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Differential regulation of CD11b on γδ T cells and monocytes in response to unripe apple polyphenols
Author(s) -
Graff Jill C.,
Jutila Mark A.
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.0207125
Subject(s) - integrin alpha m , monocyte , biology , immune system , microbiology and biotechnology , t cell , cell adhesion , immunology , biochemistry , cell
Leukocyte adhesion and migration are mediated partially by CD11b/CD18 (membrane‐activated complex‐1, CR3). Earlier studies have demonstrated a role for green tea polyphenols in down‐regulating CD11b on CD8 + T cells and monocytes. We have shown recently a stimulatory effect of unripe apple polyphenols (APP) on γδ T cells. Thus, we compared the effect of APP on bovine γδ T cell and monocyte CD11b expression. Purified bovine monocytes and monocyte‐depleted PBLs were cultured with APP. CD11b levels decreased on monocytes in response to APP. In contrast, a γδ T cell subset responded to APP by up‐regulating CD11b. The CD11b regulation was not seen on γδ T cells or monocytes treated with APP fractions depleted of tannins. The APP‐induced down‐regulation of CD11b on monocytes was inhibited by an anti‐CD11b mAb, consistent with previous studies showing that polyphenols bind CD11b. As expected, the anti‐CD11b mAb had no effect on the APP response in resting γδ T cells, as these cells lacked CD11b. Consistent with the changes in surface CD11b expression, APP‐treated γδ T cells showed increased adherence to pastic, whereas monocyte adhesion was reduced. APP also induced cytokine gene expression in γδ T cells. Some polyphenols are thought of as anti‐inflammatory agents; however, these data, as well as other ongoing studies, indicate they have a proinflammatory effect on γδ T cells. In vivo, plant polyphenols may enhance γδ T cell migration and function at sites of inflammation, where they could induce rapid, immune‐regulatory and innate‐like immune responses.