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Intercellular adhesion molecule‐1 (ICAM‐1) is involved in the cytolytic T lymphocyte interaction with a human synovial cell line
Author(s) -
Mentzer Steven J.,
Rothlein Robert,
Springer Timothy A.,
Faller Douglas V.
Publication year - 1988
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.1041370121
Subject(s) - ctl* , cell culture , microbiology and biotechnology , cell adhesion molecule , intercellular adhesion molecule 1 , biology , cell , cell–cell interaction , cytolysis , cell adhesion , t cell , cd8 , intracellular , cytotoxic t cell , antigen , immunology , immune system , biochemistry , in vitro , genetics
The cell surface molecules involved in the human cytolytic T lymphocyte (CTL)‐synovial cell interaction may play an important role in T cell interactions with connective tissue mesenchymal cells. To examine the molecular basis for the CTL‐synovial cell interaction, we immortalized synovial cell explants to establish the cell line SYN.SPP. The SYN.SPP cell line was compared to the established B lymphoblastoid cell line JY. Cell surface immunofluorescence demonstrated significantly different levels of the immunologically relevant cell surface molecules ICAM‐1 and LFA‐3. Both cell lines were used to stimulate CTL precursors. After several months in culture, CTL lines stimulated by the SYN.SPP and JY cell lines demonstrated HLA class I‐directed cytolytic activity. The cell surface molecules utilized by the anti‐SYN.SPP and anti‐JY CTL lines were identified by monoclonal antibody (MAb) inhibition. MAb recognizing the CTL cell surface molecules CD3, CD8 and LFA‐1 (CD11a) significantly inhibited CTL‐mediated lysis of both target cells. An interesting observation was that the anti‐SYN.SPP CTL line appeared to utilize the ICAM‐1 and not the LFA‐3 target cell molecule. In contrast, the anti‐Y CTL line utilized the LFA‐3 and not the ICAM‐1 membrane molecule. These results indicate that CTL interactions with connective tissue mesenchymal cells may be regulated by a unique pattern of antigen nonspecific cell‐cell interaction molecules.