INDUCTION OF AUTO-IMMUNITY TO ANTIGENS OF THE GLOMERULAR BASEMENT-MEMBRANE IN INBRED BROWN-NORWAY RATS

  • 1 January 1979
    • journal article
    • research article
    • Vol. 36  (4) , 759-767
Abstract
Induction of autoimmune antibodies [Ab] against antigens of glomerular basement membrane (GBM) was studied in 9-inbred strains of rats each with a different major histocompatibility complex H-1. Brown-Norway (BN) (H-1n), Lewis (H-1l), PvG/c (H-1c), AS2 (H-1f), AVN (H-1a), BD V (H-1d), DA (H-1a) and F344 (H-1l) rats were immunized with bovine GBM and Freund''s complete adjuvent (CFA). A pronounced linear deposition of host Ig[immunoglobulin]G (IgG1 and IgG2a) along the GBM was found in BN rats. No deposition of C3 [complement component 3] could be detected in the glomeruli nor did the animals develop proteinuria. The quantity of autoimmune Ab fixed to the GBM was low (48 .mu.g .+-. 14) which could explain the absence of C3 deposition and proteinuria. The antigenic specificity of the Ab deposited along the GBM in BN rats was shown by the fixation in vitro of the eluted Ab to the GBM and tubular basement membrane (TBM) of normal kidneys. A much weaker and irregular deposition of host IgG along the GBM was observed in PVG/c, AS2, AVN, BD V, DA and F344 rats. Of these strains, eluates from the glomeruli of PVG/c, AVN, BD V and DA rats fixed very weakly to the GBM of normal kidneys whereas eluates from AS2 and F344 rats did not fix to GBM or TBM. No deposition of host IgG was found in Lewis rats, and the eluates did not fix to normal kidneys. Congenic L.BN rats with the BN H-ln haplotype and a Lewis background did not respond. Rats are genetically predisposed to an autoimmune anti-GBM response which is not, or not exclusively, controlled by genes linked to the H-1 histocompatibility complex.