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Sulfonated human immunoglobulin enhances CD16-linked CD11b expression on human neutrophils
Hirokazu Kimura1, Masahiko Kato, Miyuki Ikeda
1Gunma Prefectural Institute of Public Health and Environmental Sciences, 378, Kamioki, Maebashi, Gunma 371-0052, Japan. kimura-hi@pref.gunma.jp
Cell Biology International
|October 31, 2003
Summary
Sulfonated human immunoglobulin (SHIG) may trigger inflammatory responses by increasing CD11b expression on neutrophils. This effect, observed in vitro, was blocked by dexamethasone and an anti-CD16 antibody, suggesting a potential mechanism for adverse reactions.
Area of Science:
- Immunology
- Cell Biology
Background:
- Intravenous immunoglobulin (IVIg) therapy can cause inflammatory side effects.
- The mechanisms behind these adverse reactions are not fully understood.
Purpose of the Study:
- To investigate whether modified human immunoglobulins, sulfonated (SHIG) or polyethylene glycol-treated (PHIG), enhance inflammatory receptor expression on neutrophils in vitro.
- Specifically, to assess the impact on alphaMbeta2 (CD11b/CD18) and Fc gamma receptor type III (FcgammaRIII) expression.
Main Methods:
- Peripheral blood neutrophils were treated with SHIG and PHIG in vitro.
- Expression of CD11b and CD16 on neutrophils was quantified using fluorescence flow cytometry.
- Cytokine levels in culture supernatants were measured using a fluorescence microsphere system.
Main Results:
- SHIG, but not PHIG, enhanced CD11b expression and induced partial neutrophil aggregation in vitro.
- SHIG-induced CD11b expression was significantly reduced by dexamethasone and an anti-CD16 monoclonal antibody.
- Neither SHIG nor PHIG altered CD16 expression or significantly changed the concentrations of measured cytokines (IL-1beta, IL-2, IL-4, IL-5, IL-6, IL-8, IL-10, RANTES, TNF-alpha, INF-gamma).
Conclusions:
- SHIG's ability to enhance CD11b expression and induce neutrophil aggregation in vitro suggests a potential mechanism for IVIg-associated excessive inflammatory responses.
- These findings highlight the importance of understanding immunoglobulin modifications and their impact on neutrophil activation.