Increased levels of galactose-deficient IgG in sera of HIV-1-infected individuals

被引:94
作者
Moore, JS
Wu, XL
Kulhavy, R
Tomana, M
Novak, J
Moldoveanu, Z
Brown, R
Goepfert, PA
Mestecky, J
机构
[1] Univ Alabama Birmingham, Dept Microbiol, Birmingham, AL 35294 USA
[2] Univ Alabama Birmingham, Dept Med, Birmingham, AL 35294 USA
关键词
HIV-1; pathogenesis; glycosylation; galactose-deficient IgG; Psathyrella velutina lectin; antibodies;
D O I
10.1097/01.aids.0000161767.21405.68
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Background: The IgG from sera of patients with chronic inflammatory diseases of autoimmune character or some chronic microbial infections is frequently deficient in galactose on N-linked glycans. However, this phenomenon has not been investigated at length in human viral infections. Objectives: To evaluate the glycosylation of serum IgG in HIV-1-positive patients. Methods: Psathyrella velutina lectin was used in enzyme-linked immunosorbent and Western blot assays to determine glycosylation. In addition, gas-liquid chromatography and mass spectrometry were utilized to confirm the galactose deficiency observed in the lectin-binding assays. Results HIV-1-infected individuals had significantly higher levels of galactose-deficient IgG than healthy controls. In fact, the galactose deficiency of the N-linked glycans observed in other diseases was even more profound in HIV-1 infection. This deficiency was primarily restricted to IgG when total serum glycoproteins were evaluated and IgG1 was the subclass most affected in all patients. Also, a significant increase in lectin binding was observed on IgG2 and IgG4 from HIV-1-positive females compared with HIV-1 -negative females. Conclusions : Identification of deficient galactosylation of serum IgG from HIV-1-infected patients extended the spectrum of diseases in which this phenomenon has been observed. In addition, the results suggest yet another aspect of immune dysfunction as a result of HIV-1 infection. (c) 2005 Lippincott Williams & Wilkins.
引用
收藏
页码:381 / 389
页数:9
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