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Item No. 31827

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Explore how neutrophils shape the immune response in health and disease. This poster highlights neutrophil pathogen defense mechanisms, including phagocytosis, degranulation, and NETosis, as well as neutrophil roles in inflammation and NET-associated pathologies.
DOWNLOAD NOWLow affinity immunoglobulin γ Fc region receptor IIIb (FcγRIIIb) has roles in neutrophil adhesion, phagocytosis, and the respiratory burst.1 It is encoded by the FCGR3B gene in humans and is comprised of two immunoglobulin-like (Ig-like) extracellular domains that bind to IgG Fc and pentraxins, such as C-reactive protein. FcγRIIIb is synthesized as a precursor with a transmembrane domain and four-residue cytoplasmic domain that are cleaved in the endoplasmic reticulum, following which a glycosylphosphatidylinositol (GPI) anchor is added, which allows for membrane association of the mature protein.2,1 It can be expressed as three different allotypes known as human neutrophil antigens HNA-1a, HNA-1b, and HNA-1c, which are characterized by differential antibody binding affinities.1 FcγRIIIb is constitutively expressed in neutrophils and a subset of basophils and is shed from the cell surface as a soluble form via proteolytic cleavage during apoptosis or following neutrophil activation.1,3 Copy number variation of FCGR3B is associated with an increased risk of systemic lupus erythematosus (SLE) and primary Sjögren's syndrome.4 Cayman's FcγRIIIb/CD16b HNA-1b allotype (human, recombinant) protein consists of 176 amino acids and has a calculated molecular weight of 20 kDa.
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1. FcγRIIB, FcγRIIIB, and systemic lupus erythematosus. Ann. N. Y. Acad. Sci. 1183(1), 69-88 (2010).
2. Function of human FcγRIIA and FcγRIIIB. Semin. Immunol. 7(1), 37-44 (1995).
3. Different proteolytic mechanisms involved in FcγRIIIb shedding from human neutrophils. Clin. Exp. Immunol. 125(1), 169-175 (2001).
4. Association of copy number variation in the FCGR3B gene with risk of autoimmune diseases. Genes Immun. 11(2), 155-160 (2010).