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Functional Association of CD9 with the Fc Receptors in Macrophages¹

Keisuke Kaji^*, Sunao Takeshita^*, Kensuke Miyake, Toshiyuki Takai and Akira Kudo^2,*

^* Department of Life Science, Tokyo Institute of Technology, Yokohama, Japan; Department of Immunology, Saga Medical School, Saga, Japan; and Department of Experimental Immunology, Institute of Development, Aging and Cancer, Tohoku University, Sendai, Japan

CD9, a member of the tetraspan family of proteins, is highly expressed on macrophages. Although a clear function for the molecule has yet to be described, we have found that the anti-CD9 mAb activates mouse macrophages. The rat anti-CD9 mAb, KMC8.8, but not the F(ab')₂, induced tyrosine phosphorylation of proteins including syk and cbl and induced cell aggregation in the mouse macrophage cell line, J774, suggesting that co-cross-linking of CD9 and FcR was required for the signal. Co-cross-linking of CD9-FcR with KMC8.8 on macrophages from three different FcR-deficient mice, FcR -chain^-/-, FcRIIB^-/-, and FcRIII^-/-, revealed that FcRIII is specific and crucial for syk phosphorylation. Although both KMC8.8 and the anti-FcRIIB/III mAb, 2.4G2, evoked similar phosphorylation patterns, only KMC8.8 induced cell aggregation. Additionally, KMC8.8 treatment led to reduce levels of TNF- production and p42/44 extracellular signal-related kinase phosphorylation relative to 2.4G2 stimulation. Immunofluorescence staining showed that co-cross-linking of CD9-FcR with KMC8.8 induced filopodium extension before cell aggregation, which was followed by simultaneous colocalization of CD9, FcRIIB/III, Mac-1, ICAM-1, and F-actin at the cell-cell adhesion site. Moreover, KMC8.8 treatment of FcR-deficient macrophages revealed that the colocalization of CD9, FcRIII, Mac-1, and F-actin requires co-cross-linking of CD9-FcRIII, whereas co-cross-linking of CD9-FcRIIB induced the colocalization of only CD9 and FcRIIB. Our results demonstrate that co-cross-linking of CD9 and FcRs activates macrophages; therefore, CD9 may collaborate with FcRs functioning in infection and inflammation on macrophages.

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