Human IgG Matched Antibody Pair Kit includes an unlabeled monoclonal capture antibody, an AP-labelled monoclonal detection antibody, native human IgG ELISA standard, and standard reconstitution buffer. This matched antibody pair kit can be used to quantify native and recombinant human IgG. Matched antibody pair kits are ideal for economical ELISA and ELISA-based assay development.

Type de test

Sandwich (quantitative)

Méthode de détection

Colorimetric

Type d'échantillon

Serum, plasma, and cell culture supernatant.

Gamme de detection

0.2-100 ng/ml

Spécificité

This matched antibody pair kit utilizes a pair of antibodies to specifically recognize the Fc part of human IgG.

Reactivité

Human, Non-Human Primates

Réactivité croisée

This matched antibody pair kit reacts with human IgG and cross reacts with IgG from non-human primates.

Notes générales

It may be necessary to optimize the reagents in this matched antibody pair kit for your sample type, immunoassay format, or instrumentation. The protocol manual outlines the recommended assay procedure to run a standard 96-well microplate sandwich ELISA using AP/pNPP system for colorimetric quantitative detection of human IgG.

Stockage

Shipped at +4°C. Store the ELISA standard at -20°C. Store all other reagents at +4°C.

Synonymes

FLJ39988, FLJ40036, FLJ40253, FLJ40587, FLJ40789, FLJ40834, G1m marker, G2m marker, G3m marker, G4m marker, HDC, Heavy chain disease protein, Human immunglobulin G, Ig gamma 1 chain C region, Ig gamma 2 chain C region, Ig gamma 3 chain C region, Ig gamma 4 chain C region, IgG heavy chain locus, IGHG 1, IGHG 2, IGHG 3, IGHG 4, IGHG1, IGHG2, IGHG3, IGHG4, Immunoglobulin Gm1, Immunoglobulin Gm3, Immunoglobulin Gm4, Immunoglobulin heavy constant gamma 1, immunoglobulin heavy constant gamma 1 (G1m marker), Immunoglobulin heavy constant gamma 2, immunoglobulin heavy constant gamma 2 (G2m marker), Immunoglobulin heavy constant gamma 3, immunoglobulin heavy constant gamma 3 (G3m marker), Immunoglobulin heavy constant gamma 4, immunoglobulin heavy constant gamma 4 (G4m marker), MGC117419, MGC45809

Avertissement

Ce produit est uniquement destiné à la recherche. Il n'est pas destiné à un usage diagnostique ou thérapeutique.

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Figure 1: Human IgG Matched Antibody Pair Kit (A270397)

Representative standard curve for Human IgG Matched Antibody Pair Kit (A270397) using pNPP as substrate.

Références (5)

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IgM, lgG and IL-6 profiles in the Trypanosoma brucei brucei monkey model of human African trypanosomiasis

Références : Human IgG Matched Antibody Pair Kit (A270397)

Résumé :

Human African trypanosomiasis (HAT) patients manifest immunological profiles, whose variations over time can be used to indicate disease progression. However, monitoring of these biomarkers in human patients is beset by several limitations which can be offset by using chronic animal models. A recent improved monkey model of HAT using a Trypanosoma brucei brucei isolate has been developed but the immunological profile has not been elucidated. The objectives of the current study was to determine the IgM, IgG and IL-6 profiles in blood and cerebrospinal fluid (CSF) in vervet monkeys infected with T. b. brucei. Three vervet monkeys were infected intravenously with 10⁵T. b. brucei, monitored for disease development and subsequently treated 28days post infection (dpi) sub-curatively using diminazene aceturate (DA) to induce late stage disease and curatively treated with melarsoprol (Mel B) at 119 dpi, respectively. Matched serum and cerebrospinal fluid (CSF) samples were obtained at regular intervals and immunospecific IgM, immunoglobulin G (IgG) were quantified by ELISA while IL-6 was assayed using a cytometric bead array (CBA) kit. Results showed that following infection, CSF IgM, IgG, IL-6 and serum IL-6 were significantly (p<0.05) elevated with peak levels coinciding with relapse parasitaemia. The IgG levels increased to reach OD peak levels of 0.442±0.5 at 126 dpi. After curative treatment with MelB, the serum IgM and Ig G levels fell rapidly to attain pre-infection levels within 35 and 49days, respectively. This shows that the profile of these immunoglobulins can be used as an indicator of curative treatment. CSF IL-6 concentrations of infected vervet monkeys showed no significant change (P>0.05) between infection and 35 dpi but levels increased significantly (P<0.05) with the highest level of 55.53pg/ml recorded at112 dpi. IL-6 elevation from 35 dpi may be indicative of parasite neuroinvasion hence can be used as possible candidate marker for late stage disease in the monkey model. Further, the marker can also be used in conjunction with IgG and IgM as markers for development of test of cure for HAT.

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A Functional Role for Antibodies in Tuberculosis

Références : Human IgG Matched Antibody Pair Kit (A270397)

Résumé :

While a third of the world carries the burden of tuberculosis, disease control has been hindered by a lack of tools, including a rapid, point-of-care diagnostic and a protective vaccine. In many infectious diseases, antibodies (Abs) are powerful biomarkers and important immune mediators. However, in Mycobacterium tuberculosis (Mtb) infection, a discriminatory or protective role for humoral immunity remains unclear. Using an unbiased antibody profiling approach, we show that individuals with latent tuberculosis infection (Ltb) and active tuberculosis disease (Atb) have distinct Mtb-specific humoral responses, such that Ltb infection is associated with unique Ab Fc functional profiles, selective binding to Fc?RIII, and distinct Ab glycosylation patterns. Moreover, compared to Abs from Atb, Abs from Ltb drove enhanced phagolysosomal maturation, inflammasome activation, and, most importantly, macrophage killing of intracellular Mtb. Combined, these data point to a potential role for Fc-mediated Ab effector functions, tuned via differential glycosylation, in Mtb control.

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Immunopathology of Japanese macaque encephalomyelitis is similar to multiple sclerosis

Références : Human IgG Matched Antibody Pair Kit (A270397)

Résumé :

Japanese macaque encephalomyelitis (JME) is an inflammatory demyelinating disease that occurs spontaneously in a colony of Japanese macaques (JM) at the Oregon National Primate Research Center. Animals with JME display clinical signs resembling multiple sclerosis (MS), and magnetic resonance imaging reveals multiple T2-weighted hyperintensities and gadolinium-enhancing lesions in the central nervous system (CNS). Here we undertook studies to determine if JME possesses features of an immune-mediated disease in the CNS. Comparable to MS, the CNS of animals with JME contain active lesions positive for IL-17, CD4+ T cells with Th1 and Th17 phenotypes, CD8+ T cells, and positive CSF findings.

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Calcineurin inhibitors dampen humoral immunity by acting directly on naive B cells

Références : Human IgG Matched Antibody Pair Kit (A270397)

Résumé :

Calcineurin inhibitors (CNI), used frequently in solid organ transplant patients, are known to inhibit T cell proliferation, but their effect on humoral immunity is far less studied. Total and naive B cells from healthy adult donors were cultured in immunoglobulin (Ig)A- or IgG/IgE-promoting conditions with increasing doses of cyclosporin, tacrolimus, rapamycin or methylprednisolone. The effect on cell number, cell division, plasmablast differentiation and class-switching was tested. To examine the effect on T follicular helper (Tfh) cell differentiation, naive CD4(+) T cells were cultured with interleukin (IL)-12 and titrated immunosuppressive drug (IS) concentrations. Total B cell function was not affected by CNI. However, naive B cell proliferation was inhibited by cyclosporin and both CNI decreased plasmablast differentiation. Both CNI suppressed IgA, whereas only cyclosporin inhibited IgE class-switching. Rapamycin had a strong inhibitory effect on B cell function. Strikingly, methylprednisolone, increased plasmablast differentiation and IgE class-switching from naive B cells. Differentiation of Tfh cells decreased with increasing IS doses. CNI affected humoral immunity directly by suppressing naive B cells. CNI, as well as rapamycin and methylprednisolone, inhibited the in-vitro differentiation of Tfh from naive CD4(+) T cells. In view of its potent suppressive effect on B cell function and Tfh cell differentiation, rapamycin might be an interesting candidate in the management of B cell mediated complications post solid organ transplantation.

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Distribution of Fc?R gene polymorphisms among two sympatric populations in Mali: differing allele frequencies, associations with malariometric indices and implications for genetic susceptibility to malaria

Références : Human IgG Matched Antibody Pair Kit (A270397)

Résumé :

Background: Genetic polymorphisms in the complex gene cluster encoding human Fc-gamma receptors (Fc?Rs) may influence malaria susceptibility and pathogenesis. Studying genetic susceptibility to malaria is ideal among sympatric populations because the distribution of polymorphic genes among such populations can help in the identification malaria candidate genes. This study determined the distribution of three FcyRs single nucleotide polymorphisms (SNPs) (Fc?RIIB-rs1050519, Fc?RIIC-rs3933769 and Fc?RIIIA-rs396991) among sympatric Fulani and Dogon children with uncomplicated malaria. The association of these SNPs with clinical, malariometric and immunological indices was also tested.

Methods: This study involved 242 Fulani and Dogon volunteers from Mali age under 15 years. All SNPs were genotyped with predesigned TaqMan(®) SNP Genotyping Assays. Genotypic and allelic distribution of SNPs was compared across ethnic groups using the Fisher exact test. Variations in clinical, malariometric and immunologic indices between groups were tested with Kruskal-Wallis H, Mann-Whitney U test and Fisher exact test where appropriate.

Results: The study confirmed known malariometric and immunologic differences between sympatric Fulani and non-Fulani tribes. Parasite density was lower in the Fulani than the Dogon (p < 0.0001). The mutant allele of Fc?RIIC (rs3933769) was found more frequently in the Fulani than the Dogon (p < 0.0001) while that of Fc?RIIIA (rs396991) occurred less frequently in the Fulani than Dogon (p = 0.0043). The difference in the mutant allele frequency of Fc?RIIB (rs1050519) between the two ethnic groups was however not statistically significant (p = 0.064). The mutant allele of rs396991 was associated with high malaria-specific IgG1 and IgG3 in the entire study population and Dogon tribe, p = 0.023 and 0.015, respectively. Parasite burden was lower in carriers of the Fc?RIIC (rs3933769) mutant allele than non-carriers in the entire study population (p < 0.0001). Carriers of this allele harboured less than half the parasites found in non-carriers.

Conclusion: Differences in the allelic frequencies of rs3933769 and rs396991 among Fulani and Dogon indirectly suggest that these SNPs may influence malaria susceptibility and pathogenesis in the study population. The high frequency of the Fc?RIIC (rs3933769) mutant allele in the Fulani and its subsequent association with low parasite burden in the entire study population is noteworthy.

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