FIG 7.

B1a B cell-deficient Bruton's tyrosine kinase X-linked immunity-deficient mice have disease during NMI infection that is more severe than that seen with wild-type mice. Wild-type (CBA) mice and Bruton's tyrosine kinase X-linked immunity-deficient (BTK^xid) mice were challenged i.p. with 1 × 10⁷ NMI cells. (A) Body weight was measured throughout infection and compared to the weight at day 0. (B) Splenomegaly was measured at 14 days postinfection. (C) Bacterial burden in the spleen was measured at 14 days postinfection by real-time PCR. (D) Histopathology in the spleen shows that inflammation was more severe in BTK^xid mice than in wild-type CBA mice. (E) Pathology scores from spleens demonstrate more inflammatory infiltrates in BTK^xid spleens than in wild-type CBA mouse spleens. One section of spleen was evaluated for each mouse. Spleens for groups were scored for histiocytic inflammation in red pulp of spleen using the following scale: 0, no inflammation (no accumulations of macrophages); 1, a few small accumulations of macrophages; 2, a few small-to-moderate accumulations of macrophages; 3, large numbers of moderate-to-large accumulations of macrophages. (F) Anti-C. burnetii-specific IgM titers were significantly higher in wild-type CBA mice than in BTK^xid mice. (G) Serum levels of TNF-α were significantly higher in wild-type CBA mice than in BTK^xid mice. *, P < 0.05; **, P < 0.01; ***, P < 0.001. These data indicate that B1a B cell-deficient BTK^xid mice have disease during NMI infection that is more severe than that seen with CBA mice. B1a B cells may play a role in regulating immune responses and producing IgM during primary infection with NMI.