Ultraviolet B-irradiated antigen-presenting cells display altered accessory signaling for T-cell activation: relevance to immune responses initiated in skin.

A principal mechanism by which ultraviolet (UV) B radiation exerts its selective and antigen-specific suppressive influence on immune responses is through its effects on the capacity of antigen-presenting cells (APC) in skin, primarily Langerhans cells (LC), to differentially activate T-cell subsets. Recent evidence has indicated that LC, following UVB radiation, lose the capacity to stimulate proliferation of CD4+ Th1, but not of Th2, clones. Additional work has shown this acquired unresponsiveness of Th1 cells to represent a long-lasting form of clonal anergy that results from a block in their ability to produce IL-2. Although not completely delineated, these defects appear to be the result of preserved delivery of the primary signal transduced by interaction of the MHC/antigen complex on APC with the T-cell receptor complex, in the absence of a viable second signal normally delivered by interaction of a co-stimulatory factor from APC with its appropriate ligand on the T cells. These findings support the notion that the outcome of certain immune responses depends greatly upon conditions that are brought to bear on APC and T cells during the time of antigen presentation.