Class II positive human dermal fibroblasts restimulate cloned allospecific T cells but fail to stimulate primary allogeneic lymphoproliferation

David H. Maurer, Weldon E. Collins, Jeffrey H. Hanke, Mai Van, Robert R. Rich, Marilyn S. Pollack

Research output: Contribution to journalArticlepeer-review

15 Scopus citations

Abstract

Recently, a number of laboratories have shown that gamma interferon (IFN-γ) is a potent modulator of HLA class II antigen expression in a variety of cell types ranging from classical antigen presenting cells to those not expected to participate in physiological antigen presentation such as fibroblasts. In order to examine the role of HLA class II expressing fibroblasts in antigen presentation, we established dermal fibroblast (FIB) strains from five HLA typed donors. After optimal preculture with IFN-γ, class II positive FIB were fully competent to restimulate proliferative responses of two DR specific T cell clones and one DP specific T cell line. However, they failed to elicit strong primary allogeneic proliferation from fully DR mismatched fresh PBMC. This failure was not due to a direct suppressive effect of FIB and could not be corrected by exogenous IL1 or by factors contained in conventional mixed leukocyte culture supernatants.

Original languageEnglish (US)
Pages (from-to)245-258
Number of pages14
JournalHuman Immunology
Volume14
Issue number3
DOIs
StatePublished - Nov 1985

Bibliographical note

Funding Information:
ACKNOWLEDGMENTS The authors wish to thank Drs. Bo Dupont, Ronald Levy, Frances Brodksy, and Nancy Reinsmoen for providing some of the monoclonal antibodies used in these studies; Drs. Robert Hartzman and Stephen Shaw for providing DP primed reagents; and Debra Schnei-bel for typing and editing the manuscript. This work was supported in part by NIH grants CA 37888, AM 33988, AI 15394, AI 21289, and AM 33990 and by NIAID contract AI 22676. Computational assistance was provided by the CLINFO project, supported by the Division of Research Resources, NIH grant RR 00350.

Copyright:
Copyright 2014 Elsevier B.V., All rights reserved.

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