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Aberrations in titre and avidity of serum IgM and IgG antibodies to microbial and food antigens in IgA deficiency.

Artikel i vetenskaplig tidskrift
Författare F Cardinale
Vanda Friman
B Carlsson
J Björkander
L Armenio
L A Hanson
Publicerad i Scandinavian journal of immunology
Volym 36
Nummer/häfte 2
Sidor 279-83
ISSN 0300-9475
Publiceringsår 1992
Publicerad vid Institutionen för invärtesmedicin, Avdelningen för infektionssjukdomar
Sidor 279-83
Språk en
Länkar www.ncbi.nlm.nih.gov/entrez/query.f...
Ämnesord Antibody Affinity, Antigens, Bacterial, immunology, Antigens, Viral, immunology, Female, Food Hypersensitivity, immunology, Humans, IgA Deficiency, Immunoglobulin G, analysis, Immunoglobulin M, analysis, Lactoglobulins, immunology, Male
Ämneskategorier Infektionsmedicin

Sammanfattning

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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