Targeted deletion of fibrinogen-like protein (FGL2) leads to increased immune reactivity.
Published: 2005
Language: eng
Number of pages: 67
Description: FGL2/Fibroleukin, a member of the fibrinogen protein family, has been shown to participate in the pathogenesis of many inflammatory diseases. Production of fgl2 deficient mice (fgl2-/-) allowed us to examine whether targeted deletion leads to altered immune function. Constitutive fgl2 expression, detected by LacZ expression, was observed in spleen, lymph nodes and bone marrow. Proportions of T cell, B cell and macrophage populations were comparable, however, increased numbers of CD11c+MHCII+ dendritic cells (DC) were found in spleen and bone marrow of fgl2-/- mice. The increase in DC number could be explained by a decrease in cells undergoing caspase-independent apoptosis in fgl2-/- mice. Functional immune assays revealed increased T cell, B cell and DC activity in response to various stimuli. Autoimmune renal disease characterized by cellular infiltration, fibrin deposition, hemorrhage, and abnormal glomerulus and tubule structure was seen in fgl2-/- mice. Collectively, this data implicates FGL2 as an important immunoregulatory protein.
Notes: Source: Masters Abstracts International, Volume: 44-02, page: 0812.

Thesis (M.Sc.)--University of Toronto, 2005.

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