       Document 0303
 DOCN  M9460303
 TI    Follicular dendritic cell function and murine AIDS.
 DT    9404
 AU    Masuda A; Burton GF; Fuchs BA; Bhogal BS; Rupper R; Szakal AK; Tew JG;
       Department of Microbiology and Immunology, Medical College of;
       Virginia/Virginia Commonwealth University, Richmond 23298.
 SO    Immunology. 1994 Jan;81(1):41-6. Unique Identifier : AIDSLINE
       MED/94178811
 AB    Infection of mice with LP-BM5 elicits an immunodeficiency state referred
       to as murine acquired immune deficiency syndrome (MAIDS). Shortly after
       infection, retrovirus particles become associated with follicular
       dendritic cells (FDC) and this study was undertaken to determine whether
       retroviruses alter FDC functions. The FDC functions examined included
       the ability to: (1) retain antigen (Ag) trapped prior to infection; (2)
       trap new Ag after infection; (3) maintain specific IgG responses; and
       (4) provide co-stimulatory signals to B cells. Mice were infected with
       LP-BM5 and the ability of their FDC to trap and retain 125I-Ag (HSA) was
       assessed. Serum anti-HSA levels were monitored and FDC co-stimulatory
       activity was indicated by increased B-cell proliferation. HSA trapped on
       FDC prior to infection began to disappear by 3 weeks and was practically
       gone by 6 weeks. Serum anti-HSA titres were maintained normally for
       about 3 weeks after infection and then declined precipitously. The
       ability of FDC to trap new Ag began to disappear around the second and
       third week of infection and was markedly depressed by the fourth week.
       However, FDC recovered from infected mice retained their ability to
       co-stimulate anti-mu- and interleukin-4 (IL-4)-activated B cells
       throughout a 5-week period. In short, the ability of FDC to trap and
       retain specific Ag and maintain specific antibody levels was markedly
       depressed after retrovirus infection. However, FDC from infected mice
       continued to provide co-stimulatory signals and these signals may
       contribute to the lymphadenopathy and splenomegaly characteristic of
       MAIDS.
 DE    Animal  Antibody Specificity/IMMUNOLOGY  Antigen-Antibody
       Complex/IMMUNOLOGY/METABOLISM  Antigens/METABOLISM  Dendritic
       Cells/*IMMUNOLOGY  IgG/BLOOD  Lymph Nodes/IMMUNOLOGY  Mice  Mice, Inbred
       C57BL  Murine Acquired Immunodeficiency Syndrome/*IMMUNOLOGY
       Ovalbumin/IMMUNOLOGY  Serum Albumin/IMMUNOLOGY  Spleen/IMMUNOLOGY
       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).

