Table 1 Mucosal diseases associated with quantitative or qualitative changes in T-bet
From: Transcriptional regulation of the mucosal immune system mediated by T-bet
Disease | Changes in T-bet | Experimental/clinical observation | Host |
|---|---|---|---|
Asthma | Absent97 | Spontaneous asthma | Mouse |
Reduced expression in T cells from airways and peripheral blood in patients with asthma | Human | ||
Increased risk of asthma and predictor of response to GC therapy | Human | ||
Pulmonary TB | Absent6 | Increased susceptibility | Mouse |
IBD | Absent5 | Resistance to Th1 models of colitis and heightened susceptibility to Th2 model of colitis | Mouse |
Absent in innate immune cells63 | Spontaneous TNFα-dependent colitis | Mouse | |
Over-expression5 | Heightened susceptibility to Th1 model of colitis | Mouse | |
Elevated T-bet expression in gut lamina propria T cells from patients with Crohn's disease | Human | ||
Celiac disease | Elevated T-bet expression in duodenal biopsies and peripheral blood T cells, monocytes and B cells in patients with celiac disease | Human | |
Periodontitis | Increased T-bet expression in lesions from patients with active disease | Human | |
Oral GvHD | Increased90 | Increased T-bet expression in CD8+ T cells in oral lesions | Human |
Helicobacter infection | Absent119 | Resistance to Helicobacter felis induced gastritis and gastric adenocarcinoma | Mouse |
Colorectal cancer | Increased112 | Increased expression of T-bet in CRC specimens was associated with a favorable prognosis | Human |
Absent in innate immune cells64 | Drives colitis-associated CRC | Mouse | |
Genital HSV infection | Absent11 | Increased susceptibility to infection | Mouse |
Genetic polymorphism123 | Increased susceptibility | Human | |
HPV infection and cervical neoplasia | Increased113 | Increased T-bet expression in tumor-infiltrating T-cells was associated with a favorable prognosis | Human |