Given the lack of specificity in clinical manifestations and chest CT changes in PTB, it is difficult to differentially diagnose PTB from lung cancer, lung tuberosity or other lung diseases.
Mtb is a parasitic bacterium. The host immune system plays an important role in the pathogenesis and defense mechanism of Mtb, and the main immune response is cell-mediated immunity (CMI). Research has shown that the Mtb strains could stimulate CD4 + T cell proliferation3. After infection, Mtb initially activates innate immunity, then natural receptors on the surface of macrophages recognize Mtb and produce phagolysosomes to finally clear the bacteria. During this process, the level of CD4 + T cells increases in the peripheral blood of patients, which in turn increases the ratio of CD4+/CD8 + T cells, resulting in immune system disorders that contribute to disease progression4–7. The results of this study supported the aforementioned conclusions, which confirmed that the cellular immune function of tuberculosis patients was up-regulated.
The role of B cells in immunity against PTB remains controversial. Some scholars believed that most of the studies on PTB patients examined B cells isolated from peripheral blood and not inflamed Mtb-affected tissues, which led to inconsistent conclusions on B cell levels in PTB8. There were experimental results to prove that inhibitory anti-PstS1 B cell responses arise during active tuberculosis9. The result of this study showed that the expression of B cells was higher in PTB. The possible reason is that after Mtb infection, B cells proliferate and are accumulated at the site of pulmonary inflammation, where they secrete type I interferons to inhibit Mtb proliferation and delay the migration of neutrophils to the lesion. In turn, the expression of B cells in peripheral blood is increased, which prompts the up-regulation of humoral immune function.
NK cells are the main effector cells of innate immunity, which possess potent cytolytic capacity without MHC-restriction. After attachment of Mtb to the natural cytotoxicity receptor (NCR) NKp44 on NK cells, the cells can directly or indirectly control mycobacterial growth through cytotoxic mechanisms and macrophage activation10. Portevin D et al. found that NK cells were previously thought to be functionally impaired during TB11. This study proved that the expression of NK cells was significantly lower in PTB supported the conclusion and we speculate that due to the dysfunction of innate immunity, which led to decline in ability to inhibit the proliferation of Mtb that resultes in colonization of tuberculosis bacteria in lungs, which in turn causes tuberculosis.
CRP is considered as an acute clinical indicator, and its level is often related to the severity of the disease. A previous study revealed a lower median CRP in PTB compared to bacterial pneumonia12, and our study supported this conclusion. We found that the levels of CRP in PTB and CAP were much higher than the control groupand CAP group has much higher level of CRP than PTB. Since CRP is a component of the innate immune response, it suggests that the innate immunity factors in PTB patients is not as strong as CAP.