Protective modulation of class II MHC gene expression in tubular epithelium by target antigen-specific antibodies. Cell-surface directed down-regulation of transcription can influence susceptibility to murine tubulointerstitial nephritis

T. P. Haverty, M. Watanabe, E. G. Neilson, C. J. Kelly

Research output: Contribution to journalArticlepeer-review

25 Scopus citations

Abstract

We have been studying the factors which permit autoimmune injury to the kidney leading to interstitial nephritis. Nonsusceptible mice develop L3T4+ effector T cells which do not recognize their 3M-1 target Ag, nor produce interstitial lesions in the kidney unless proximal tubular class II MHC Ag expression is increased, for example, by rIFN-γ. Anti-tubular basement membrane/α3M-1-Ab, normally present in such mice after immunization with 3M-1, produce an opposite result by diminishing class II transcription and expression. This unique antibody-ligand interaction on the surface of proximal tubular epithelium secreting 3M-1 serves as a novel protective regulatory response in interstitial parenchyma. The in vitro studies conveyed in this current report suggest that 3/4 M-1-Ab mediate this protective effect by reducing the transcription of mRNA encoding class II gene products. These findings, within the overall complexity of a nephritogenic immune response, demonstrate the important role certain elements may play in maintaining functional nonsusceptibility to autoimmune injury.

Original languageEnglish (US)
Pages (from-to)1133-1141
Number of pages9
JournalJournal of Immunology
Volume143
Issue number4
StatePublished - 1989

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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