| 1. |
- Nilssen, D E, et al.
(author)
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B-cell activation in duodenal mucosa after oral cholera vaccination in IgA deficient subjects with or without IgG subclass deficiency.
- 1993
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In: Scandinavian journal of immunology. - 0300-9475. ; 38:2, s. 201-8
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Journal article (peer-reviewed)abstract
- Alterations in duodenal Ig-producing cells induced by two oral cholera vaccinations were studied by two-colour immunofluorescence in mucosal tissue sections from adults with selective IgA deficiency (IgAD), either with (n = 7) or without (n = 9) frequent infections, infection-prone patients with combined IgAD and IgG subclass deficiency (IgGSD) (n = 7), and normal control subjects (n = 11). The proportion of IgG-producing cells prior to immunization tended to be lower in the symptomatic IgAD subjects than in the clinically healthy ones. In the first subgroup the absolute number of IgG cells per intestinal length unit was significantly increased after immunization (P < 0.04), and this tendency was also observed in the healthy IgAD subjects (6/9) and in those with combined deficiency (5/7). Very few IgAD subjects responded with an increase of IgM-producing cells. The normal controls responded variably in all major immunocyte classes, in the order IgA > IgG > IgM. Compared with these controls, the patients with combined IgAD and IgGSD showed significantly increased IgG1 (P < 0.01) and reduced IgG2 (P < 0.006) proportions, which was in accordance with their serum subclass levels. Our study showed that oral cholera vaccination preferentially activates intestinal IgG-producing cells in IgAD subjects. This result agreed with data recently obtained by ELISPOT in the same patients with regard to antibody-forming cells specific for cholera toxin. Both methods suggested that IgG rather than IgM antibodies are elicited as compensation for a lacking IgA response. However, our overall results showed that intestinal B-cell activation is quite variable after oral cholera vaccination. Although such vaccination might be of importance for enhancing mucosal immunity also in IgAD patients, a concurrent gut disease could possibly be aggravated by IgG-mediated mucosal immunopathology in the absence of anti-inflammatory IgA antibodies.
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| 2. |
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| 3. |
- Andersson, A, et al.
(author)
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Genes for C4b-binding protein alpha- and beta-chains (C4BPA and C4BPB) are located on chromosome 1, band 1q32, in humans and on chromosome 13 in rats
- 1990
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In: Somatic Cell and Molecular Genetics. - 0740-7750. ; 16:5, s. 493-500
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Journal article (peer-reviewed)abstract
- C4b-binding protein is involved in the regulation of the complement system. It is a multimeric protein composed of seven identical alpha-chains and a single copy of a unique beta-chain. The latter was identified only recently and its structure determined by cDNA cloning. Both subunits in C4b-binding protein belong to the same superfamily of proteins composed predominantly of tandemly arranged short consensus repeats (SCR) approximately 60 amino acid residues in length. The gene for the human alpha-chain is known to be located in a gene cluster on chromosome 1, band 1q32, which is called the regulators of complement activation (RCA) gene cluster. We have used cDNA probes for both alpha- and beta-chains of human C4b-binding protein to localize their genes with an in situ hybridization technique. We find the genes for both chains to be located on chromosome 1, band 1q32, in the human. This suggests that the beta-chain gene is also a member of the RCA gene cluster and that the alpha- and beta-chain genes are located close to each other. The cDNA probes for the alpha- and beta-chains also were used to screen mouse-rat somatic cell hybrids using Southern blotting to localize their genes in the rat. Both the alpha- and beta-chain genes were shown to be located on chromosome 13 in the rat. These are the second and third genes to be located on rat chromosome 13, and the results suggest that the genes for the alpha- and beta-chains together with the gene for coagulation factor V represent a conserved chromosomal region in rat and man.
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| 4. |
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| 5. |
- Cardinale, F, et al.
(author)
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Aberrations in titre and avidity of serum IgM and IgG antibodies to microbial and food antigens in IgA deficiency.
- 1992
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In: Scandinavian journal of immunology. - 0300-9475. ; 36:2, s. 279-83
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Journal article (peer-reviewed)abstract
- The antibody levels and relative avidity of serum IgM and IgG antibodies against E. coli O antigens, poliovirus type 1 and beta-lactoglobulin were determined with enzyme-linked immunosorbent techniques in IgA deficient (IgAd) patients with frequent respiratory tract infections and healthy IgAd individuals. Healthy individuals with normal immunoglobulin levels served as controls. The IgM antibody levels against the bacterial, viral and food antigens and the IgG antibody levels against the bacterial antigens were significantly higher in the IgAd group with recurrent infections than in the group of healthy IgAd individuals. The symptomatic IgAd group had significantly higher levels of the IgG antibodies against the bacterial antigen, also when compared with controls. In contrast the healthy IgAd individuals had the highest avidities of IgM antibodies to the viral and food antigens. The high avidities of antibodies could be a compensatory host defence mechanism in IgAd. These aberrations may appear as a consequence of increased mucosal exposure in IgAd to antigens such as E. coli or beta-lactoglobulin, but presumably not to poliovirus which is only exceptionally present in the milieux. They could also be a result of the previously suggested dysregulation of antibody responses in IgAd.
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| 6. |
- Hanson, L A, et al.
(author)
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Sensitization and development of tolerance via the gut.
- 1993
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In: Pediatric allergy and immunology : official publication of the European Society of Pediatric Allergy and Immunology. - 0905-6157. ; 4:3 Suppl, s. 16-20
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Journal article (peer-reviewed)
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