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Age associated changes in the distribution of lpr gene-induced B220-positive T cells in lymphoid organs of MRL/Mp-lpr/lpr mice using dual exposure microphotographs of double immunofluorescence staining.

Homozygous MRL/Mp-lpr/lpr [MRL/lpr] mice, which have an autosomal recessive mutant lpr gene and exhibit defects in Fas antigen, spontaneously develop autoimmune disease with progressive expansion and accumulation of characteristic abnormal CD4-CD8-double negative T cells that express B220 surface antigen, a B cell-specific surface marker in normal mice. We analyzed the distribution and age related changes of lpr gene-induced abnormal T cells (B220-positive lpr T cells) in the lymphoid organs of MRL/lpr mice. We studied cryostat sections of the spleen, peripheral lymph nodes, mesenteric lymph nodes, and Peyer's patches at different stages using FITC [fluorescein isothiocyanate)-conjugated monoclonal antibodies directed against B220 (RA3-6B2) and PE (phycoerythrin)-conjugated anti-mouse CD3 (2C11) monoclonal antibody, examining dual-exposure microphotographs of double-immunofluorescence stained preparations. We observed that in aged MRL/lpr mice, B220-positive abnormal lpr T cells were not present in the thymus-dependent area, and the majority of the follicular area cells were displaced by lpr T cells. These findings suggest that the cellular trafficking of B220-positive lpr T cells differs from that of conventional T cells and that these lpr-derived T cells play a role in the follicle.