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Department of Immunology, University of Texas M.D. Anderson Cancer Center, Houston, TX 77030
Cutaneous exposure to low dose (2 kJ/m2) ultraviolet B
radiation impairs the induction of contact hypersensitivity (CHS)
responses to haptens applied to UV-irradiated skin and induces
hapten-specific suppressor T lymphocytes (Ts). Cells collected from the
draining lymph nodes of UV-irradiated, FITC-sensitized mice have
impaired Ag-presenting activity and induce Ts cells upon injection into
syngeneic recipients. This study investigates whether Ts cells
originate in the UV-irradiated donor mice or are induced in lymph node
cell recipients and the mechanism of suppression. Using congenic mice,
we determined that the Ts cells in recipient animals were derived from
T cells in the draining lymph nodes of the UV-irradiated donors. Cell
lines and clones established from unirradiated and UV-irradiated,
FITC-sensitized mice were CD4+, CD8-,
TCR-
/ß+, MHC restricted, and hapten specific. The T
cells proliferated in response to APC sensitized in vivo, but not to
APC coupled in vitro with FITC. Cell lines from unirradiated mice were
Th1 like, producing large amounts of IFN-
, but little IL-4 or IL-10,
whereas cloned Ts cells from UV-irradiated mice produced IL-10, but no
IL-4 or IFN-
. Ts cells blocked APC functions and IL-12 production in
vitro. Injection of 5 x 104 cloned Ts cells into
untreated recipients suppressed the induction of CHS. These results
suggest that UV radiation can induce a distinct T regulatory type
1-like Ts population that may block the activation of Th1 cell-mediated
immune responses.
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