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J Allergy Clin Immunol. 2004 Jun;113(6):1211-7.

Epigallocatechin gallate attenuates adhesion and migration of CD8+ T cells by binding to CD11b.

Author information

1
Department of Surgical Oncology, Faculty of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan. kz-kawai@mvd.biglobe.ne.jp

Abstract

BACKGROUND:

Although green tea polyphenol catechin has been reported to have antiallergic and anti-inflammatory activities, the precise mechanisms of its effect on the immune system have been poorly investigated.

OBJECTIVE:

In this study, we aimed to elucidate the mechanisms of the anti-inflammatory effect of catechin. For this purpose, we studied the effect of 2 kinds of catechin, epigallocatechin gallate (EGCG) and epicatechin gallate, on peripheral blood CD8+ T cells, which play the key role in immune responses.

METHODS:

Isolated peripheral blood mononuclear cells or CD8+ T cells were incubated without or with catechin, and the changes in the surface expression of integrin molecules were investigated by flow cytometry and the direct binding of catechin to CD11b molecule by competitive ELISA. Also, the effect of catechin on the ability of CD8+ T cells to bind intracellular adhesion molecule 1 and to migrate in response to chemokines was evaluated by using the adhesion and migration assays.

RESULTS:

The 2 catechins directly bound to CD11b expressed on CD8+ T cells, which caused a consequent decrease of flow-cytometric CD11b expression. The effect was more prominent with EGCG than epicatechin gallate, and the impaired expression of CD11b induced by EGCG resulted in decreased ability of CD8+ T cells to adhere intercellular adhesion molecule 1, and consequently decreased migration in response to chemokines.

CONCLUSION:

We concluded that catechin, especially EGCG, by downregulating CD11b expression on CD8+ T cells and, in consequence, inhibiting infiltration of these cells into the sites of inflammation, is a promising new potent anti-inflammatory agent.

PMID:
15208607
DOI:
10.1016/j.jaci.2004.02.044
[Indexed for MEDLINE]

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