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IgA Fc receptors.
Renato C Monteiro1, Jan G J Van De Winkel
11INSERM E0225, Bichat Medical School, 16 rue Henri Huchard, Paris 75870, France. monteiro@bichat.inserm.fr
Annual Review of Immunology
|January 14, 2003
Summary
The myeloid-specific IgA Fc receptor (FcalphaRI or CD89) plays a crucial role in mucosal defense and IgA nephropathy. Human FcalphaRI transgenic mice revealed its function in antibacterial defense and disease development.
Area of Science:
- Immunology
- Cell Biology
Background:
- The IgA receptor family includes various surface receptors involved in IgA transport, catabolism, and deposition.
- The myeloid-specific IgA Fc receptor (FcalphaRI or CD89) is a key receptor expressed on immune cells.
- FcalphaRI lacks intrinsic signaling domains but associates with the FcR gamma-chain for activation.
Purpose of the Study:
- To review the biology of FcalphaRI (CD89).
- To elucidate the in vivo role of FcalphaRI using human FcalphaRI transgenic mice.
- To explore the implications of FcalphaRI in mucosal defense, IgA nephropathy, and disease treatment.
Main Methods:
- Review of existing literature on IgA receptors.
- Generation and utilization of human FcalphaRI transgenic (Tg) mice.
- Analysis of FcalphaRI expression and function in vivo.
Main Results:
- FcalphaRI is expressed on neutrophils, eosinophils, monocytes/macrophages, dendritic cells, and Kupffer cells.
- FcalphaRI Tg mice demonstrated FcalphaRI expression on Kupffer cells, highlighting its role in mucosal defense.
- Studies identified a role for soluble FcalphaRI in IgA nephropathy development via circulating IgA-FcalphaRI complexes.
- Recent work suggests human IgA's therapeutic potential in infectious and neoplastic diseases.
Conclusions:
- FcalphaRI is critical for antibacterial defense, particularly involving serum IgA.
- Soluble FcalphaRI is essential in the pathogenesis of IgA nephropathy.
- Human IgA and FcalphaRI hold promise for treating infectious and neoplastic diseases.