Evidence map›Paper›PMID 26923204›Full record

ReviewNature reviews. Nephrology2016

Plasma cells as an innovative target in autoimmune disease with renal manifestations.

Falk Hiepe, Andreas Radbruch

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Nephrology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 125 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
125citing papers in PubMed, 1 pooled it
10.9field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

125 citing papers in PubMed, 1 synthesis or guideline pooled it, 199 citations in OpenAlex.

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  9. Selective ablation of dsDNA-specific plasma cells improves lupus nephritis in NZB/W mice.Proceedings of the National Academy of Sciences of the United States of America · 2026
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  19. Cxcl9Communications biology · 2025
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65 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 1 country.

Falk HiepeCharité - Universitätsmedizin Berlin and Deutsches Rheumaforschungszentrum Berlin, ein Institut der Leibniz-Gemeinschaft, Charitéplatz 1, Berlin 10117, Germany.
Andreas RadbruchCharité - Universitätsmedizin Berlin and Deutsches Rheumaforschungszentrum Berlin, ein Institut der Leibniz-Gemeinschaft, Charitéplatz 1, Berlin 10117, Germany.
German Rheumatism Research Centre · DELeibniz Association · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autoantibodies are secreted by plasma cells and have an essential role in driving the renal manifestations of autoimmune diseases such as systemic lupus erythematosus and antineutrophil cytoplasmic autoantibody-associated vasculitis. Effective depletion of autoreactive plasma cells might be the key to curative treatment of these diseases. Two major plasma-cell compartments exist: short-lived plasmablasts or plasma cells, which result from differentiation of activated B cells, and long-lived plasma cells, which result from secondary immune responses. Long-lived plasma cells reside in survival niches in bone marrow and inflamed tissue and provide the basis of humoral memory and refractory autoimmune disease activity. Unlike short-lived plasmablasts, long-lived plasma cells do not respond to conventional immunosuppression or to therapies that target B cells. Existing therapies that target long-lived plasma cells, such as proteasome inhibitors and antithymocyte globulin, as well as promising approaches that target survival factors, cell homing or surface molecules, deplete the whole memory plasma cell pool, including cells that secrete protective antibodies. By contrast, we have developed a novel strategy that uses an affinity matrix to deplete pathogenic long-lived plasma cells in an autoantigen-specific manner without removing protective plasma cells. Targeting B-cell precursors to prevent replenishment of autoreactive long-lived plasma cells should also be considered.

Indexed as

AutoantibodiesAutoimmune DiseasesB-LymphocytesBoronic AcidsBortezomibGlomerulonephritisHumansImmunologic MemoryImmunosuppressive AgentsKidney DiseasesLupus NephritisOligopeptidesPeptidesPlasma CellsProteasome InhibitorsThreonineAutoantibodiesBoronic AcidsBortezomibcarfilzomibCTCE-9908delanzomibImmunosuppressive AgentsOligopeptidesPeptidesProteasome InhibitorsThreonine

Identifiers

PMID26923204
OpenAlexW2289710622

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.