Alveolar carcinoma: a review.

ST2 selectively and stably expressed on the surface of T-helper 2 (Th2) but not Th-1 cells is a ligand for recently identified Interleukin-33 (IL-33). We have studied the susceptibility to and severity of the two T cell mediated inflammatory process: multiple low dose streptozotocin induced diabetes and Con-A induced hepatitis, in ST2 deficient (ST2-/-) and “wild-type: BALB/C mice. After diabetes induction (40mg STZ/kg b.w. for 5 days) ST2-/- mice developed glycemia and glycosuria. β cell loss and intra-islet mononuclear infiltrates while “wild type” mice did not develop any biochemical signs and histology revealed only peri-insulitis. When injected with Con-A (12 mg/kg b.w) ST2-/- mice developed significantly enhanced hepatitis as evaluated by liver function test 8 and 24 hours after induction and quantitative analysis of the hepatocytes necrosis. Analysis of cellular make up of the pancreatic lymph nodes and pancreata (in diabetes) and liver infiltrating cells (in ConA induced hepatitis) and their cytokines content by FACS analysis and cytokine expression by RT-PCR revealed the enhanced infiltration of Th-1 and Th-17 cells and higher content and expression of proinflammatory cytokines: IFN-γ, IL-17 and TNF. We therefore concluded that attenuation of IL-33-ST2 axis facilitates the induction of Th-1/Th-17 mediated inflammatory autoimmunity.