Tuberculosis and scavenger receptors: Exploring their relationship.

Abstract

Tuberculosis (TB) remains a significant global health concern, particularly in low- and middle-income countries. Several risk factors are associated with TB infection and its progression from infection to disease onset, including host factors, microbial factors, environmental factors, and socio-economic status. Host genetic factors play a significant role in determining susceptibility to acquiring infection, progression to active disease, and the severity of the disease. Innate immunity is essential in the initial defense, advancement, and long-term control of mycobacterial infection. Among various cell surface and intracellular receptors mediating mycobacteria uptake, scavenger receptors play a crucial role in innate immunity. Scavenger receptors are classified into 12 classes, with class B comprising SR-B1 (SCARB-1), SR-B2 (LIMP2), and SR-B3 (CD36). SR-B1 and CD36 are involved in the uptake and phagocytosis of Mycobacterium tuberculosis (Mtb). Scavenger receptors promote cytokine production and modulate cytokine production during antimycobacterial responses. The SR-B1 and CD36 genes contain various single nucleotide polymorphisms in their intronic and exonic regions. These polymorphisms may influence the expression of the genes, leading to changes in Mtb uptake and antimycobacterial response. In this current review, we have explored the importance of scavenger receptors in TB pathogenesis. Additionally, we have summarized SNPs in SR-B1 and CD36 genes and their effect on protein expression.