IgG subclasses in bacterial infections.
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Age Factors↗
Biomedical subjects
C I Smith
Publications and source records attributed to C I Smith.
Detection of immunoglobulin genes in individuals with immunoglobulin class or subclass deficiency. Evidence for a pretranslational defect.
Individuals with IgA class or IgG or IgA subclass deficiencies, as well as patients with the phenotypic expression of common variable hypogammaglobulinemia with undetectable IgA, were investigated for immunoglobulin structural gene defects. In total, more than 100 donors were studied using Southern blots. In none of these individuals did we find evidence for structural C alpha- or C gamma-gene deletions. Digestion with BamHI, PstI and PvuII, did not reveal any polymorphism in the samples analyzed with the alpha gene probe. We were unable to detect alpha-chain mRNA in lymphocytes from 8 individuals with undetectable serum and salivary IgA.
Dysgammaglobulinemia↗
Aberrant pattern of anti-carbohydrate antibodies in immunoglobulin class or subclass-deficient donors.
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Autoantibodies↗
Development of anti-polysaccharide antibodies in asplenic children.
Splenectomized patients are highly susceptible to infections with capsulated bacteria and an impaired response to vaccination with bacterial polysaccharides has frequently been observed in these individuals. Based partly on experimental animal data, an important role for the spleen in the production of specific anti-carbohydrate antibodies, i.e. mostly IgG2 in normal adults, has been suggested. We therefore determined the immunoglobulin class and subclass pattern of serum antibodies from asplenic patients against protein and carbohydrate antigens. Normal levels of total serum IgM, IgG2 and specific IgM and IgG2 anti-polysaccharide antibodies were observed, suggesting only a minor role for the spleen in determining the antibody repertoire. The data imply that the impaired phagocytic capacity and/or the inability to mount a sufficiently rapid antibody response are the main factors underlying the increased susceptibility to bacterial infections noted in these patients.
Adult↗
Gastrointestinal morbidity among World War II prisoners of war: 40 years on.
A study of Australian male World War II veterans was conducted to assess clinically the gastrointestinal ill-effects which were present 40 years after the stress of internment as prisoners of war of the Japanese. A random sample of 170 surviving members of the captured Eighth Army Division resident in Sydney in 1983 (ex-POW) was compared with a similar sample of veterans who fought in Southeast Asia during the War, but were not imprisoned (non-POW). Duodenal ulcers and strongyloidiasis were more prevalent in the ex-POW group than in the non-POW group. The increased rate of duodenal ulcer (24.7%, compared with 10.5%; P = 0.0005) was confirmed by a higher proportion of ex-POWs currently taking cimetidine (9.0%, compared with 2.3%; P = 0.008). Strongyloidiasis had been found in 9.7% of all veterans, but in 15% of ex-POWs and in 19% of those who had worked on the Burma-Thailand railway. No other significant differences in gastrointestinal disease were found.
Aged↗
Bone-marrow grafting induces acetylcholine receptor antibody formation.
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Adolescent↗
Enzyme-linked immunosorbent assay for subclass distribution of human IgG and IgA antigen-specific antibodies.
In this study we describe an ELISA using monoclonal antibodies to IgG 1, 2, 3, 4, IgA1 and IgA2 for determining the subclass distribution of human-specific antibodies. No cross-reactivity of the subclass-specific reagents under the conditions used was observed. The sensitivity was 0.5 ng/ml for IgG1, 3, 4; 1.5 ng/ml for IgG2 and 50 ng/ml for IgA1 and IgA2. The reproducibility as described by the coefficient of variation calculated on repeated runs was 8-26% if the data were obtained by relating the absorbance values to a positive serum run in the assay, 17-58% when relating the OD figures to those of a standard myeloma plate. The method may be considered semiquantitative with high sensitivity and specificity, easy to handle and with small day-to-day variation. The assay has been applied to a number of antigens of protein and polysaccharide nature.
Antibodies, Monoclonal↗
Transfer of IgA deficiency to a bone-marrow-grafted patient with aplastic anaemia.
IgA deficiency developed in a 2-year-old boy with aplastic anaemia who received a bone-marrow graft from his HLA-identical, 6-year-old, IgA-deficient sister. Southern blot analysis revealed the presence of alpha-genes in both children, thus suggesting a defect of lymphocyte stem-cell differentiation as a cause of IgA deficiency. Tissue typing showed homozygosity of HLA A1, B8, DR3, the haplotype associated with IgA deficiency in healthy people. Despite normal serum levels of IgG subclasses in both donor and recipient, both children showed a relative lack of specific IgG2 anticarbohydrate antibodies. This suggests that their IgA deficiency is part of a more fundamental aberration of immunoglobulin class and subclass distribution.
Anemia, Aplastic↗
Heterogeneity of T-cell beta-chain gene rearrangements in human leukaemias and lymphomas.
The state of T-cell receptor beta-chain gene rearrangement in human T-cell leukaemias has been analysed. All forms of leukaemia tested (T-CLL, ALL, PLL, Sezary syndrome and ATL) exhibit rearrangements of C beta genes confirming the clonality of these neoplasias. However we find no evidence for common gene rearrangements nor for restricted rearrangement patterns within this type of neoplasia. We find evidence of T-cells with C beta 1 and C beta 2 rearrangements, sometimes associated with Igh JH rearrangements, but several cases of T-cell leukaemia with a marker inversion of chromosome 14 (q11;q32) do not have Igh JH rearrangements. The results suggest that TCR beta gene rearrangement occurs early in T-cell ontogeny but that this rearrangement is most often irrelevant to leukaemogenesis.
Cell Line↗
beta 2-Microglobulin secretion from lymphoid cells: a study at the cellular level.
A protein plaque assay was developed for the detection of human lymphocytes secreting beta 2-microglobulin. The development of plaques required production of beta 2-microglobulin by viable cells at an estimated rate exceeding 25 molecules per second. It has previously been suggested that beta 2-microglobulin secretion is restricted to certain lymphoid cell subpopulations. However, both T- and B-cells were shown to form plaques in normal donors and immunodeficient patients after activation with various mitogens. A close correlation between beta 2-microglobulin production and DNA synthesis was evident. However, secretion of immunoglobulin did not correlate with the proportion of cells secreting beta 2-microglobulin.
B-Lymphocytes↗
Kinetics of the spontaneously occurring common variable hypogammaglobulinemia: an analysis of two individuals with previously normal immunoglobulin levels.
Two males with previously normal serum immunoglobulin levels who spontaneously developed common variable hypogammaglobulinemia were investigated. In one patient serum samples obtained before and after the development of hypogammaglobulinemia were analyzed. A parallel decrease in serum IgM, IgG (all 4 subclasses), IgA (both subclasses) as well as kappa and lambda light chains was found. Serum IgD and IgE also decreased but reached a minimum level before the other immunoglobulin classes. A bone marrow aspirate obtained before the development of hypogammaglobulinemia in this patient showed 1.2% plasma cells, whereas the frequency was only 0.1% when low serum immunoglobulins were recorded. These observations demonstrate the existence of adult onset hypogammaglobulinemia.
Adult↗
Rabbit anti-human beta 2 microglobulin antibodies: a T-cell mitogen.
Rabbit anti-beta 2 microglobulin antibodies have been described as a potent mitogen for human B lymphocytes. However, when fractionated after activation, only the T-cell enriched population is actively dividing. The induction of proliferation in purified T cells requires the presence of non-T cells. Daudi cells (which do not express beta 2 microglobulin on their cell surface) were shown to produce 'macrophage replacing factors' which supported anti-beta 2-induced T cell division. Non-T cells could be effectively replaced by addition of interleukin 2 containing cell supernatants, 12-O-tetradecanoyl-phorbol-13-acetate (TPA), or teleocidin B. Thus, anti-beta 2 appears to selectively activate T cells. In contrast to other T cell mitogens, anti-beta 2 microglobulin antibodies did not induce secondary immunoglobulin production in B cells from peripheral blood or spleen.
Animals↗
Ontogeny of IgG2 antibodies against S. aureus teichoic acid in normal and immunodeficient children.
Anti-teichoic acid antibodies of various subclasses were found to be effectively transported across the placenta during pregnancy. In adults these antibodies are mainly of the IgG2 subclass although substantial amounts of specific IgG1 antibodies may also be found. During ontogeny, specific IgG1 antibodies develop during the second year of life whereas specific IgG2 antibodies appear markedly later. In IgG2 deficient children, prolonged deficiency of specific anti-teichoic acid antibodies was observed, suggesting a lack of maturation of the appropriate idiotype(s). In children who received a bone marrow transplant from adult donors, engraftment of IgG2 producing cells could be seen, thus transferring the ability to produce specific antibodies.
Adolescent↗
Immunoglobulin synthesis in a patient with C4 deficiency: functional immaturity of peripheral blood lymphocytes.
Peripheral blood lymphocytes from a systemic lupus erythematosus patient with homozygous C4 deficiency were stimulated in vitro. Although T cell independent stimulation (Epstein-Barr virus) induced normal proportions of IgM secreting cells. IgG and IgA secreting cells were almost absent. Virtually no immunoglobulin secretion was obtained after T cell dependent stimulation (pokeweed mitogen). Cell fractionation experiments indicated that the low pokeweed mitogen response, at least with regard to IgG and IgA production, was mainly due to impaired B-lymphocyte function. The serum IgG subclass distribution pattern of specific antibodies against certain carbohydrate antigens demonstrated a relative lack of IgG2 antibodies. The findings were consistent with functional immaturity of B lymphocytes in the patient.
B-Lymphocytes↗
Gm allotypes in IgA deficiency.
Gm phenotypes were examined in 90 Swedish IgA-deficient (less than 0.05 g/litre of serum IgA) donors and 40 normal first and second degree relatives of six of these donors. The G1m1,2, G3m5 and Km1 frequency in the group of IgA-deficient donors did not differ from that found in the normal population. Among the relatives, HLA and/or Gm identical normal sibs were observed. Anti-IgA antibodies were present in 29 of the IgA-deficient donors and anti-IgG in seven. No association between the two was found. A statistically significant association between the G1m-2 phenotype and the presence of anti-IgA antibodies was observed. When subdivided according to HLA type, a non-random distribution of Gm phenotypes was seen in HLA-B8/DR3 positive individuals with anti-IgA antibodies (HLA-B8/DR3 being the haplotype associated with IgA deficiency). These data suggest an association between IgA deficiency, anti-IgA and the studied Gm allotypes.
Dysgammaglobulinemia↗
False-positive Waaler-Rose test in IgA deficiency.
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Antibodies, Anti-Idiotypic↗
Immunoglobulin subclass distribution of human anti-carbohydrate antibodies: aberrant pattern in IgA-deficient donors.
The IgG and IgA subclass distribution of anti-carbohydrate antibodies in normal and immunodeficient donors was investigated. In normal donors, the specific anti-dextran antibodies were mainly of the IgG2 and IgA2 subclass, although substantial amounts of antibodies could also be of the IgG1 subclass. In children, IgG1 was the predominant subclass expressed. An aberrant IgG subclass distribution pattern of specific antibodies occurred in some IgA-deficient donors, with preferential expression of IgG1 and IgG3 anti-dextran antibodies.
Adult↗
Detection of IgA heavy chain constant region genes in IgA deficient donors: evidence against gene deletions.
Sixty-six donors with selective IgA deficiency and one patient with selective IgA2 deficiency were investigated for immunoglobulin gene defects using restriction enzyme digestions and Southern blot analysis. All patients carried alpha 1 and alpha 2 genes in their genome, suggesting that large deletions are uncommon causes for IgA deficiency. Digestion with Bam HI, Pst I and Pvu II, did not reveal any polymorphism in the studied samples.
Chromosome Deletion↗