The landscape of different molecular modules in an immune microenvironment during tuberculosis infection.
Nan ZhangXizi LuoJuanJuan HuangHongyan SongXinyue ZhangHonglan HuangShishun ZhaoGuo-Qing WangPublished in: Briefings in bioinformatics (2021)
Tuberculosis is a chronic inflammatory disease caused by Mycobacterium tuberculosis. When tuberculosis invades the human body, innate immunity is the first line of defense. However, how the innate immune microenvironment responds remains unclear. In this research, we studied the function of each type of cell and explained the principle of an immune microenvironment. Based on the differences in the innate immune microenvironment, we modularized the analysis of the response of five immune cells and two structural cells. The results showed that in the innate immune stress response, the genes CXCL3, PTGS2 and TNFAIP6 regulated by the nuclear factor kappa B(NK-KB) pathway played a crucial role in fighting against tuberculosis. Based on the active pathway algorithm, each immune cell showed metabolic heterogeneity. Besides, after tuberculosis infection, structural cells showed a chemotactic immunity effect based on the co-expression immunoregulatory module.
Keyphrases
- innate immune
- mycobacterium tuberculosis
- nuclear factor
- pulmonary tuberculosis
- stem cells
- induced apoptosis
- hiv aids
- single cell
- cell cycle arrest
- toll like receptor
- oxidative stress
- machine learning
- endoplasmic reticulum stress
- cell death
- emergency department
- signaling pathway
- deep learning
- immune response
- human immunodeficiency virus
- long non coding rna
- pi k akt