Interleukin-10 production by lung macrophages in CBA xid mutant mice infected with Mycobacterium tuberculosis Introduction It is well established that mice need to mount a T helper type 1 (Th1) response, mediated by the cytokines interleukin- 12 (IL-12), IL-23, and interferon-c (IFN-c), to successfully express host resistance to infection with Mycobacterium tuberculosis.1–5 In contrast, a Th2 response is not protective, although it remains unclear to what extent it might interfere with the overall course of the disease. Most evidence in the mouse model favours a lack of involvement in the expression of initial protective immunity,6,7 whereas much later during the disease process lung macrophages accumulate large amounts of IL-10 in mouse strains prone to reactivation disease.8 This includes mice on the CBA background of inbred strains. In this mouse, a well characterized mutation designated xid in the cytoplasmic signalling enzyme Bruton’s protein kinase