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Ludwig Boltzmann Institute for Cell Biology and Immunobiology of the Skin, Department of Dermatology, University of Münster, Münster, Germany;
Ben May Institute for Cancer Research, University of Chicago, Chicago, IL 60637
Hapten sensitization through UV-exposed skin induces
hapten-specific tolerance that can be adoptively transferred by
injecting T lymphocytes into naive recipients. The exact phenotype of T
cells responsible for inhibiting the immune response and their mode of
action remain unclear. Evidence exists that CTLA-4 negatively regulates
T cell activation. We addressed whether CTLA-4 is involved in the
transfer of UV-induced tolerance. Injection of lymph node cells from
mice that were sensitized with dinitrofluo-robenzene (DNFB) through
UV-irradiated skin inhibited induction of contact hypersensitivity
against DNFB in the recipient animals. When CTLA-4+ cells
were depleted, transfer of suppression was lost. Likewise,
significantly fewer lymphocytes enriched for CTLA-4+ cells
were necessary to transfer suppression than unfractionated cells.
Expression of CTLA-4 appears to be functionally relevant, since in vivo
injection of a blocking anti-CTLA-4 Ab was able to break UV-induced
tolerance and inhibited transfer of suppression. Upon stimulation with
dendritic cells in the presence of the water-soluble DNFB analogue,
DNBS, CTLA-4+ T cells from DNFB-tolerized mice secreted
high levels of IL-10, TGF-ß, and IFN-
; low levels of IL-2; and no
IL-4, resembling the cytokine pattern of T regulatory 1 cells. Ab
blocking of CTLA-4 resulted in inhibition of IL-10 release.
Accordingly, transfer of tolerance was not observed when recipients
were treated with an anti-IL-10 Ab. Hence we propose that T cells,
possibly of the T regulatory 1 type, transfer UV-mediated suppression
through the release of IL-10. Activation of CTLA-4 appears to be
important in this process.
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