Synovial T lymphocyte recognition of organisms that trigger reactive arthritis.

Reactive arthritis (ReA) is believed to be "triggered' by infection with certain bacteria. When the proliferative responses of mononuclear cells (MC) obtained from the synovial fluid (SF) of ReA patients were examined, it was found that they responded maximally to the specific organism responsible for the preceding infection. The response was shown to be due to Class II MHC-restricted T cells by inhibition experiments using cyclosporin A and monoclonal antibodies.

Interleukin 3 stimulates proliferation via protein kinase C activation without increasing inositol lipid turnover.

Interleukin 3 (IL-3) is required for the survival and proliferation of the FDCP-Mix 1 multipotent stem cell line. IL-3 or phorbol esters can rapidly translocate protein kinase C from a cytosolic to a membrane-bound form in these cells. Phorbol esters were able to partially replace the requirement of FDCP-Mix 1 cells for IL-3.

The haemopoietic growth factors interleukin 3 and colony stimulating factor-1 stimulate proliferation but do not induce inositol lipid breakdown in murine bone-marrow-derived macrophages.

The haemopoietic growth factors interleukin 3 (IL-3) and colony stimulating factor-1 (CSF-1) stimulate the survival and proliferation of murine normal bone-marrow-derived macrophages. To establish whether these growth factors elicit their effects via the hydrolysis of phosphatidylinositol(4,5)bisphosphate [PtdIns(4,5)P2] to form the second messengers inositol (1,4,5)trisphosphate [Ins(1,4,5)P3] and diacylglycerol, macrophages were labelled with tracer quantities of [3H]inositol. Treatment of these cells with either IL-3 or CSF-1 did not alter the levels of PtdIns(4,5)P2 or Ins(1,4,5)P3.