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Intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 cooperatively contribute to the cutaneous Arthus reaction.

Authors
  • Orito, Hidemitsu
  • Fujimoto, Manabu
  • Ishiura, Nobuko
  • Yanaba, Koichi
  • Matsushita, Takashi
  • Hasegawa, Minoru
  • Ogawa, Fumihide
  • Takehara, Kazuhiko
  • Sato, Shinichi
Type
Published Article
Journal
Journal of Leukocyte Biology
Publisher
Wiley
Publication Date
May 01, 2007
Volume
81
Issue
5
Pages
1197–1204
Identifiers
PMID: 17299025
Source
Medline
License
Unknown

Abstract

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-alpha 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-alpha 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.

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