MHC genes

Manning C., Wakeland E. and Potts W. (1992). Communal nesting patterns in mice implicate MHC genes in kin recognition. Nature 360, 581-583. 

Until now the reasons for why allergies affect only some patients and not others are not evident. It is also not known what causes an allergy to a specific allergen. A positive correlation between the rate of occurrence of major histocompatibility complex (MHC) genes (especially DR locus) and the frequency of allergies to specific allergens is being verified. 

Odor types distinctive of H2b and Hdh genotypes already appear in the urine of 1-day-old mouse pups (Yamazaki et ah, 1992a). At that age, the normal intestinal bacterial flora is not yet present and hence is not necessary for the odor (Yamazaki et ah, 1992b). In addition to MHC, gene(s) on the X and Y chromosomes and other autosomal genes contribute to individual odors (Yamazaki etal, 1986,1990). 

Some very hydrophobic antigens are presented by neither a class I nor a class II MHC molecule but by members of the CD1 family, leukocyte surface proteins that are not encoded in the MHC gene region.266 271 272... 

Corriveau RA, Huh GS, Shatz CJ. Regulation of class I MHC gene expression in the developing and mature CNS by neural activity. Neuron 1998 21(3) 505-520. 

In theory, all genes coding for products that are involved in the induction and maintenance of self-tolerance and in regulating immune effector functions as well as organ-specific functions may be involved in defining individual susceptibility. The most clearly established genetic association is with specific alleles within the MHC gene complex. However, with rare exceptions, a specific MHC haplotype is not sufficient for development of autoimmune disease. 

Damoiseaux JG,Cautain B, Bernard I, Mas M, van Breda Vriesman PJ, Druet P, Fournie G, Saoudi A A dominant role forthe thymus and MHC genes in determining the peripheral CD4/CD8T cell ratio in the rat. J. Immunol. 1999 163 2983-2989. 

The so-called resistant strains, however, show a different response to mercury exposure. These resistant strains also show an increase in MHC expression molecules on B-cells, but this response is extremely short-lived, and increases in serum IgE were not observed (Dubey et al. 1991a Prouvost-Danon et al. 1981). The difference in the responses of the so-called resistant and susceptible strains may be found in the activation of Thl cells and the increase in secretion of -interferon by the Thl cells of resistant animals (van der Meide et al. 1993). The susceptible strains do not show an increase in -interferon production with mercury exposure. Because -interferon inhibits the proliferation of Th2 cells, the absence of this response in the susceptible strains may allow the Th2 cell-stimulated production of autoantibodies to occur, whereas in the resistant strains the production of antibodies is curtailed. Thus, differences in the activation of Thl versus Th2 cells may underlie the differences in susceptibility of various individuals. Studies using in-bred strains of mice and rats have determined that the susceptibility to the different immune reactions is governed by both MHC genes as well as other genes (Aten et al. 

The type I muscle MHC gene is located on chromosome 14 in both humans and mouse. This gene also codes for cardiac )6MHC, although they are not the identical protein. The skeletal muscle type II MHCs are on chromosome 17 in humans (11 in mice). There is also a cardiac a MHC and embryonic and neonatal cardiac and skeletal MHCs. 

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