Protein tyrosine phosphatase non-receptor type 2 and inflammatory bowel disease

Figure 3 Loss of protein tyrosine phosphatase non-receptor type 2 affects several aspects of T cell development. Loss of protein tyrosine phosphatase non-receptor type 2 (PTPN2) in innate immune cells results in enhanced secretion of pro-inflammatory cytokines, including IFN-γ, IL-6 and IL-1β. In CD4⁺ T cells, these cytokines are involved in driving Th1 and Th17 development. Loss of PTPN2 in CD4⁺ T cells further potentiates the IFN-γ/IL-6-induced activation of STAT1/STAT3, what further strengthens the development of Th1/Th17 cells. Further, loss of PTPN2 results in enhanced TCR signaling strength what drives aberrant activation and proliferation of naïve T cells and escape of auto-reactive T cells from negative selection. Ultimately, this leads to the generation of increased levels of effector and memory T cells. DC: Dendritic cell; IFN: Interferon; M: Macrophage; TNF: Tumour necrosis factor; IL: Interleukin; STAT: Signal transducer and activator of transcription; TCR: T-cell receptor.