Moreover, when co-inoculation of anti-Acr IgA TBA61 mAb and mouse IFNγ via i.n. route in Balb/c mice with IL-4 depletion by a neutralizing anti-IL4 mAb, a significant reduction of bacterial burdens can be observed compared with IgA and IFNγ treatment in wild-type mice after H37Rv infection (21) (Table 2). Here, CD79A is linked to infection.