Autoantibodies against C1q in Systemic Lupus Erythematosus Are Antigen-Driven

Schaller, Monica; Bigler, Cornelia; Danner, Doris; Ditzel, Henrik J.; Trendelenburg, Marten

doi:10.4049/jimmunol.0902642

Cited by 51 publications

(43 citation statements)

References 58 publications

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“…15,16 Patients affected by SLE are characterized by a hyperactivity of cells of the immune system. 30 A hyperactive state has been recently demonstrated in dendritic cells, which have been suggested to play a pathogenic role in SLE. 15,16 Dendritic cells continuously circulate from the bloodstream throughout the periphery, towards the draining lymph nodes, and can be activated by several danger signals derived from either exogenous or endogenous agents.…”

Section: Discussionmentioning

confidence: 98%

“…[14][15][16][28][29][30] These endogenous dendritic cell activators are capable of triggering the production of pivotal cytokines for the development of autoimmunity such as the type I IFN. 31,32 Consistent with our earlier report, 8 focal aggregations of dendritic cells as well as dendritic cells contacting each other were identified in Barrett's tissue specimens and adenocarcinoma specimens.…”

Section: Discussionmentioning

confidence: 99%

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Expression of C1q Complement Component in Barrett’s Esophagus and Esophageal Adenocarcinoma

Bobryshev

Lord

2010

Journal of Gastrointestinal Surgery

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Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

Expression of C1q Complement Component in Barrett’s Esophagus and Esophageal Adenocarcinoma

Bobryshev

Lord

2010

Journal of Gastrointestinal Surgery

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“…32 The anti-ADAMTS13 mAbs showed somatic hypermutation typical for an antigen-driven, affinity matured immune response, which is a process dependent on CD4 1 T-cell help. [40][41][42]48 The average nucleic acid mutation rate was 12% for the V H and the V L chain regions, with the highest mutation rate in mAbs using the V H 1-3 germ-line gene (average, 15%; range, 13.5-18.4%) and the lowest in V H 1-69 mAbs (average, 4.8%; range, 2.9-5.7%).…”

Section: Discussionmentioning

confidence: 99%

The splenic autoimmune response to ADAMTS13 in thrombotic thrombocytopenic purpura contains recurrent antigen-binding CDR3 motifs

Schaller¹,

Vogel

Kentouche

et al. 2014

Blood

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Key Points• The spleen harbors ADAMTS13-specific memory B cells following acute acquired TTP.• The splenic anti-ADAMTS13 antibody repertoire is characterized by a set of unique and novel CDR3 motifs, 4 shared by 2 patients.Acquired thrombotic thrombocytopenic purpura (TTP) is the consequence of a severe ADAMTS13 deficiency resulting from autoantibodies inhibiting ADAMTS13 or accelerating its clearance. Despite the success of plasma exchange the risk of relapse is high. From 2 patients (A and B), splenectomized for recurrent episodes of acquired TTP, the splenic B-cell response against ADAMTS13 was characterized through generation of human monoclonal anti-ADAMTS13 autoantibodies (mAbs) by cloning an immunoglobulin G (IgG) 4 k-and IgG 4 l-Fab library using phage display technology and by Epstein-Barr virus transformation of switched memory B cells (CD19 1 /CD27 1 /IgG 1 ). Sequence analysis of the anti-ADAMTS13 IgGs of both patients revealed that the V H gene use was limited in our patients to V H 1-3 (55%), V H 1-69 (17%), V H 3-30 (7%), and V H 4-28 (21%) and contained 8 unique and thus far not reported heavy-chain complementarity determining region 3 motifs, of which 4 were shared by the 2 patients. The discovery of several highly similar anti-ADAMTS13 autoantibodies in 2 unrelated TTP patients suggests that the autoimmune response is antigen driven, because the probability that such similar immunoglobulin rearrangements happen by chance is very low (<10 29). (Blood. 2014;124(23):3469-3479)

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“…It is reasonable that native CRP under certain circumstances (such as inflammation with low pH) may dissociate into subunits, deposit and expose neo-epitopes on tissue surfaces and consequently become target for autoantibodies. This scenario could be parallel to the development of anti-C1q antibodies in SLE [55].…”

Section: Discussionmentioning

confidence: 99%

C-reactive protein, immunoglobulin G and complement co-localize in renal immune deposits of proliferative lupus nephritis

et al. 2013

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Autoantibodies against C1q in Systemic Lupus Erythematosus Are Antigen-Driven

Abstract: Material

Cited by 51 publications

References 58 publications

Expression of C1q Complement Component in Barrett’s Esophagus and Esophageal Adenocarcinoma

Expression of C1q Complement Component in Barrett’s Esophagus and Esophageal Adenocarcinoma

The splenic autoimmune response to ADAMTS13 in thrombotic thrombocytopenic purpura contains recurrent antigen-binding CDR3 motifs

C-reactive protein, immunoglobulin G and complement co-localize in renal immune deposits of proliferative lupus nephritis

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