Immunochemical study on the Role of ${\beta}_2$ Integrin in the Activation of Monocytes Upon Direct Contact with T Lymphocytes

T 세포 접촉에 의한 단핵구 활성화에서 ${\beta}_2$ Integrin의 역할에 관한 면역화학적 연구

  • Lee, Suck-Cho (Department of Periodontology and Research Institute of Oral Bio-Science, College of Dentistry, Chonbuk National University) ;
  • Lee, Ho (Department of Periodontology and Research Institute of Oral Bio-Science, College of Dentistry, Chonbuk National University) ;
  • Oh, Kwi-Ok (Institute of Dentistry, College of Dentistry, Seoul National University) ;
  • Kim, Hyung-Seop (Department of Periodontology and Research Institute of Oral Bio-Science, College of Dentistry, Chonbuk National University)
  • 이석초 (전북대학교 치과대학 치주과학교실, 전북대학교 구강생체과학연구소) ;
  • 이호 (전북대학교 치과대학 치주과학교실, 전북대학교 구강생체과학연구소) ;
  • 오귀옥 (서울대학교 치학 연구소) ;
  • 김형섭 (전북대학교 치과대학 치주과학교실, 전북대학교 구강생체과학연구소)
  • Published : 1999.06.30

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 $IL-1{\beta}$ by monocytes. In this reactions, adhesion molecules play an important part, yet the role of them in Tmonocytes interaction remain unclear. This study was undertaken in an effort to elucidate, 1) the influence of 1.25(OH)$_2D_3-induced$ 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-1${\beta}$ production by THP-1. $IL-1{\beta}$ production was higher when THP-1 had been previously exposed to 1.25(OH)$_2D_3$ as compared to control, with ${\alpha}$- 1.25(OH)$_2D_3$ dose-dependent and exposure time-dependent manner. It was shown that 1.25(OH)$_2D_3$ also increased the expression of ${\beta}_2$ integrin adhesion receptor Mac-1(CD11b/CD18) dose- and timedependently, but did not increase the expression of human leukocyte antigen- D(HLA-D) and intercellular adhesion molecule-1(ICAM-1). The $IL-1{\beta}$ 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 $IL-1{\beta}$ 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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