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J. Exp. Med.,
Volume 189, Number 8, April 19, 1999 1285-1294
By
From the Department of Immunology, University of Texas M.D. Anderson Cancer Center, Houston,
Texas 77030
Induction of antigen-specific suppression elicited by environmental insults, such as ultraviolet
(UV)-B radiation in sunlight, can inhibit an effective immune response in vivo and may contribute to the outgrowth of UV-induced skin cancer. Although UV-induced DNA damage is
known to be an initiating event in the immune suppression of most antigen responses, the underlying mechanism(s) of such suppression remain undefined. In this report, we document that Fas ligand (FasL) is critical for UV-induced systemic immune suppression. Normal mice acutely
exposed to UV exhibit a profound suppression of both contact hypersensitivity and delayed
type hypersensitivity (DTH) reactions and the development of transferable antigen-specific suppressor cells. FasL-deficient mice exposed to UV lack both transferable suppressor cell activity and primary suppression to all antigens tested, with the exception of the DTH response to
allogeneic spleen cells. Interestingly, suppression of this response is also known to occur independently of UV-induced DNA damage. Delivery of alloantigen as protein, rather than intact cells, restored the requirement for FasL in UV-induced immune suppression of this response.
These results substantiate that FasL/Fas interactions are essential for systemic UV-induced suppression of immune responses that involve host antigen presentation and suggest an interrelationship between UV-induced DNA damage and FasL in this phenomenon. Collectively, our
results suggest a model whereby UV-induced DNA damage disarms the immune system in a
manner similar to that observed in immunologically privileged sites.
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