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Studies of delayed systemic effects of ultraviolet B radiation (UVR) on the induction of contact hypersensitivity, 2. Evidence that interleukin‐10 from UVR‐treated epidermis is the critical mediator
Author(s) -
Kurimoto I.,
Kitazawa T.,
Streilein J. W.
Publication year - 2000
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1046/j.1365-2567.2000.00934.x
Subject(s) - immune system , immunology , epidermis (zoology) , immunity , lymphatic system , medicine , lymph , lymph node , ultraviolet radiation , spleen , histamine , pathology , chemistry , endocrinology , anatomy , radiochemistry
Summary Acute, low‐dose ultraviolet B radiation (UVR) alters cutaneous immunity at the local site as well as systemically. Within 2–3 days of UVR exposure, recipient mice lose their capacity to develop contact hypersensitivity (CH) when hapten is painted on unexposed skin. This loss correlates temporally with a functional deficit among dendritic antigen‐presenting cells within non‐draining lymph nodes and spleen. In the experiments described, the delayed systemic immune deficiency following acute, low‐dose UVR exposure was found to be eliminated with neutralizing anti‐interleukin‐10 (IL‐10) antibody. Intracutaneous injection of IL‐10 generated a deficiency of systemic immunity as well as a functional deficit among lymph node dendritic cells that was similar to that induced by UVR. The skin itself was found to be the source of the IL‐10 responsible for these defects, and epidermis (presumably keratinocytes) rather than mast cells was found to be the source of IL‐10 within UVR‐exposed skin. The potential relationships are discussed between the delayed systemic immune deficit created by acute, low‐dose UVR, and the systemic immune deficits caused by chronic, high‐dose UVR and by a single, high‐dose UVR exposure.