MHC control of autoimmune anti-TBM reaction in the Norway rat.

The RT1 control of anti-TBM reaction presupposed in rat kidney transplantations has been revealed in immunization experiments performed in similar strain combinations. The anti-TBM reaction proven by immunofluorescence and in some cases even tubulointerstitial nephritis with giant cell infiltration developed in kidneys of BN rats immunized with BP.1N (or BP) kidney homogenate in CFA. On the contrary, BN.1B recipients of BP (or BP.1N) kidney homogenate in CFA displayed no anti-TBM reaction. This is in perfect correlation with the absence of TIN and anti-TBM reaction in chronically rejected BP kidneys grafted to BN.1B (RT1b-identical) recipients. In accord with the literature data, LEW.1N animals carrying no TBM antigen(s) did not develop anti-TBM reaction detectable on their own kidneys following BP.1N immunization. In our experiments the adjuvant effect of alloantigenic difference was necessary for the immunization with syngeneic BN kidney and CFA did not induce any anti-TBM signs in BN recipients' own kidneys. The existence of some anti-TBM antigen Ir genes linked to the rat MHC can thus be assumed. However, there was no clear-cut association of glomerular changes with MHC in immunization experiments. On the basis of the data presented here the contribution of an anti-TBM component and TIN to the subacute rejection of RT1n-matched rat kidney grafts seems to be confirmed in the special (BP.1N to BN) strain combination previously described.