Abstract

Although strong associations, and genetic linkage between the Human Leukocyte Antigen (HLA) complex and susceptibility to a wide variety of autoimmune diseases has been documented for the last 30 years, the mechanisms by which genes in the major histocompatibility complex (MHC) mediate susceptibility to autoimmunity remain poorly understood.’ While the primary functions of the MHC Class I and Class II molecules—antigen presentation of peptides to the receptors on T-cells, and T-cell positive and negative selection in the thymus—are now well documented and at least partially delineated, the precise molecular mechanisms by which particular alleles of MHC Class I or Class II molecules increase or decrease susceptibility to autoimmune diseases have not yet been worked out.

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