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Involvement of CD11b/CD18 in enhanced neutrophil adhesion by Fcγ receptor stimulation
Author(s) -
Kusunoki Takashi,
Tsuruta Satoru,
Higashi Hideo,
Hosoi Susumu,
Hata Daisuke,
Sugie Katsuji,
Mayumi Mitsufumi,
Mikawa Haruki
Publication year - 1994
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 - 10.1002/jlb.55.6.735
Subject(s) - biology , stimulation , integrin alpha m , cd18 , adhesion , receptor , immunology , microbiology and biotechnology , neuroscience , biochemistry , materials science , composite material
Neutrophils showed a rapid and transient adhesion to immunoglobulin G (IgG)‐coated plates compared with their adhesion to bovine serum albumin (BSA)‐coated plates: the adhesion reached a peak after 15 min of incubation and then gradually returned to almost the basal state in 60 min. The addition of monomeric IgG or anti‐FcγRII monoclonal antibody (mAb) (IV.3) suppressed the increase in adhesion, whereas anti‐FcγRIII mAb (3G8) was hardly effective, indicating that the interaction of FcγR, especially FcγRII, with coated IgG is involved in the process. Adhesion was also blocked by cytochalasin B, suggesting that functional actin filament structures are crucial. Protein kinase inhibitors, erbstatin and genistein, inhibited the adhesion in a dose‐dependent manner. The adhesion was inhibited by anti‐CDllb (Ml/70) and anti‐CD18 (MHM23, TS1/18) mAbs. Moreover, neutrophils from a patient with complete leukocyte adhesion deficiency syndrome did not show increased adhesion to IgG‐coated plates. The adhesion of neutrophils to fibrinogen‐ and BSA‐coated plates was also increased when FcγR was stimulated in the fluid phase with soluble aggregated IgG, which was also inhibited by anti‐CDllb mAb. Stimulation of neutrophil FcγR with soluble aggregated IgG enhanced the expression of CDllb in concert with the enhanced adhesion. These data collectively suggest that stimulation via FcγR evokes a tyrosine kinase‐dependent and actin filament‐dependent intracellular signal that enhances the specific and nonspecific adhesive activity of neutrophils, presumably through the activation of CDllb/CD18. J. Leukoc. Biol. 55: 735–742; 1994.