PMID- 15840592
OWN - NLM
STAT- MEDLINE
DCOM- 20051028
LR  - 20070906
IS  - 1462-0324 (Print)
IS  - 1462-0324 (Linking)
VI  - 44
IP  - 9
DP  - 2005 Sep
TI  - Induction of systemic lupus erythematosus-like syndrome in syngeneic mice by 
      immunization with activated lymphocyte-derived DNA.
PG  - 1108-14
AB  - OBJECTIVES: Systemic lupus erythematosus (SLE) is the prototype of autoimmune 
      disease and the mechanisms underlying the disease have not yet been elucidated. 
      Thus, animal models of SLE would facilitate investigation of pathogenetic 
      mechanisms involved in the development of the disease. This study characterizes a 
      murine model of SLE-like syndrome induced by syngeneic activated 
      lymphocyte-derived DNA (referred to as ALD DNA). METHODS: Normal BALB/c mice were 
      immunized subcutaneously with highly purified ALD DNA. Anti-double-stranded DNA 
      (anti-dsDNA) antibodies were determined by enzyme-linked immunosorbent assay. 
      Other SLE-associated autoantibodies were examined by indirect immunofluorescence 
      and anti-ENA (extractable nuclear antigen) profile assay. Pathological changes 
      were analysed by light microscopy and electron microscopy. Kidney cryostat 
      sections were viewed by immunofluorescence for the presence of glomerular IgG and 
      C3 deposits. Proteinuria was measured by Coomassie brilliant blue assay. RESULTS: 
      High levels of anti-dsDNA antibodies and other autoantibodies frequently 
      appearing in SLE were detectable in the sera of ALD DNA-immunized mice. 
      Glomerulonephritis and glomerular deposition of IgG plus C3 were observed in the 
      kidney sections. Moreover, proteinuria was seen in the immunized mice. 
      CONCLUSIONS: SLE-like syndrome can be induced by ALD DNA in normal mice. This 
      induced model may be useful for elucidating the mechanisms involved in 
      autoimmunity to DNA and the development of SLE.
FAU - Qiao, B
AU  - Qiao B
AD  - Department of Immunology, Shanghai Medical College of Fudan University, P.R. 
      China.
FAU - Wu, J
AU  - Wu J
FAU - Chu, Y W
AU  - Chu YW
FAU - Wang, Y
AU  - Wang Y
FAU - Wang, D P
AU  - Wang DP
FAU - Wu, H S
AU  - Wu HS
FAU - Xiong, S D
AU  - Xiong SD
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20050419
PL  - England
TA  - Rheumatology (Oxford)
JT  - Rheumatology (Oxford, England)
JID - 100883501
RN  - 0 (Antibodies, Antinuclear)
RN  - 0 (Complement C3)
RN  - 0 (Immunoglobulin G)
RN  - 0 (Immunoglobulin Isotypes)
RN  - 9007-49-2 (DNA)
SB  - IM
CIN - Rheumatology (Oxford). 2005 Sep;44(9):1086-9. PMID: 15914499
MH  - Animals
MH  - Antibodies, Antinuclear/biosynthesis
MH  - Autoimmunity
MH  - Complement C3/analysis
MH  - DNA/*immunology
MH  - *Disease Models, Animal
MH  - Female
MH  - Immunization
MH  - Immunoglobulin G/biosynthesis
MH  - Immunoglobulin Isotypes/biosynthesis
MH  - Lupus Erythematosus, Systemic/*etiology/immunology
MH  - Lupus Nephritis/immunology/pathology
MH  - Lymphocyte Activation/*immunology
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Proteinuria/immunology
EDAT- 2005/04/21 09:00
MHDA- 2005/10/29 09:00
CRDT- 2005/04/21 09:00
PHST- 2005/04/21 09:00 [pubmed]
PHST- 2005/10/29 09:00 [medline]
PHST- 2005/04/21 09:00 [entrez]
AID - keh656 [pii]
AID - 10.1093/rheumatology/keh656 [doi]
PST - ppublish
SO  - Rheumatology (Oxford). 2005 Sep;44(9):1108-14. doi: 10.1093/rheumatology/keh656. 
      Epub 2005 Apr 19.