
Cellular responses to human chondrocytes: absence of allogeneic responses in the presence of HLA‐DR and ICAM‐1
Author(s) -
JOBANPUTRA P.,
CORRIGALL V.,
KINGSLEY G.,
PANAYI G.
Publication year - 1992
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/j.1365-2249.1992.tb07952.x
Subject(s) - immunology , peripheral blood mononuclear cell , chondrocyte , cytokine , phytohaemagglutinin , microbiology and biotechnology , tumor necrosis factor alpha , major histocompatibility complex , biology , t cell , icam 1 , in vitro , cell adhesion molecule , cartilage , antigen , immune system , anatomy , biochemistry
SUMMARY To assess the accessory cell function of human articular chondrocytes, we assessed the ability of human chondrocytes to stimulate allogeneic peripheral blood mononuclear cells (PBMC) and to support phytohacmagglutinin (PHA)‐induced proliferation of highly purified T cells. We also examined the surface expression of HLA‐DR and ICAM‐1 on the chondrocytes both unstimulated and stimulated with cytokines in vitro . Chondrocytes failed to stimulate allogeneic PBMC despite the constitutive expression of MHC class I molecules and the cytokine‐induced expression of class II molecules but were able to support T cell proliferation to PHA, IFN‐γ and to a limited extent, IL‐1β, induced class II expression on chondrocytes. ICAM‐1 was present on 94–99% of freshly isolated cells; this declined with culture (17–59%; P<0.005) but was readily induced by IFN‐γ, IL‐1β, and tumour necrosis factor‐alpha. Alloreactivity and, presumably, autoreactivity to chondrocytes requires factors in addition to the surface expression of DR and ICAM‐1. However the presence of these molecules suggests a capacity for cell‐cell interactions in inflammatory sites such as the cartilage pannus junction.