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Sulfonated human immunoglobulin enhances CD16‐linked CD11b expression on human neutrophils
Author(s) -
Kimura Hirokazu,
Kato Masahiko,
Ikeda Miyuki,
Nagai Akira,
Okada Yasunori,
Naito Shigeto,
Oshima Shigeru,
Taniguchi Koichi,
Kozawa Kunihisa,
Morikawa Akihiro
Publication year - 2003
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1016/j.cellbi.2003.07.003
Subject(s) - cd16 , integrin alpha m , tumor necrosis factor alpha , antibody , flow cytometry , in vivo , immunology , immunoglobulin g , biology , in vitro , receptor , microbiology and biotechnology , receptor expression , cd64 , chemistry , antigen , biochemistry , cd3 , cd8
Abstract Intravenous human immunoglobulin therapy infrequently results in excessive inflammatory responses in vivo; these effects are not fully understood. We assessed whether sulfonated human immunoglobulin (SHIG) or polyethylene glycol‐treated human immunoglobulin (PHIG) enhanced expression of inflammatory receptors on peripheral blood neutrophils in vitro, such as αMβ2 (CD11b/CD18) and Fc gamma receptor type III (FcγRIII). CD11b and CD16 expression on neutrophils was measured by fluorescence flow cytometry. Various cytokines were assessed using a highly sensitive fluorescence microsphere system. SHIG enhanced /induced CD11b expression and partial aggregations on neutrophils, but PHIG did not. No detection of aggregation IgG was observed in SHIG and PHIG . SHIG‐induced CD11b expression was inhibited by treatment of corticosteroid (dexamethasone) and by anti‐CD16 monoclonal antibody. Concentrations of various cytokines such as interleukin (IL)‐1β, IL‐2, IL‐4, IL‐5, IL‐6, IL‐8, IL‐10, RANTES, tumor necrosis factor (TNF)‐α, and interferon (INF)‐γ in culture supernatant were not significantly changed by SHIG or PHIG. SHIG and PHIG did not enhance CD16 on neutrophils. SHIG enhanced CD16‐linked CD11b expression on neutrophils in vitro. CD11b induction was inhibited by dexamethasone and by anti‐CD16 antibody. These in vitro results suggest that aggregations and enhancement of CD11b on neutrophils by SHIG may induce excessive inflammatory responses in vivo.