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Abstract
The modulation of leukocyte cell surface adhesion molecules may influence the development of cellular events that determine the course of the inflammatory process. Direct interaction between activated T cells and monocytes resulted in a large production of IL-1β by monocytes. In this reactions, adhesion molecules play an important part, yet the role of them in T-monocytes interaction remain unclear. This study was undertaken in an effort to elucidate, 1) the influence of 1.25(OH)2D3-induced differentiation on the monocyte responsiveness to direct contact with T lymphocytes, and 2) the role of adhesion molecules on the T-monocyte direct interaction. Initially, I observed that direct contact of monocyte cell line THP-1 with stimulated fixed T cell line HuT78 markedly induces IL-1β production by THP-1.
IL-1β production was higher when THP-1 had been previously exposed to 1.25(OH)2D3 as compared to control, with α-1.25(OH)2D3 dose-dependent and exposure time-dependent manner. It was shown that 1.25(OH)2D3 also increased the expression of β2 integrin adhesion receptor Mac-1(CD11b/CD18) dose- and time- dependently, but did not increase the expression of human leukocyte antigen-D(HLA-D) and intercellular adhesion molecule-1(ICAM-1). The IL-1β producing activity of THP-1 cells correlated well with the ability to induce the Mac-1 expression on THP-1 surface. Monoclonal antibody raised against relevant cell surface glycoproteins on THP-1 were tested for their ability to block the response of THP-1 to T cells. Antibody to Mac-1 only partially blocked IL-1β production by THP-1, whereas antibodies to ICAM-1 and HLA-D did not.
These data indicate that regulation of Mac-1 expression on THP-1 cells can alter the responsiveness of these cells to contact by activated T cells, however other unknown structures on the THP-1 cells may be involved in this process also.
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