Journal List > J Korean Acad Periodontol > v.29(2) > 1049085

J Korean Acad Periodontol. 1999 Jun;29(2):333-348. Korean.
Published online June 30, 1999.
Copyright © 1999 Korean Academy of Periodontology
Immunochemical study on the Role of β2 Integrin in the Activation of Monocytes Upon Direct Contact with T Lymphocytes
Suck-Cho Lee, Ho Lee, Kwi-Ok Oh,* and Hyung-Seop Kim
Department of Periodontology and Research Institute of Oral Bio-Science, College of Dentistry, Chonbuk National University, Korea.
*Institute of Dentistry, College of Dentistry, Seoul National University, Korea.

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.