TY - JOUR
T1 - Ultraviolet B - irradiated antigen-presenting cells display altered accessory signaling for T-cell activation
T2 - Relevance to immune responses initiated in skin
AU - Simon, Jan C.
AU - Krutmann, Jean
AU - Elmets, Craig A.
AU - Bergstresser, Paul R.
AU - Cruz, Ponciano D
PY - 1992/6
Y1 - 1992/6
N2 - 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+ Thl, 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.
AB - 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+ Thl, 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.
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U2 - 10.1111/1523-1747.ep12462236
DO - 10.1111/1523-1747.ep12462236
M3 - Article
C2 - 1588126
AN - SCOPUS:0026549714
SN - 0022-202X
VL - 98
SP - S66-S69
JO - Journal of Investigative Dermatology
JF - Journal of Investigative Dermatology
IS - 6 SUPPL.
ER -