Beyond IgG, studies using human FcαR CD89 transgenic mice point towards the potential for IgA mediated FcR functions to impact Mtb. Opsonization of H37Rv with human monoclonal IgA targeting the alpha crystallin Mtb protein HspX prior to high dose intranasal challenge of these mice leads to decreased pulmonary bacterial burden early after infection compared to non-transgenic littermates. The gene discussed is CD79A; the disease is infection.