Fig. 11.

Proposed model of IL-2-induced intestinal epithelial homeostasis. At lower concentrations, IL-2 promoted tyrosine phosphorylation-dependent interactions between Jak3 and p52ShcA leading to increased proliferation (27). A higher concentration could recruit phosphatases (e.g., SHP1) at this complex through Shc leading to decrease in phosphorylation and disruption of this complex. Less phosphorylated form of Jak3 translocates to the nucleus inhibiting (possibly the transcription factor responsible) its own transcription and hence downregulation of jak3-mRNA leading to higher IL-2-induced apoptosis in IEC. Nuclear targeted Jak3 might also influence the transcription factors for Shc expression.