Different Gm allotype amounts in human intravenous immunoglobulin (IVIG) preparations; survival of foreign Gm allotypes in immunodeficient patients

Oxelius, Vivi‐Anne; Eibl, Martha M.

doi:10.1046/j.1365-2249.1996.d01-851.x

Cited by 22 publications

(30 citation statements)

References 9 publications

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“…Particular Gm genotypes are found in populations of IgG subclass de®ciencies [21], IgA de®ciency [6,16] and common variable immunode®ciency [7], often with increased frequency of the genotype G2m(±n±n) on the IGHG2 locus. From patients with hypogammaglobulaemia treated with intravenous immunoglobulin G it is known that G2m(n) is accumulated more than other given foreign Gm allotypes [23].…”

Section: Discussionmentioning

confidence: 99%

“…Methods to separate G2m(±n) from G2m(n), and also G3m(g) from G3m(b), molecules have been published. Different half-lives of Gm allotypes within IgG1, IgG2 and IgG3, and a particularly prolonged survival for G2m(n) were noticed in hypogammaglobulinaemic patients given intravenous gammaglobulin preparations [23]. The opposite Gm haplotypes Gm(f; n; b) and Gm(a; Àn; g), studied in homozygous forms from children with bronchial asthma give rise to different pathways of immune regulation [10].…”

Section: Discussionmentioning

confidence: 99%

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Serum Gm Allotype Development During Childhood

et al. 1999

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Oxelius V-A, Aurivillius M, Carlsson A-M, Musil K. Serun Gm Allotype Development During Childhood. Scand J Immunol 1999;50:440±446 Gm allotypes are genetic variants of the immunoglobulin heavy G chains (IGHG) of IgG molecules, coded from chromosome 14q32, characterized by differences in amino acid epitopes of the constant heavy G chains and inherited in the Mendelian manner. Gm allotypes have in¯uence on IgG subclass levels, and serum Gm allotype levels have been given for different Gm genotypes in adults. Four hundred and thirty healthy children, aged 1±15 years, were examined for serum Gm allotypes and IgG subclasses from the six most common Gm genotypes and different age groups were measured using competitive enzyme-linked immunosorbant assay and radial immunodiffusion methods. Quantities (in g/l) of G1m(a) and G1m(f) of IgG1, G2m(n) and G2m(± n) of IgG2 and G3m(g), and G3m(b) of IgG3 are given. Different maturation rates of the alternative Gm allotypes within IgG1, IgG2 and IgG3 were shown. G2m(n) development was strikingly retarded compared with G2m(±n) from the g2 locus. This was found comparing IgG2 levels from homozygous G2m(±n±n) and G2m(nn) individuals, but was also seen in heterozygous G2m(n±n) genotypes. From the g1 locus G1m(f) levels dominated signi®cantly, but inconstantly, over G1m(a) levels in heterozygous G1m(af) individuals. In homozygous G1m genotypes, G1m(aa) compared with G1m(ff) of the same age, one or the other dominated, sometimes signi®cantly. Serum levels of G3m(b) from the g3 locus of homozygous G3m(bb) individuals were increased signi®cantly compared with G3m(g) levels of homozygous G3m(gg) individuals, in ages over 3 years. However, in heterozygous G3m(gb) individuals G3m(b) dominance was not evident. There is a relatively rapid development of G1m(f) molecules and a retarded development of G2m(n) in the Gm(f;n;b) haplotype. In comparison, G1m(a) is retarded and G2m(±n) is enhanced in the Gm(a;±n;g) haplotype. The retarded serum G2m(n) development is comparable with serum IgA development during childhood. Different maturation rates of Gm allotypes within the same IgG subclass provide further explanation for the variation of the antibody response during childhood. Quantitative Gm allotype determinations give information of the activity from IGHG genes. The genetic variation constitutes an additional basis for evaluation of IgG antibodies in different diseases in childhood.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Serum Gm Allotype Development During Childhood

et al. 1999

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“…G2M(n) differs from G2M(nϪ), the alternative immunochemically distinguished IgG2 allotype, by the presence of methionine instead of a valine residue at CH2 position 52 in the Fc part of the IgG2 molecule (20). Furthermore, the two IgG2 allotypes differ with regard to physicochemical properties, maturation during childhood, and catabolic rate (21)(22)(23).…”

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confidence: 99%

Homozygosity for the IgG2 Subclass Allotype G2M(n) Protects against Severe Infection in Hereditary C2 Deficiency

Jönsson

Oxelius

Truedsson

et al. 2006

The Journal of Immunology

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Homozygous C2 deficiency (C2D) is the most common deficiency of the classical complement pathway in Western countries. It is mostly found in patients with autoimmune disease or susceptibility to bacterial infections and in healthy persons. We wished to assess to what extent other immunological factors might explain differences of susceptibility to infections in C2D. For this reason, 44 Swedish patients with C2D were stratified with regard to the severity of documented infections. Investigations of IgG subclass levels, IgG subclass-specific GM allotypes, concentrations of factor B, properdin, and factor H, and polymorphisms of mannan-binding lectin and the Fc receptors FcγRIIa and FcγRIIIb were performed. Homozygosity for the G2M*n allele, which is known to promote Ab responses to polysaccharide Ags, was strongly associated with the absence of severe infections (p < 0.001) in the patients, suggesting a major protective role. The combination of mannan (or mannose)-binding lectin and C2 deficiency was found to be a minor susceptibility factor for invasive infection (p = 0.03). Low concentrations of IgG2 and factor B might sometimes contribute to susceptibility to infection. Other factors investigated did not appear to be important. In conclusion, the findings indicated that efficient Ab responses to polysaccharides are protective against severe infection in C2D. Implications with regard to vaccination should be considered.

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“…Furthermore the IGHG*bf-n/*bf-n diplotype (=B2/B2-cells), which was infrequent in children with a family history of allergy and atopy, is common in IgG2 deficiency and in common variable immunodeficiency (23,24). Infants hospitalised with the most severe RSV (Respiratory Syncytial Virus) exhibited increased frequency of the B2-cells (25).…”

Section: Discussionmentioning

confidence: 99%

“…The IgG allotypes are inherited in a Mendelian fashion and expressed randomly in allelic exclusion. The IgG allotypes are separate entities with distinct immunochemical and functional characteristics, such as fractionation rates, electrophoretic rates (7), half-life times (8) and maturation rate during childhood (9). Four subsets of B cells have been identified, based on the alternative protein expressions from the IGHG3, IGHG1 and IGHG2 genes (10), the IGHG*bfn haplotype (=B1-cells) is typed by IgG3*b, IgG1*f and IgG2*n; the IGHG*bf-n haplotype (=B2 cells) is typed by IgG3*b, IgG1*f and IgG2*-n, the IGHG*gan haplotype (=B3-cells) is typed by IgG3*g, IgG1*a and IgG2*n and the IGHG*ga-n haplotype (=B4-cells) is typed by IgG3*g, IgG1*a and IgG2*-n allotypes in serum (6) ( Table 1).…”

Section: Introductionmentioning

confidence: 99%