Cellular and Humoral Mechanisms Involved in the Control of Tuberculosis

Figure 1

Pathogenesis of tuberculosis. TB pathogenesis can be divided in four well-defined events. Inhalation of the mycobacteria is followed by its interaction with resident macrophages through cellular receptors and its internalization. Macrophage bactericidal mechanisms are then activated, including RNI and ROI generation. The efficient killing of mycobacteria depends on pathogen and host factors. Inflammatory cell recruitment: survived mycobacteria proliferate within macrophages inducing the production of proinflammatory cytokines. The local inflammatory environment induces the recruitment of several cell types including monocytes, neutrophils, and dendritic cells to the site of infection. High levels of TNF-α contribute to control Mtb growth and granuloma formation. Control of mycobacteria proliferation: arrival of immune cells to the site of infection including T cells, which become organized in characteristic structures called granulomas efficiently stop mycobacteria proliferation and contain the mycobacteria within the granuloma walls preventing its spread. Characteristic of this structure is the presence of foam cells resulting from the differentiation of chronically activated macrophages. Mycobacteria containment eventually becomes stable (latent) infection. Postprimary TB: mycobacteria persistence associated with a failure in the immunosurveillance system increases the risk that latent disease becomes reactivated, inducing the damage of nearby bronchi and conditioning the spreading of the Mtb to other areas of the lung and the transmission of the disease.