Figure 1.

Innate and adaptive immune responses induced by the MTB. Upon entering the pulmonary alveoli via the respiratory tract, MTB is first recognized by resident immune cells such as alveolar macrophages, immature dendritic cells (iDCs), and natural killer (NK) cells. Following capture by iDCs, which migrate from the site of infection to the lymph nodes, the bacteria induces their differentiation into mature dendritic cells (mDCs) with enhanced antigen-presenting and MHC expression capacity. Through the assistance of CD28-CD80 and CD40-CD40L, MHC I and MHC II molecules on dendritic cells recognize and activate CD4⁺ and CD8⁺ T lymphocytes. CD4⁺ T lymphocytes differentiate into Th1, Th2, or Th17 subsets depending on the microenvironmental cytokines and contribute to the control of MTB infection. Th1 and Th2 immunity counterbalance each other and maintain immune homeostasis. CD8⁺ T lymphocytes further differentiate into cytotoxic T lymphocytes (CTLs) that produce granzyme, perforin, Fas-FasL, IFN-γ, TNF-α, and other molecules to activate macrophages and eliminate the bacteria. Depending on the interplay between innate and adaptive immune responses and the virulence of MTB, infection can lead to either recovery, latent tuberculosis infection (LTBI), or active tuberculosis (ATB).