidence was provided that the translocation occurred by the toxin pathway, and it cannot be excluded that the toxin was only instrumental in accumulating the peptide on the surface of the cells and in the endocytic pathway. 

Mudzinski SP, Christian TP, Guo E, Cirenza E, Hazlett KR, Gosselin EJ Expression of HLA-DR (major histocompatibility class II) on neutrophils of patients treated with granulocyte-macrophage colony-stimulating factor for mobilization of stem cells (letter). Blood 1995 86 2452-2453. 

Hansch GM, Radsak M, Wagner C, Reis B, Koch A, Breitbart A, Andrassy K Expression of major histocompatibility class II antigens on polymorphonuclear neutrophils in patients with Wegener s granulomatosis. Kidney Int 1999 55 1811-1818. 

Shirayoshi Y, Burke PA, Appella E, Ozato K (1988) Interferon induced transcription of a major histocompatibility class I gene accompanies binding of inducible nuclear factors to the interferon consensus sequence. Proc Natl Acad Sci USA 85 5884 5888 Silacci P, Mottet A, Steimle V, Reith W, Mach B (1994) Developmental extinction of major histocompatibility complex class II gene expression in plasmocytes is mediated by silencing of the transactivator gene CIITA. J Exp Med 180 1329- 1336... 

Lobigs M, Chelvanayagam G, Mullbacher A (2000) Proteolytic processing of peptides in the lumen of the endoplasmic reticulum for antigen presentation by major histocompatibility class I. Eur J Immunol 30 1496-1506... 

Proteasomes are the major cytosolic and nuclear protein degradation machineries and they are also responsible for the proteolysis of misfolded, ER-dislocated (endoplasmic reticulum) proteins [1-3]. Proteasomal protein turnover takes place in an ubiquitin-dependent manner. The proteasome-generated products - ohgopeptides varying in length from 3 to up to 30 amino acid residues - are further processed by aminopeptidases. In higher vertebrates, antigenic peptides are selected from the peptide pool produced by proteasomes and downstream aminopeptidases for presentation on the outer cell surface by major histocompatibility class 1 (MHCl) protein complexes. In this way, proteasomes are essential factors in the detection and eradication of virally infected cells. 

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