Role of Mysm1 in lymphocyte activation. (A-B) Mysm1 promoter–driven β-galactosidase reporter activity in the splenic (A) T cells and (B) B cells, stimulated in vitro with LPS (1 μg/mL), anti-CD40 agonist Ab (5 μg/mL) and IL-4 (5 ng/mL), or PMA (50 ng/mL) and ionomycin (500 ng/mL), for 48 hours. The data were collected using phenotypically normal Mysm1^+/tm1a cells, and presented as fold change versus the background β-galactosidase activity in wild-type cells undergoing identical treatment. Significant induction of Mysm1-driven β-galactosidase reporter activity was observed (*P < .05, **P < .01, using t test). (C) Reduced induction of the CD69 activation marker on Mysm1^tm1a/tm1a splenic T cells, stimulated in vitro with PMA and ionomycin, as above, over a 5-day time course. (D) Reduced expression of CD54 on Mysm1^tm1a/tm1a splenic B cells, stimulated in vitro with LPS (1 μg/mL), or anti-CD40 (2.5 μg/mL) and IL-4 (5 ng/mL), over 5 days; MFI indicates mean fluorescence intensity. Bars represent means ± SEM from 4 mice; *P < .05, **P < .01, ***P < .001 using 2-way ANOVA.