Fig. 5. Evidence of immune complexes and infection of T_FH cells within CLNs of chronically SIV-infected rhesus macaques.

Model figure depicting the interaction of FDCs, B cells, and T_FH cells (A) within the GC of a secondary lymphoid organ. FDCs trap and retain antigens in the form of specific antibody-antigen immune complexes allowing them to provide antigen to interact with BCRs on GC B cells. FDCs express adhesion molecules, FcR, and complement receptors 1 and 2 (CR1/CR2) on their cell surface. The ICs bind to FcRs and CRs (also known as CD35/CD21) on the FDC dendrites. T_FH cells also express high levels of PD-1, which leads to decreased T_FH proliferation. The interaction of FDCs and B cells within the GC of CLNs (B). Cells from CLNs of chronically SIV-infected rhesus macaques were stained for CD20, CD35 and p27 expression. Representative profiles at 60x magnification indicate formation of immune-complexes, resulting from co-localization of CD20 (blue), p27 (green) and CD35 (red) signals. The arrows indicate the regions of colocalization. The antigen on the surface of FDCs could interact with B cells in the follicles of CLNs. Figure C shows transfer of viral p27 antigen (green) from CD35⁺ FDCs (red) to PD-1^hi T_FH (blue) cells in GC of CLNs. The Figure shows antigen carrying FDCs in proximity to T_FH cells, with some of the T_FH cells being actually infected (colocalization of blue and green). The formation of the complex between CD20 (B cells) and (PD-1^hi) T_FH cells, with (p27) antigen shared at their membranes was shown in figure D. This showed that FDCs can infect B cells and T_FH cells in the CLNs.