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Ultraviolet B‐exposed major histocompatibility complex class II positive keratinocytes and antigen‐presenting cells demonstrate a differential capacity to activate T cells in the presence of staphylococcal superantigens
Author(s) -
SKOV L.,
BAADSGAARD O.
Publication year - 1996
Publication title -
british journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.304
H-Index - 179
eISSN - 1365-2133
pISSN - 0007-0963
DOI - 10.1046/j.1365-2133.1996.112847.x
Subject(s) - superantigen , major histocompatibility complex , mhc class ii , antigen , keratinocyte , biology , antigen presenting cell , immunology , antigen presentation , t cell , enterotoxin , microbiology and biotechnology , chemistry , immune system , in vitro , biochemistry , escherichia coli , gene
Summary In this study we tested the capacity of ultraviolet B (UVB)‐irradiated major histocompatibility complex (MHC) class II + keratinocytes, monocytes and dendritic cells to activate T cells in the presences of Staphylococcus enterotoxin B. We demonstrated that UVB irradiation of MHC class II + keratinocytes does not change their capacity to activate T cells in the presence of Staphylococcus enterotoxin B. In contrast. UVB irradiation of antigen T cells after UVB irradiation was not due to factors relased form UVB‐irradiated cells. The interferon‐γ induced uupregulation of HLA‐DR and intercellular adhesion molecule‐l on accessory cell function of interferon‐γ pretreated monocytes. Differential requirements for and UVB regulation of costimulatory molecules may be involved. Since blocking of the B7/CD28 pathway affects the capacity of dendritic cells but not keratinocytes to activate T cells in the presence of Staphylococcus enterotoxin B. Thus. MHC class II + keratinocytes in the presence of superantigens released from staphylococci may activate T cells and maintain inflammation despite UVB treatment.