Immunochemical study on the Role of beta2 Integrin in the Activation of Monocytes Upon Direct Contact with T Lymphocytes.
10.5051/jkape.1999.29.2.333
- Author:
Suck Cho LEE
1
;
Ho LEE
;
Kwi Ok OH
;
Hyung Seop KIM
Author Information
1. Department of Periodontology and Research Institute of Oral Bio-Science, College of Dentistry, Chonbuk National University, Korea.
- Publication Type:Original Article
- MeSH:
Antibodies;
Antigens, CD18*;
Cell Line;
HLA-D Antigens;
Humans;
Intercellular Adhesion Molecule-1;
Leukocytes;
Membrane Glycoproteins;
Monocytes*;
T-Lymphocytes*
- From:The Journal of the Korean Academy of Periodontology
1999;29(2):333-348
- CountryRepublic of Korea
- Language:Korean
-
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-1beta 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-1beta production by THP-1. IL-1beta production was higher when THP-1 had been previously exposed to 1.25(OH)2D3 as compared to control, with alpha-1.25(OH)2D3 dose-dependent and exposure time-dependent manner. It was shown that 1.25(OH)2D3 also increased the expression of beta2 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-1beta 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-1beta 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.
