REDUCED ANTIGEN-PRESENTING FUNCTION OF HUMAN EPSTEIN-BARR-VIRUS (EBV)-B CELLS AND MONOCYTES AFTER UVB RADIATION IS ACCOMPANIED BY DECREASEDEXPRESSION OF B7, INTERCELLULAR-ADHESION MOLECULE-1 (ICAM-1) AND LFA-3

Citation
Ib. Kremer et al., REDUCED ANTIGEN-PRESENTING FUNCTION OF HUMAN EPSTEIN-BARR-VIRUS (EBV)-B CELLS AND MONOCYTES AFTER UVB RADIATION IS ACCOMPANIED BY DECREASEDEXPRESSION OF B7, INTERCELLULAR-ADHESION MOLECULE-1 (ICAM-1) AND LFA-3, Clinical and experimental immunology, 101(3), 1995, pp. 461-467
Citations number
31
Categorie Soggetti
Immunology
ISSN journal
00099104
Volume
101
Issue
3
Year of publication
1995
Pages
461 - 467
Database
ISI
SICI code
0009-9104(1995)101:3<461:RAFOHE>2.0.ZU;2-I
Abstract
In this study, the effect of ultraviolet-B (UVB) radiation on antigen- presenting function was studied, to investigate whether antigen-presen ting cells (APC) are inhibited by WE through a common mechanism. Two t ypes of human APC were used: EBV-B cells and monocytes, and these were irradiated in vitro with single low doses of WE (range 0-200 J/m(2)). Irradiation of EBV-B cells or monocytes resulted in similar dose-depe ndent reduction in APC function, when determined by the allogeneic mix ed leucocyte reaction (MLR) or Candida albicans- or tetanus toxoid-spe cific T cell response. Our study shows that the reduced APC function w as not likely to be caused by alterations in antigen processing or cyt okine production. However, UVB-irradiated APC displayed marked changes in adhesion molecule expression. Irradiated EBV-B cells showed reduce d expression of ICAM-1 (30%), LFA-3 (25%) and B7-1 (35%), while expres sion of HLA-DR, CD19 and LFA-1 was not affected. WB irradiation of mon ocytes did result in reduction in the expression of HLA-DR (30%), LFA- 3 (40%), ICAM-1 (65%) and B7-1 and B7-3 (90%), but had no effect on CD 14, LFA-1 and ICAM-3 expression. Addition of nonirradiated cells (but not the supernatant of these cells) or CD28 antibodies partly restored T cell activation, indicating that UVB-induced reduction in APC funct ion is at least partly mediated via impairment of co-stimulatory molec ule expression.