In contrast, infection of BALB.Xid mice, which have a deficiency in B cell receptor signaling and severe reductions in the mucosal CD5+ B cell compartment, revealed a defect in antigen-stimulated IL-10 production, reduced SEA-specific IgM and IgA titers, increased IFNγ and IL-4 production, elevated IgE and IgG1 titers, increased tissue egg burdens and higher mortality (Gaubert et al., 1999). The gene discussed is CD5; the disease is infection.