Steroid-sensitive mechanism of soluble immune response suppressor production in steroid-responsive nephrotic syndrome

H. W. Schnaper, T. M. Aune

Research output: Contribution to journalArticlepeer-review

29 Scopus citations

Abstract

Soluble immune response suppressor (SIRS), a lymphokine that suppresses antibody production and delayed type hypersensitivity in vivo, has been detected in urine and serum from certain patients with nephrotic syndrome. In the present paper, the relationship bteween SIRS production and nephrotic syndrome is further characterized. A striking correlation was found between detection of SIRS and the presence of steroid-responsive nephrotic syndrome (SRNS). A potential mechanism of SIRS production in SRNS patients was identified, in that (a) lymphocytes from patients produced SIRS without requiring activation by exogenous agents, and (b) incubation of normal lymphocytes with serum from patients activated the cells to secrete SIRS in culture. Although SIRS disappears rapidly from urine or serum after initiation of corticosteroid therapy, hydrocortisone (10-6-10-7 M) did not block secretion of SIRS by activated suppressor cells. It did, however, inhibit in vitro activation of lymphocytes to produce SIRS by concanavalin A, interferon, or SRNS patient serum. The association of suppressor cell activation with SRNS and the sensitivity of both to steroids suggest that the pathogeneses of albuminuria and SIRS production are related.

Original languageEnglish (US)
Pages (from-to)257-264
Number of pages8
JournalJournal of Clinical Investigation
Volume79
Issue number1
DOIs
StatePublished - 1987

ASJC Scopus subject areas

  • Medicine(all)

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