Selective deficiency of immunoglobulin A2.

Loghem, Erna van; Zegers, B. J. M.; Bast, E. J. E. G.; Kater, L.

doi:10.1172/jci111155

Cited by 21 publications

(5 citation statements)

References 28 publications

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“…24 Immunoglobulin A subclass deficiency Several case reports have described IgA subclass de¢-ciencies in symptomatic patients. 25 In apparently healthy blood donors, the selective absence of either IgA1 or IgA2 is more common than de¢ciency of total IgA. 26 …”

Section: Transient Immunoglobulin a Deficiencymentioning

confidence: 99%

The clinical significance of immunoglobulin A deficiency

2007

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Section: Transient Immunoglobulin a Deficiencymentioning

confidence: 99%

The clinical significance of immunoglobulin A deficiency

2007

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“…Selective deficiency of the major IgA subclass, IgAl, has not been reported, but selective deficiency of IgA2 in a mother and daughter has been described [8],…”

Section: Introductionmentioning

confidence: 99%

IgG Anti-IgA1 and Anti-IgA2 Antibodies: Their Measurement by an Enzyme-Linked Immunosorbent Assay and Their Relationship to Disease

Petty¹,

Sherry²,

Johannson³

1986

Int Arch Allergy Immunol

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IgG anti-IgA antibodies were measured by an enzyme-linked immunosorbent assay using one IgA1 and one IgA2 (ml) myeloma and a pooled IgA protein preparation as antigens. Class-specific anti-IgA antibodies occurred in 0.8% of non-IgA-deficient sera and 24.3% of IgA-deficient sera. Antibodies reacting with IgA1 only occurred in 2.6% of non-IgA-deficient sera and 6.7% of IgA-deficient sera. Antibodies reacting with IgA2 only occurred in 0.6% of non-IgA-deficient sera and 2.7% of IgA-deficient sera. The prevalence of anti-IgA in IgA deficients with inflammatory disease was higher (81.8%) than in IgA deficients without disease (24.1 %) and was accounted for by class-specific antibodies.

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“…The remaining 210 Em(1)-positive samples noted in table IV were either from heterozygotes or from individuals of unknown zygosity and included samples from persons deficient in IgGl (Xap) [25], IgG2 (Muz) [26], IgG3 (Bar) [27], IgA2 (Bie) [28] or IgG1, IgG2, IgG4 and IgAl (Tak, Tou) [29, 301. Because Em(1) is present in all but a few haplotypes, we have not calculated the frequencies of haplotypes associated with Em(1) but of those that were found Em(1-) in the various populations.…”

Section: Resultsmentioning

confidence: 99%

A Genetic Marker of Human IgE Heavy Chains, Em(1)¹

1984

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A monoclonal anti-IgE antibody was obtained that reacted with some IgE myeloma proteins and with all but a few normal sera. Family studies proved that a genetic marker of IgE had been detected. This allotype, called Em(1), segregates in association with certain Gm-Am haplotypes. The available quantitative evidence warrants the conclusion that human IgE has genetic variants, but no subclasses. Samples from various populations of five continents, representative for the respective prevalent Gm-Am haplotypes, were tested for Em(1). Em(1) was absent mainly in haplotypes carrying A2m(2) and G2m(n). These closely linked genes are located in a chromosomal region that comprises the gamma 2-gamma 4-epsilon-alpha 2 CH genes. A hypothesis for the generation of Em(1) is given.

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Selective deficiency of immunoglobulin A2.

Cited by 21 publications

References 28 publications

The clinical significance of immunoglobulin A deficiency

The clinical significance of immunoglobulin A deficiency

IgG Anti-IgA1 and Anti-IgA2 Antibodies: Their Measurement by an Enzyme-Linked Immunosorbent Assay and Their Relationship to Disease

A Genetic Marker of Human IgE Heavy Chains, Em(1)¹

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Selective deficiency of immunoglobulin A2.

Cited by 21 publications

References 28 publications

The clinical significance of immunoglobulin A deficiency

The clinical significance of immunoglobulin A deficiency

IgG Anti-IgA1 and Anti-IgA2 Antibodies: Their Measurement by an Enzyme-Linked Immunosorbent Assay and Their Relationship to Disease

A Genetic Marker of Human IgE Heavy Chains, Em(1)1

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Product

Resources

About

A Genetic Marker of Human IgE Heavy Chains, Em(1)¹