NDLI: Absence of CD59 exacerbates systemic autoimmunity in MRL/lpr mice.

Please wait, while we are loading the content...

Pneumococcal surface protein A inhibits complement deposition on the pneumococcal surface by competing with the binding of C-reactive protein to cell-surface phosphocholine.

Primary MHC-class II(+) cells are necessary to promote resting VÎ´2 cell expansion in response to (E)-4-hydroxy-3-methyl-but-2-enyl-pyrophosphate and isopentenyl pyrophosphate.

Atypical activation of the unfolded protein response in cystic fibrosis airway cells contributes to p38 MAPK-mediated innate immune responses.

ZBTB7B (Th-POK) regulates the development of IL-17-producing CD1d-restricted mouse NKT cells.

Broad cross-presentation of the hematopoietically derived PR1 antigen on solid tumors leads to susceptibility to PR1-targeted immunotherapy.

Endothelial cell peroxisome proliferator-activated receptor Î³ reduces endotoxemic pulmonary inflammation and injury.

Tumor-associated macrophages promote invasion while retaining Fc-dependent anti-tumor function.

Glutamine suppresses airway neutrophilia by blocking cytosolic phospholipase A(2) via an induction of MAPK phosphatase-1.

Paneth cell-mediated multiorgan dysfunction after acute kidney injury.

Neutrophil extracellular traps entrap and kill Borrelia burgdorferi sensu stricto spirochetes and are not affected by Ixodes ricinus tick saliva.

Differential expression of neurotensin and specific receptors, NTSR1 and NTSR2, in normal and malignant human B lymphocytes.

Absence of CD59 exacerbates systemic autoimmunity in MRL/lpr mice.

5-Lipoxygenase mediates RANKL-induced osteoclast formation via the cysteinyl leukotriene receptor 1.

TRAF binding is required for a distinct subset of in vivo B cell functions of the oncoprotein LMP1.

IFN-Î³ limits Th9-mediated autoimmune inflammation through dendritic cell modulation of IL-27.

Mechanism of action of inhibition of allergic immune responses by a novel antedrug TLR7 agonist.

CCR1-mediated STAT3 tyrosine phosphorylation and CXCL8 expression in THP-1 macrophage-like cells involve pertussis toxin-insensitive G (14/16) signaling and IL-6 release.

Autoimmunity: twenty years in the Fas lane.

Pathogenic long-lived plasma cells and their survival niches in autoimmunity, malignancy, and allergy.

Year: 2012 Volume: 189 Issue: 10

Year: 2012 Volume: 189 Issue: 9

Year: 2012 Volume: 189 Issue: 8

Year: 2012 Volume: 189 Issue: 7

Year: 2012 Volume: 189 Issue: 6

Year: 2012 Volume: 189 Issue: 5

Year: 2012 Volume: 189 Issue: 4

Year: 2012 Volume: 189 Issue: 3

Year: 2012 Volume: 189 Issue: 2

Year: 2012 Volume: 189 Issue: 1

Year: 2012 Volume: 188

Year: 2011 Volume: 187

Year: 2011 Volume: 186

Year: 2010 Volume: 185

Year: 2010 Volume: 184

Year: 2009 Volume: 183

Year: 2009 Volume: 182

Year: 2008 Volume: 181

Absence of CD59 exacerbates systemic autoimmunity in MRL/lpr mice.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Eisenberg, Robert A. Song, Wen-Chao Miwa, Takashi Madaio, Michael P. Maldonado, Michael A. Zhou, Lin
Description	Country affiliation: United States Author Affiliation: Miwa T ( Department of Pharmacology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.)
Abstract	CD59 is a GPI-anchored membrane regulator of complement expressed on blood cells as well as peripheral tissues. It protects host cells from complement injury by inhibiting formation of the membrane attack complex. Recent studies in mice have suggested also a role of CD59 in T cell immune response that was mechanistically independent of complement. In the present study, we investigated the function of CD59 in the MRL/lpr model of murine lupus. We backcrossed the Cd59a knockout (Cd59a(-/-)) mouse onto the MRL/lpr background and compared Cd59a(+/+)-MRL/lpr and Cd59a(-/-)-MRL/lpr littermates for the development of systemic autoimmunity. We found that CD59a deficiency significantly exacerbated the skin disease and lymphoproliferation characteristic of MRL/lpr mice. It also increased autoantibody titers and caused a higher level of proteinuria in male MRL/lpr mice. Bone marrow transfer experiments indicated that CD59a expression on both bone marrow-derived cells and peripheral tissues played a role in lymphoproliferation, whereas the skin disease phenotype is determined mainly by local CD59a expression. Importantly, C3 gene deletion or C5 neutralization with a blocking mAb in Cd59a(-/-)-MRL/lpr mice did not rescue the proautoimmune phenotype associated with CD59a deficiency. These results together suggest that CD59a inhibits systemic autoimmunity in MRL/lpr mice through a complement-independent mechanism.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1201621
Journal	The Journal of Immunology
Issue Number	11
Volume Number	189
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2012-12-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Antigens, Cd59 Immunology Autoantibodies Biosynthesis Autoimmunity Lupus Erythematosus, Systemic Anemia, Hemolytic Genetics Animals Antibodies Pharmacology Complement C3 Deficiency Complement C5 Antagonists & Inhibitors Dermatitis Pathology Gene Expression Hemoglobinuria Mice Mice, Inbred Mrl Lpr Mice, Knockout Proteinuria Sex Factors Skin T-lymphocytes Research Support, N.i.h., Extramural Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

IL-21 receptor is required for the systemic accumulation of activated B and T lymphocytes in MRL/MpJ-Fas(lpr/lpr)/J mice.

Absence of CD59 exacerbates systemic autoimmunity in MRL/lpr mice 1

Complement receptor of the immunoglobulin superfamily reduces murine lupus nephritis and cutaneous disease.

Brief report: increased expression of a short splice variant of CTLA-4 exacerbates lupus in MRL/lpr mice.

Deficiency in activation-induced cytidine deaminase promotes systemic autoimmunity in lpr mice on a C57BL/6 background.

A Bacterial Artificial Chromosome Transgene with Polymorphic Cd72 Inhibits the Development of Glomerulonephritis and Vasculitis in $MRL-Fas^{lpr}$ Lupus Mice

Knocking out of CD38 accelerates development of a lupus-like disease in lpr mice.

B cell-derived IL-10 does not regulate spontaneous systemic autoimmunity in MRL.Fas(lpr) mice.

Cholera toxin B accelerates disease progression in lupus-prone mice by promoting lipid raft aggregation.

Absence of CD59 exacerbates systemic autoimmunity in MRL/lpr mice.

Similar Documents

IL-21 receptor is required for the systemic accumulation of activated B and T lymphocytes in MRL/MpJ-Fas(lpr/lpr)/J mice.

Absence of CD59 exacerbates systemic autoimmunity in MRL/lpr mice 1

Complement receptor of the immunoglobulin superfamily reduces murine lupus nephritis and cutaneous disease.

Brief report: increased expression of a short splice variant of CTLA-4 exacerbates lupus in MRL/lpr mice.

Deficiency in activation-induced cytidine deaminase promotes systemic autoimmunity in lpr mice on a C57BL/6 background.

A Bacterial Artificial Chromosome Transgene with Polymorphic Cd72 Inhibits the Development of Glomerulonephritis and Vasculitis in $MRL-Fas^{lpr}$ Lupus Mice

Knocking out of CD38 accelerates development of a lupus-like disease in lpr mice.

B cell-derived IL-10 does not regulate spontaneous systemic autoimmunity in MRL.Fas(lpr) mice.

Cholera toxin B accelerates disease progression in lupus-prone mice by promoting lipid raft aggregation.

Absence of CD59 exacerbates systemic autoimmunity in MRL/lpr mice.