The Differentially Expressed Genes Responsible for the Development of T Helper 9 Cells From T Helper 2 Cells in Various Disease States: Immuno-Interactomics Study

Background T helper (Th) 9 cells are a novel subset of Th that develop independently from Th2 and characterized by the secretion interleukin (IL)-9. Studies have suggested involvement Th9 in variable diseases such as allergic pulmonary (eg, asthma, chronic obstructive airway disease, rhinosinusitis, nasal polyps, hypoplasia), metabolic acute leukemia, myelocytic breast cancer, lung melanoma, pancreatic cancer), neuropsychiatric disorders Alzheimer disease), autoimmune Graves Crohn colitis, psoriasis, systemic lupus erythematosus, scleroderma, rheumatoid arthritis, multiple sclerosis, inflammatory bowel atopic dermatitis, eczema), infectious tuberculosis, hepatitis). However, there is dearth information on its other metabolic, neuropsychiatric, diseases. Objective This study aims to identify significant differentially altered genes conversion cells, their regulating microRNAs (miRs) publicly available Gene Expression Omnibus data sets mouse model using silico analysis unravel various pathogenic pathways involved disease processes. Methods Using expressed (DEGs) identified 2 (GSE99166 GSE123501) we performed functional enrichment network analyses pathways, protein-protein interactions, miR-messenger RNA associations, disease-gene associations related implicated cells. Results We extracted 260 common downregulated, 236 upregulated, 634 DEGs expression profiles GSE99166 GSE123501. Codifferentially ILs, cytokines, receptors, transcription factors (TFs) were enriched 7 crucial Kyoto Encyclopedia Genes Genomes Ontology. constructed interaction predicted top regulatory miRs differentiation pathways. also pulmonary, autoimmune, well carcinomas where may play role. Conclusions hitherto unexplored possible between states. Some important including CCL1 (chemokine [C-C motif] ligand 1), CCL20 20), IL-13, IL-4, IL-12A, IL-9; IL-12RB1, IL-4RA (interleukin receptor alpha), CD53 (cluster 53), CD6 6), CD5 5), CD83 83), CD197 197), IL-1RL1 1 receptor-like CD101 101), CD96 96), CD72 72), CD7 7), CD152 (cytotoxic lymphocyte–associated protein 4), CD38 38), CX3CR1 [C-X3-C CTLA2A CTLA28, CD196 196); TFs, FOXP3 (forkhead box P3), IRF8 (interferon factor 8), FOXP2 P2), RORA (RAR-related orphan AHR (aryl-hydrocarbon receptor), MAF (avian musculoaponeurotic fibrosarcoma oncogene homolog), SMAD6 (SMAD family member JUN (Jun proto-oncogene), JAK2 (Janus kinase 2), EP300 (E1A binding p300), ATF6 (activating BTAF1 (B-TFIID TATA-box associated BAFT (basic leucine zipper factor), NOTCH1 (neurogenic locus notch homolog GATA3 (GATA 3), SATB1 (special AT-rich sequence BMP7 (bone morphogenetic PPARG (peroxisome proliferator–activated gamma, able some could target DEGs. The scarcity studies role highlights lacunae this field. Our provides rationale for exploring diabetes mellitus, diabetic nephropathy, hypertensive ischemic stroke, steatohepatitis, liver fibrosis, obesity, adenocarcinoma, glioblastoma glioma, malignant neoplasm stomach, neuroblastoma, osteosarcoma, carcinoma, prostate stomach carcinoma.