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January 24, 2010 | History

Targeted deletion of fibrinogen-like protein (FGL2) leads to increased immune reactivity 1 edition

Targeted deletion of fibrinogen-like protein (FGL2) leads to increased ...
Cheryl Koscik

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Targeted deletion of fibrinogen-like protein (FGL2) leads to increased immune reactivity.

Published 2005 .
Written in English.

About the Book

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.

Edition Notes

Source: Masters Abstracts International, Volume: 44-02, page: 0812.

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

Electronic version licensed for access by U. of T. users.

GERSTEIN MICROTEXT copy on microfiche (1 microfiche).

The Physical Object

Pagination
67 leaves.
Number of pages
67

ID Numbers

Open Library
OL19217161M
ISBN 10
0494073225

History Created December 11, 2009 · 2 revisions Download catalog record: RDF / JSON

January 24, 2010 Edited by WorkBot add more information to works
December 11, 2009 Created by WorkBot add works page