Anti-Human IgG3 [Clone HP6050] – Biotin

Purified human myeloma protein

This Biotinylated antibody is formulated in 0.01 M phosphate buffered saline (150 mM NaCl) PBS pH 7.4, 1% BSA and 0.09% sodium azide as a preservative.

Liquid

This biotinylated antibody is stable when stored at 2-8°C. Do not freeze.

Research Use Only

2 – 8° C Wet Ice

Clone HP6050 activity is directed against the hinge region of human IgG3.

Humans produce five classes of immunoglobulins, IgM, IgD, IgA, IgE, and IgG¹. IgG is the most abundant class¹ and functions in the humoral immune response². There are four subclasses of IgG, and they are numbered according to decreasing abundance as IgG1 through IgG4. The four subclasses are highly conserved and consist of four polypeptide chains: two identical heavy chains and two identical light chains¹. While the general structure is very similar between IgG subclasses, differences in their constant regions in the hinge and upper CH2 domain as well as in glycosylation affect their binding to antigens (e.g. pathogenic proteins, polysaccharides, allergens), C1q and Fc receptors, leading to differences in functionality. As a result, each IgG subclass has a unique response skewed to specific antigens.

IgG3 is a pro-inflammatory antibody that potently induces effector function¹. However, IgG3 has a relatively shorter half-life compared to other IgG antibodies, and this is thought to deter an excessive inflammatory response. IgG3 is also unique relative to the other IgG subclasses in that its hinge is elongated due to duplications of the hinge exon. Additionally, many IgG3 allelic forms exist. IgG3 antibodies are the first subclass to respond to viral infection, with IgG1 following.

HP6050 was generated by immunizing a BALB/c mouse with purified human myeloma protein³. Spleen cells were fused with Sp2/0-Ag14 myeloma cells.

IgG3 is produced by B cells and is present in serum.

IgG-Fc receptors, C1q

1 Vidarsson G, Dekkers G, Rispens T. Front Immunol. 5:520. 2014.
2 Rispens T, Huijbers MG. Nat Rev Immunol. 23(11):763-778. 2023.
3 Reimer CB, Phillips DJ, Aloisio CH, et al. Hybridoma. 3(3):263-275. 1984.
4 Jefferis R, Reimer CB, Skvaril F, et al. Immunol Lett. 10(3-4):223-252. 1985.