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J. Exp. Med.,
Volume 187, Number 7, April 6, 1998 1133-1138
By
From the * Department of Dermatology, Case Western Reserve University, and University Hospitals of
Cleveland, Cleveland, Ohio 44106; the Complement component 3 (C3), a critical regulator of innate immunity, may also play a role in
the regulation of cognate immunity, such as contact sensitivity responses. Because ultraviolet
(UV) radiation also activates C3 in the skin, we determined whether the immunosuppressed
state that results when a contact sensitizer is applied through UVB-exposed skin requires the
presence and activation of C3. This question was addressed through the use of C3-deficient
mice, blockade of C3 cleavage to C3b, and accelerated degradation of iC3b by soluble complement receptor 1 (sCR1). Both C3-modulated systems totally reversed the failure to induce a contact sensitivity response to dinitrofluorobenzene (DNFB) upon primary sensitization at the
UV-exposed site, as well as immunologic tolerance to a second DNFB immunization through
normal skin. Treatment with sCR1 reduced the infiltration of CD11b+ leukocytes into the
epidermis and dermis of UV-irradiated skin but did not reverse the UV-induced depletion of
epidermal class II MHC+CD11blo Langerhans cells. These data, taken together with previous
results showing abrogation of locally induced UV immunosuppression by in vivo anti-CD11b
treatment, suggest a novel mechanism by which ligation of the leukocyte Department of Pathology, Harvard Medical School, Boston,
Massachusetts 02115; and the § Veterans Affairs Hospital, Cleveland, Ohio 44106
2 integrin, CD11b,
by iC3b molecules formed from C3 activation in UV-exposed skin, modifies cutaneous CD11b+ cells such that skin antigen-presenting cells are unable to sensitize in a primary immune response, but actively induce antigenic tolerance.
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