Serum Gm Allotype Development During Childhood

Oxelius, Vivi‐Anne; Aurivillius, Magnus; Carlsson, Anna; Musil, Kristina

doi:10.1046/j.1365-3083.1999.00618.x

Cited by 29 publications

(52 citation statements)

References 18 publications

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“…A streptococcal M protein peptide (aa 367-375) and its myosin homolog (aa 114-122) selectively stimulated JDM lymphocytes (cytotoxic response, increased lymphocyte proliferation, and tumor necrosis factor ␣ production) when JDM peripheral blood mononuclear cells were compared with controls (6); stimulation that is compatible with immune activation (37). In addition, these streptococcal peptides also elicited limited T cell receptor V␤ usage (12,15,18) using a T cell capture analysis (6). Further evidence for an activated immune response compatible with a preceding infection in JDM is obtained from gene expression profiles of muscle of untreated children with JDM, which show an increase in IFN-␣/␤ inducible immune genes (9).…”

Section: Pachman Et Almentioning

confidence: 99%

History of infection before the onset of juvenile dermatomyositis: Results from the National Institute of Arthritis and Musculoskeletal and Skin Diseases Research Registry

Pachman

Lipton

Ramsey‐Goldman

et al. 2005

Arthritis & Rheumatism

135

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Objective. To obtain data concerning a history of infection occurring in the 3 months before recognition of the typical weakness and rash associated with juvenile dermatomyositis (JDM). Methods. Parents or caretakers of children within 6 months of JDM diagnosis were interviewed by the registry study nurse concerning their child's symptoms, environment, family background, and illness history. Physician medical records were reviewed, confirming the JDM diagnosis. Results. Children for which both a parent interview and physician medical records at diagnosis were available (n ‫؍‬ 286) were included. Diagnoses were as follows: definite/probable JDM (n ‫؍‬ 234, 82%), possible JDM (n ‫؍‬ 43, 15%), or rash only (n ‫؍‬ 9, 3%). The group was predominantly white (71%) and had a girl:boy ratio of 2:1. Although the mean age at onset was 6.7 years for girls and 7.3 years for boys, 25% of the children were <4 years old at disease onset. In the 3 months before onset, 57% of the children had respiratory complaints, 30% had gastrointestinal symptoms, and 63% of children with these symptoms of infection were given antibiotics. Conclusion. This study provides evidence that JDM affects young children. The symptoms of the typical rash and weakness often follow a history of respiratory or gastrointestinal complaints. These data suggest that the response to an infectious process may be implicated in JDM disease pathogenesis.

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Section: Pachman Et Almentioning

confidence: 99%

History of infection before the onset of juvenile dermatomyositis: Results from the National Institute of Arthritis and Musculoskeletal and Skin Diseases Research Registry

Pachman

Lipton

Ramsey‐Goldman

et al. 2005

Arthritis & Rheumatism

135

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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).…”

mentioning

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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“…The IGHG2*n allele is also found in the IGHG*gan (B3) haplotype, but only very infrequently so (<1-2%). (5,9). Thus, the IgG2*n allotype is mainly a marker for the IGHG*bfn haplotype (=B1-cells).…”

Section: Discussionmentioning

confidence: 99%

“…In heterozygous individuals the IgG3*g and IgG3*b are about 50:50%, respectively, of the IgG3 amount. The method is described in detail elsewhere (6,9). The study was approved by the Institutional Review Board at Umeå University, Sweden.…”

Section: Ighg Genotyping By Serum Igg Allotypesmentioning

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%

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Immunoglobulin constant heavy G chain genes as risk factors in childhood allergies

Oxelius

Bråbäck

Ahlstedt

et al. 2006

Clin Experimental Allergy

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Serum Gm Allotype Development During Childhood

Cited by 29 publications

References 18 publications

History of infection before the onset of juvenile dermatomyositis: Results from the National Institute of Arthritis and Musculoskeletal and Skin Diseases Research Registry

History of infection before the onset of juvenile dermatomyositis: Results from the National Institute of Arthritis and Musculoskeletal and Skin Diseases Research Registry

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

Immunoglobulin constant heavy G chain genes as risk factors in childhood allergies

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