Fig. 6

SLAMF7 tempers B cell activation to restrict T cell activation resulting in concomitant modulation of EAE severity. A Clinical scores of μMT mice reconstituted with either WT B cells (n = 8) or SLAMF7^−/− B cells (n = 7) and subjected to EAE induced with rmMOG_1–125. B Expression of IL-17A in peripheral blood CD4⁺ T cells from mice in A. C Expression of RORγt in peripheral blood CD4⁺ T cells from mice in A. D–K Isolated splenic B cells from WT mice (n = 4) were cultured for 4 days with SLAMF7 activation (SLAMF7 cross-linking) or without (mock) and surface and soluble markers of B cell activation were assessed. Changes in autofluorescence (D), MHC-II MFI (E), GL7 expression (F), and PD-L1 MFI (G) on B cells cultured with or without SLAMF7 activation. Changes in the levels of cytokines and chemokines from supernatant of B cells cultured with and without SLAMF7 activation including Eotaxin (H), IL-17 (I), TNF⍺ (J), and CCL5 (K). L–O EAE was induced in WT mice and splenic CD3⁺ T cells were harvested on day 60. T cells were labeled with CellTrace Violet and co-cultured with splenic B cells isolated from either WT or SLAMF7^−/− mice for 4 days in the presence and absence of MOG_35–55 peptide. L Percent change in the frequency of proliferating CD8⁺ T cells comparing unstimulated cells to MOG_1–125 stimulated cells. M Percent change in PD-1 expression on CD8⁺ T cells comparing unstimulated cells to MOG_35–55 stimulated cells. N Percent change in CD69 expression on CD8⁺ T cells comparing unstimulated cells to MOG_35–55 stimulated cells. O Frequency of CD80⁺ unstimulated B cells isolated from the spleens of WT or SLAMF7^−/− mice. Data in A–O representative of an individual experiment. Groups in A compared with two-way ANOVA with Sidak’s correction for multiple comparisons. Groups in B, C and H–O compared with a two-way unpaired t-test. Data in D–G compared with a mixed-effects model with FDR correction for multiple comparisons via Benjamini and Hochberg method. *p < 0.05, **p < 0.01