Absence of complement receptor 3 results in reduced binding and ingestion of Mycobacterium tuberculosis but has no significant effect on the induction of reactive oxygen and nitrogen intermediates or on the survival of the bacteria in resident and interfe

We show that, although CR3 plays a role in the uptake of viable Mtb, the receptor plays no role in the subsequent survival of the bacteria. The finding holds true for resident Mϕs and for interferon-gamma (IFN-γ) activated Mϕs, both in the absence and presence of serum opsonins. Activation of Mϕ populations with IFN-γ significantly inhibits the growth of Mtb in host Mϕs and enhances the production of ROI and RNI. However, the presence of CR3 was not critical in any of these mechanisms. Furthermore, we demonstrate that the control of intracellular growth of Mtb in IFN-γ activated Mϕs is not mediated by a direct effect of RNI.