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Activated complement component 3 (C3) is required for ultraviolet induction of immunosuppression and antigenic
C Hammerberg1, S K Katiyar, M C Carroll
1Department of Dermatology, Case Western Reserve University, and University Hospitals of Cleveland, Cleveland, Ohio 44106, USA.
The Journal of Experimental Medicine
|May 16, 1998
Summary
Complement component 3 (C3) activation in UV-exposed skin is crucial for UV-induced immune suppression. Blocking C3 prevents UV radiation from inhibiting contact sensitivity responses and tolerance induction.
Area of Science:
- Immunology
- Dermatology
- Complement System
Background:
- Complement component 3 (C3) regulates innate immunity and may influence adaptive immunity like contact sensitivity.
- Ultraviolet (UV) radiation activates C3 in the skin, suggesting a role in UV-induced immunosuppression.
Purpose of the Study:
- To investigate if C3 presence and activation are required for the immunosuppressive state induced by applying contact sensitizers to UVB-exposed skin.
- To elucidate the mechanism of UV-induced immunosuppression involving C3 and leukocyte integrin CD11b.
Main Methods:
- Utilized C3-deficient mice, C3 cleavage blockade, and soluble complement receptor 1 (sCR1) to modulate C3 activity.
- Assessed contact sensitivity responses to dinitrofluorobenzene (DNFB) in UV-exposed skin.
- Analyzed leukocyte infiltration and Langerhans cell populations in UV-irradiated skin.
Main Results:
- C3 modulation reversed the failure to induce contact sensitivity and tolerance at UV-exposed sites.
- sCR1 treatment reduced CD11b+ leukocyte infiltration but did not affect UV-induced depletion of Langerhans cells.
- Previous studies showed anti-CD11b treatment abrogated UV immunosuppression.
Conclusions:
- C3 activation in UV-exposed skin is essential for UV-induced immunosuppression of contact sensitivity and tolerance.
- Ligation of CD11b by iC3b on cutaneous CD11b+ cells modifies their function, impairing sensitization and inducing tolerance.