FOLLICULAR DENDRITIC CELL-FUNCTION AND MURINE AIDS

Infection of mice with LP-BM5 elicits an immunodeficiency state referr ed to as murine acquired immune deficiency syndrome (MAIDS). Shortly a fter infection, retrovirus particles become associated with follicular dendritic cells (FDC) and this study was undertaken to determine whet her retroviruses alter FDC functions. The FDC functions examined inclu ded 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 infecte d with LP-BM5 and the ability of their FDC to trap and retain I-125-Ag (HSA) was assessed. Serum anti-HSA levels were monitored and FDC co-s timulatory activity was indicated by increased B-cell proliferation. H SA trapped on FDC prior to infection began to disappear by 3 weeks and was practically gone by 6 weeks. Serum anti-HSA titres were maintaine d normally for about 3 weeks after infection and then declined precipi tously. The ability of FDC to trap new Ag began to disappear around th e 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 tra p and retain specific Ag and maintain specific antibody levels was mar kedly depressed after retrovirus infection. However, FDC from infected mice continued to provide co-stimulatory signals and these signals ma y contribute to the lymphadenopathy and splenomegaly characteristic of MAIDS.