       Document 0253
 DOCN  M9640253
 TI    Sequential occurrence of IgM, IgM/IgG, and gp120-IgM/IgG complement
       complexes on CD4+ lymphocytes in relation to CD4+ blood lymphocyte
       depletion in HIV+ hemophilia patients: results of a 10-year study.
 DT    9604
 AU    Daniel V; Susal C; Weimer R; Zipperle S; Kropelin M; Zimmermann R;
       Huth-Kuhne A; Opelz G; Department of Transplantation Immunology,
       Institute of; Immunology, Heidelberg, Germany.
 SO    Immunol Lett. 1995 Jul-Aug;47(1-2):97-102. Unique Identifier : AIDSLINE
       MED/96087587
 AB    The concept of autoimmune mechanisms playing an integral role in the
       pathogenesis of HIV disease is rapidly gaining ground. In this study, we
       determined IgM and IgG antibodies, complement fragments and gp120 on the
       surface of CD4+ lymphocytes using double-fluorescence flow cytometry.
       Sequential analysis demonstrated an inverse relationship of
       autoantibodies and CD4+ lymphocyte counts in the peripheral blood. HIV+
       patients without autoantibodies (16/104 = 15%) had the highest CD4+
       blood cell counts (324 +/- 264/microliters; mean +/- SD). CD4+ counts
       were successively lower in patients with complement-fixing IgM (243 +/-
       240/microliter), complement-fixing IgG and IgM (139 +/- 138/microliter),
       or gp120-IgM/IgG complement complexes on the surface of CD4+ cells (38
       +/- 45/microliter, P = 0.03). Individual patient profiles show that IgM
       autoantibodies typically are formed early after HIV infection and appear
       to deplete CD4+ lymphocytes very slowly, whereas complement-fixing IgG
       autoantibodies are generated at a later stage and deplete CD4+
       lymphocytes more efficiently. The presence of both soluble gp120 and
       complement-fixing autoantibodies on CD4+ lymphocytes is associated with
       very low CD4+ cell counts and coincides with progression to terminal
       disease. Early during HIV infection autoantibody production is rather
       unstable, but it becomes more stable with disease progression and
       persists in advanced stages of the disease. These data suggest that
       autoantibody formation against CD4+ lymphocytes is a pathogenic
       mechanism for CD4+ cell depletion.
 DE    Antigen-Antibody Complex/*BLOOD  Autoantibodies/BLOOD  Complement
       3d/*ANALYSIS  CD4 Lymphocyte Count  CD4-Positive
       T-Lymphocytes/*IMMUNOLOGY  Hemophilia/BLOOD/*IMMUNOLOGY  Human  HIV
       Envelope Protein gp120/BLOOD/IMMUNOLOGY  HIV
       Seropositivity/BLOOD/*IMMUNOLOGY  IgG/BLOOD  IgM/BLOOD
       Lymphopenia/BLOOD/*IMMUNOLOGY  JOURNAL ARTICLE

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

