Delineating the role of transcription factor Atf3 in Mycobacterium tuberculosis infected macrophages
Mycobacterium tuberculosis (Mtb) is the causative agent of tuberculosis. The infection begins with the inhalation of bacterium into pulmonary alveoli. After inhalation, the first line of host defense starts with the recognition of Mtb by phagocytic cells of the innate immune system such as macrophages, which express numerous pattern recognition receptors (PRRs) that recognise Mtb antigenic molecules called pathogen associated molecular patterns (PAMPs). Recognition of danger signals derived from Mtb by innate immune receptors leads to activation of specific transcriptional programs, culminating in the production of potent inflammatory mediators, including pro-inflammatory cytokines and chemokines. The innate immunity is important for controlling early onset of infection. The tight regulation of cytokines and chemokines, which are produced as a consequence of innate immunity, is required for containing infection. Host transcription factors play a key role in this process. Activating transcription factor-3 (ATF3), a stress-inducible eukaryotic gene, is a member of the ATF/CREB (cAMP- response element-binding) family of bZip transcription factors was highly upregulated in the heatmap of TFs among all other CREB members. We studied the role of Atf3 during Mtb infection.