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Intercellular adhesion molecule‐1 and vascular cell adhesion molecule‐1 cooperatively contribute to the cutaneous Arthus reaction
Author(s) -
Orito Hidemitsu,
Fujimoto Manabu,
Ishiura Nobuko,
Yanaba Koichi,
Matsushita Takashi,
Hasegawa Minoru,
Ogawa Fumihide,
Takehara Kazuhiko,
Sato Shinichi
Publication year - 2007
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1189/jlb.1006623
Subject(s) - arthus reaction , cell adhesion molecule , icam 1 , proinflammatory cytokine , intercellular adhesion molecule 1 , inflammation , vcam 1 , immunology , infiltration (hvac) , intercellular adhesion molecule , cell adhesion , tumor necrosis factor alpha , biology , chemistry , microbiology and biotechnology , cell , biochemistry , materials science , composite material
Immune complex (IC)‐induced inflammation is mediated by inflammatory cell infiltration, a process that is highly regulated by expression of multiple adhesion molecules. The roles and interactions of ICAM‐1 and VCAM‐1, the major regulators of leukocyte firm adhesion, were examined in the cutaneous reverse‐passive Arthus reaction using ICAM‐1‐deficient (ICAM‐1 −/− ) mice and blocking mAb against VCAM‐1. Within 8 h, IC challenge of wild‐type mice induced edema, hemorrhage, interstitial accumulation of neutrophils and mast cells, as well as production of TNF‐α and IL‐6. All of these inflammatory parameters were reduced significantly in ICAM‐1 −/− mice. The blockade of VCAM‐1 in wild‐type mice did not affect any inflammatory parameters. In contrast, ICAM‐1 −/− mice treated with anti‐VCAM‐1 mAb had significantly reduced edema, hemorrhage, and neutrophil infiltration. Furthermore, VCAM‐1 blockade in ICAM‐1 −/− mice suppressed cutaneous TNF‐α and IL‐6 production. Thus, VCAM‐1 plays a complementary role to ICAM‐1 in the cutaneous Arthus reaction by regulating leukocyte accumulation and proinflammatory cytokine production.