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cells and enhances (or modulates) interleukin-1 (IL-1), IL-6, IL-8, IL-10, IL-12
and tumor necrosis factor a production by human keratinocytes (26). The
modulation of circulating cytokines accounts for systemic NB-UVB-induced
immunosuppression in human subjects (22, 26). Intercellular adhesion
molecule 1 (ICAM-1) is observed on cells in inflammatory skin diseases
(including PLEVA) that can cause pruritus (2729). UVB irradiation has been
found to suppress the expression of ICAM-1 in cultured human keratinocytes
(29). UVB has been reported to decrease the release of histamine from mast
cells. UVB phototherapy given two to three times a week for 4 weeks
decreased the itch response of the skin when histamine was injected, or
when a mast cell degranulator, compound (48/80), was injected (30). Duthie
et al. (31) concluded that UVB light possibly suppresses the function of
neoplastic clonal T-cell populations in the skin and so serves as an immune
up-regulator. These UVB-induced alterations may partly account for its
immunotherapeutic role in preventing the progression of the disease.