Murine interstitial nephritis: VII. Suppression of renal injury after treatment with soluble suppressor factor TsF1

E. G. Neilson, C. J. Kelly, M. D. Clayman, W. H. Hines, T. Haverty, M. J. Sun, N. Blanchard

Research output: Contribution to journalArticlepeer-review

10 Scopus citations

Abstract

We prepared soluble suppressor T cell factor (TsF1) from donor spleens harvested from mice primed with tubular antigen-derivatized lymphocytes to analyze both its functional interactions with a larger suppressor T cell network and its influence on the nephritogenic effector T cell response producing interstitial nephritis to a parenchymal antigen. Our findings indicate that TsF1 is antigen-specific, genetically restricted by I-J in its direct mediation of suppression, and capable of inhibiting the development of interstitial lesions. TsF1 also provides an inducing signal for the activation of effector Ts-2 suppressors following presentation by accessory cells. The induction of a Ts-2 effect, however, requires that the factor-presenting cell and the recipient of such cells share homology at I-J, and that the TsF1, the precursor Ts-2 cells, and the recipient of the Ts-2 effect share the same Igh-V allotype. Finally, the results of this current report clearly demonstrate a possible therapeutic role for soluble suppressor factors in the management of interstitial renal disease.

Original languageEnglish (US)
Pages (from-to)1518-1524
Number of pages7
JournalJournal of Immunology
Volume139
Issue number5
StatePublished - 1987

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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