Systemic suppression of human peripheral blood phagocytic leukocytes afterwhole-body UVB irradiation

Citation
L. Leino et al., Systemic suppression of human peripheral blood phagocytic leukocytes afterwhole-body UVB irradiation, J LEUK BIOL, 65(5), 1999, pp. 573-582
Citations number
45
Categorie Soggetti
Immunology
Journal title
JOURNAL OF LEUKOCYTE BIOLOGY
ISSN journal
07415400 → ACNP
Volume
65
Issue
5
Year of publication
1999
Pages
573 - 582
Database
ISI
SICI code
0741-5400(199905)65:5<573:SSOHPB>2.0.ZU;2-7
Abstract
We examined systemic effects of whole-body UVB irradiation on human periphe ral blood phagocytes. We found that 24 h after a single erythemal dose of U VB radiation two phagocyte functions, adhesion and phagocytosis, were reduc ed by 50%. This functional suppression was accompanied by a significant dec rease in the expression of complement receptors (CR1 and CR3) and IgG Fc re ceptors (FcRII and FcRIII), The greatest reduction (47%) was observed in CR 3, which is important for both adhesion and phagocytosis. A kinetic analysi s showed that both CR1 and CR3 levels started to decrease 15 min after the UVB exposure, reaching the lowest levels at 4.5- and 24-h time points, resp ectively. The down-modulation of CRs after whole-body UVB exposure was not due to a defective receptor synthesis or translocation from internal stores to plasma membrane because the maximal CR levels in stimulated cells were not affected by UVB. No change in the serum soluble ICAM-1 was detected aft er UVB, which rules out CD11b epitope masking by sICAM-1. UVB did not relea se low-receptor-density myeloid progenitor cells from storage pools into ci rculation, Interleukin 10, a mediator of UVB-induced immunosuppression, was unable to modulate CR expression in vitro. Wiles seven suberythemal whole- body UVB exposures were,given repeatedly within 2 weeks, a significant decr ease in CR expression Tvas seen, which was greatest after three irradiation s, Our data suggest that an exposure to UVB has systemic effects in humans which, possibly due to the down-modulation of preexisting cell-surface rece ptors, suppress some important functions of circulating phagocytic cells.