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THE ROLE OF CSF-1 IN THE PATHOGENESIS OF LUPUS NEPHRITIS

Award Number: F32DK078416
ORGANIZATION: NATIONAL INSTITUTE OF DIABETES & DIGESTIVE & KIDNEY DISEASES
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS
PERIOD OF PERFORMANCE START DATE: 03/15/2009
PERIOD OF PERFORMANCE END DATE: 03/14/2010

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THE ROLE OF CSF-1 IN THE PATHOGENESIS OF LUPUS NEPHRITIS - DESCRIPTION (provided by applicant): Nephritis is a common complication of the human autoimmune disease systemic lupus erythematosus (SLE). Mice of the MRL-Faslpr strain spontaneously develop a disease that is similar to SLE. It has been shown that macrophages (MO) are prominent in lupus nephritis in the MRL-Faslpr strain and that upon activation, MO destroy renal resident cells during inflammation. Colony Stimulating Factor-1 (CSF-1), the principal MO growth factor, is required to promote lupus nephritis in MRL-Faslpr mice. The actions of CSF-1 are mediated exclusively by the CSF-1 receptor (CSF-1 R). There are three individual CSF-1 isoforms, a cell surface CSF-1 (csCSF), a secreted proteoglycan (spCSF) and a secreted glycoprotein (sgCSF). We hypothesize that CSF-1 and CSF-1 R bearing cells are central in the pathogenesis of lupus nephritis. In order to test this hypothesis, we propose: 1) to determine whether over-expressing CSF-1 systemically accelerates lupus nephritis and the systemic illness in MRL-Faslpr mice; 2) to determine the role(s) of the individual CSF-1 isoforms in lupus nephritis and systemic illness in MRL-Faslpr mice; and 3) to determine whether eliminating CSF-1 signaling during disease in MRL-Faslpr mice can halt the progression of lupus nephritis and the systemic illness. These aims will allow us to evaluate the potential therapeutic value of blocking/eliminating CSF-1 mediated signals in the treatment of lupus nephritis and other macrophage-mediated illnesses. Kidney inflammation is a major cause of morbidity and mortality in lupus patients. This inflammation is mediated in large part by a subset of white blood cells known as macrophages that destroy tissue within the kidney. It has been shown that CSF-1, the principle macrophage growth factor, promotes kidney inflammation in mice that spontaneously develop a disease that shares many of the characteristics of human lupus. We will use these mice to determine the specific mechanisms of CSF-1 dependent inflammation and establish whether the CSF-1 pathway is a potential therapeutic target for lupus and other macrophage-mediated kidney diseases in humans..


Issue Date FY	Funding FY	Legal Entity Name	Legal Entity Address	Legal Entity City	Legal Entity State	Legal Entity Zip Code	Legal Entity COUNTY	Legal Entity COUNTRY	Assistance Listing	Award Code	Budget Year	Action Date	Action Type	Action Amount

Issue Date FY: 2009 ( Subtotal = $53,354 )
2009	2009	ADVANCED IMMUNE THERAPEUTICS INC	47 HALL STREET	WELLESLEY	MA	02481	NORFOLK	USA	Diabetes, Digestive, and Kidney Diseases Extramural Research	001	3	7/23/2009	CHANGE OF GRANTEE / TRAINING INSTITUTION / AWARDING INSTITUTION	$53,354
2009	2008	BRIGHAM & WOMEN`S HOSPITAL	10 VINING STREET	BOSTON	MA	02115	SUFFOLK	USA	Kidney Diseases, Urology and Hematology Research	000	2	7/23/2009	NON-COMPETING CONTINUATION	$0
														Subtotal = $53,354

Issue Date FY: 2008 ( Subtotal = $51,278 )
2008	2008	BRIGHAM & WOMEN'S HOSPITAL	10 VINING STREET	BOSTON	MA	02115	SUFFOLK	USA	Kidney Diseases, Urology and Hematology Research	000	2	2/13/2008	NON-COMPETING CONTINUATION	$51,278
														Subtotal = $51,278

Issue Date FY: 2007 ( Subtotal = $49,646 )
2007	2007	BRIGHAM & WOMEN'S HOSPITAL	10 VINING STREET	BOSTON	MA	02115	SUFFOLK	USA	Kidney Diseases, Urology and Hematology Research	000	1	3/6/2007	NEW	$49,646
														Subtotal = $49,646

Grand Total All Awards = $154,278

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THE ROLE OF CSF-1 IN THE PATHOGENESIS OF LUPUS NEPHRITIS

Award Number: F32DK078416

ORGANIZATION: NATIONAL INSTITUTE OF DIABETES & DIGESTIVE & KIDNEY DISEASES

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS

PERIOD OF PERFORMANCE START DATE: 03/15/2009

PERIOD OF PERFORMANCE END DATE: 03/14/2010

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