Cytokines and growth factors play critical roles in normal homeostasis of immune functions. TGF-beta1 is the dominant negative regulator of inflammatory responses. We have earlier generated TGF-beta1 null mice that exhibit multifocal inflammation associated with increased adhesion of leukocytes to endothelium, aberrant expression of MHC class-I and -II antigens, and autoimmune manifestations similar to Sjogren syndrome. Moreover, depletion of CD8 cells ameliorated health status of TGF-beta1 null mice. To delineate role of TGF-beta1 in aberrant MHC expression, TGF-beta1 null mice were generated in the MHC-I and MHC-II deficient backgrounds. TGF-beta1 X MHC-I null mice exhibit increased longevity with reduced inflammation, diminished autoimmune manifestations and significantly elevated myelopoiesis. These studies are now extended to study role of this growth factor in craniofacial development.Macrophage migration inhibitory factor (MIF) is a major protein constituent of the anterior pituitary gland released into the bloodstream during endotoxemia. For many years, MIF had been thought to be a T cell product associated with delayed-type hypersensitivity reactions. The identification of MIF as a pituitary stress hormone provides an important link in the regulation of systemic inflammatory responses by CNS. Additionally, there is a compelling evidence that suggests a strong link between MIF and cell cycle suggesting MIF as an inhibitor in G0 phase. In order to delineate the precise role of MIF in vivo, we have analyzed its expression profile during embryogenesis which seems to parallel organogenesis and tissue speciation. We have generated transgenic mice with MIF-LacZ transgene wh
