Fig. 2.

Overview of the mechanisms of innate and adaptive immunity in response to invasion by MTB in humans. Following MTB recognition by APCs, such as macrophages, antigens are presented to CD4⁺ T lymphocytes via MHC II molecules, and the activated CD4⁺ T lymphocytes will differentiate into Th1 (microenvironment with IFN-γ and IL-12), Th2 (IL-2 and IL-4), and Th17 (TGF-β and IL-23) cells. Th1 cells secrete IFN-γ and facilitate the clearance of MTB, while Th2 inhibits the action of Th1 and can also stimulate the production of antibodies by B cells to kill MTB. Th17 secretes cytokines that recruit neutrophils, macrophages, etc., to play an anti-inflammatory effect. NK cells promote the maturation of APCs, such as DCs, and can activate other immune cells, including macrophages and CTLs. Polarization of macrophages in different cytokine environments results in different immune effects. The complexities of host immunity to MTB highlight the need for further research to better understand the underlying mechanisms of host defense response. APCs antigen-presenting cells, CTL cytotoxic T lymphocyte, MHC II histocompatibility complex II, IFN-γ interferon-γ, IL interleukin, Mφ macrophage, PRR pattern recognition receptor, Th cells helper T cells, TGF transforming growth factor, DC dendritic cell, NK cell natural kill cell, Fas-FasL Fas and Fas ligand, TNF tumor necrosis factor, MTB Mycobacterium tuberculosis, GM-CSF granulocyte–macrophage colony-stimulating factor, M1 type I macrophage, M2 type II macrophage