Regulation of HLA Antigen Expression in Human Kidney

The expression of class II, and even of class I, MHC products in many sites in normal kidney may be low enough to be rate-limiting for antibody-mediated or T cell-mediated injury involving these structures (e.g. rejection). In certain human diseases and in experimental animal models, renal expression of class I and II MHC antigens is capable of large quantitative changes accompanied by shifts in sites of expression. These alterations may be induced by local or systemic processes, and can at times be controlled or reversed by pharmacological intervention (e.g. cyclosporin). The interferons, especially γ-interferon, are probably involved in these changes, but many other influences may also participate. The study of MHC induction may prove to be useful in the clinical and pathological assessment of renal disease, and in understanding the pathogenesis of some forms of renal injury, such as rejection and interstitial nephritis. At present, further studies are needed to unravel the significance of these changes.