Document 0529
 DOCN  M9480529
 TI    Intestinal mucosal immunoglobulins during human immunodeficiency virus
       type 1 infection.
 DT    9410
 AU    Janoff EN; Jackson S; Wahl SM; Thomas K; Peterman JH; Smith PD;
       Department of Medicine, VA Medical Center, Minneapolis, MN 55417.
 SO    J Infect Dis. 1994 Aug;170(2):299-307. Unique Identifier : AIDSLINE
       MED/94308593
 AB    In intestinal fluid samples from 39 human immunodeficiency virus type 1
       (HIV-1)-infected patients, IgA and IgG levels were equivalent, whereas
       in 10 controls, IgA levels were significantly higher than those of IgG
       (P < .05). Intestinal IgA in patients contained predominantly monomeric
       IgA1, whereas IgA1 and IgA2 subclass levels in controls were nearly
       equivalent and primarily polymeric. The predominance of IgG and
       monomeric IgA1 in mucosal fluid samples from HIV-1-infected patients
       suggests exudation of serum immunoglobulins into the intestine. The
       decreased proportion of mucosal plasma cells producing IgA and IgA2 in
       the HIV-1-infected patients (P < .01) may also contribute to the
       abnormal intestinal immunoglobulin levels. Intestinal IgG reacted with
       most HIV-1 antigens, whereas specific IgA was present in only 10 of 17
       patients and reacted with only envelope (gp120 and gp160) and, less
       often, core (p17 and p24) antigens. Aberrant mucosal antibody responses
       and decreased integrity of the mucosal barrier may contribute to the
       intestinal dysfunction and infections that characterize HIV-1 infection.
 DE    Diarrhea/*COMPLICATIONS/IMMUNOLOGY  Duodenum/IMMUNOLOGY  Human  HIV
       Antibodies/ANALYSIS  HIV Infections/COMPLICATIONS/*IMMUNOLOGY
       HIV-1/*IMMUNOLOGY  IgA/BLOOD  IgA, Secretory/ANALYSIS
       IgG/ANALYSIS/BLOOD  IgM/ANALYSIS/BLOOD  Immunoglobulins/*ANALYSIS/BLOOD
       Intestinal Mucosa/*IMMUNOLOGY  Plasma Cells/IMMUNOLOGY  Support,
       Non-U.S. Gov't  Support, U.S. Gov't, Non-P.H.S.  Support, U.S. Gov't,
       P.H.S.  JOURNAL ARTICLE

       SOURCE: National Library of Medicine.  NOTICE: This material may be
       protected by Copyright Law (Title 17, U.S.Code).