Abstract
Complement receptor type 1 (CR1), and type 2 (CR2) are expressed on the surface of B-cells and follicular dendritic cells (FDCs) in lymphoid follicles of mice. The importance of CR1 and CR2 in humoral immune response is well documented. Retrovirus-induced immunodeficiency syndrome, murine AIDS (MAIDS), results in abnormal humoral immune responses, destruction of lymphoid structures, and loss of FDC functions, namely trapping of antigens (Ags) and their retention on the cell surface. We investigated the expression of CR1 and CR2 in the spleen and lymph nodes of mice with MAIDS. Flow cytometry and immunohistochemistry revealed the existence of a correlation between the decrease in the expression of CR1 and CR2 by B-cells and the progression of the disease. However, expression of CR1 and CR2 by FDCs was maintained in the later stage of the disease in which lymphoid follicles were destroyed and the ability of FDCs to trap and retain Ag was severely impaired or lost. Moreover, FDCs expressing CR1 and CR2 but not FDCs-specific Ag (FDC-M1 antigen) proliferated in destroyed lymphoid structures. Although the ability of FDCs to trap and retain Ag in vivo was impaired, FDCs trapped immune complexes supplemented with complements in cryostat sections. In addition, FDCs proliferating in MAIDS displayed the same ultrastructural characteristic as normal FDCs, and expressed CD23. We conclude that decreased CR1 and CR2 expression in B-cells and continuous CR1 and CR2 expression in dysfunctional FDCs is important in the pathogenesis of MAIDS.
