Evidence map›Paper›PMID 29556239›Full record

ReviewFrontiers in immunology2018

Plasma Cell Differentiation Pathways in Systemic Lupus Erythematosus.

Susan Malkiel, Ashley N Barlev, Yemil Atisha-Fregoso, Jolien Suurmond, Betty Diamond

Abstract readReview
In one paragraph

Review in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers.

0numbers the graph read from it
0cells of the map it votes in
89citing papers in PubMed
–field-weighted citation impact
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

89 citing papers in PubMed.

  1. InterferonFrontiers in immunology · 2020
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29 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

5 authors.

Susan MalkielCenter of Autoimmune Musculoskeletal and Hematopoietic Diseases, The Feinstein Institute for Medical Research, Northwell Health, Manhasset, NY, United States.
Ashley N BarlevCenter of Autoimmune Musculoskeletal and Hematopoietic Diseases, The Feinstein Institute for Medical Research, Northwell Health, Manhasset, NY, United States.
Yemil Atisha-FregosoCenter of Autoimmune Musculoskeletal and Hematopoietic Diseases, The Feinstein Institute for Medical Research, Northwell Health, Manhasset, NY, United States.
Jolien SuurmondCenter of Autoimmune Musculoskeletal and Hematopoietic Diseases, The Feinstein Institute for Medical Research, Northwell Health, Manhasset, NY, United States.
Betty DiamondCenter of Autoimmune Musculoskeletal and Hematopoietic Diseases, The Feinstein Institute for Medical Research, Northwell Health, Manhasset, NY, United States.

Funding

The Monoclonal Antibody and Reagent CoreP01AI073693 · NIAID · FEINSTEIN INSTITUTE FOR MEDICAL RESEARCH · PI MEGGAN MACKAY · 2008 to 2026
$45.8M
NIAID NIH HHS P01 AI073693
6 · The paper itself

Abstract

Plasma cells (PCs) are responsible for the production of protective antibodies against infectious agents but they also produce pathogenic antibodies in autoimmune diseases, such as systemic lupus erythematosus (SLE). Traditionally, high affinity IgG autoantibodies are thought to arise through germinal center (GC) responses. However, class switching and somatic hypermutation can occur in extrafollicular (EF) locations, and this pathway has also been implicated in SLE. The pathway from which PCs originate may determine several characteristics, such as PC lifespan and sensitivity to therapeutics. Although both GC and EF responses have been implicated in SLE, we hypothesize that one of these pathways dominates in each individual patient and genetic risk factors may drive this predominance. While it will be important to distinguish polymorphisms that contribute to a GC-driven or EF B cell response to develop targeted treatments, the challenge will be not only to identify the differentiation pathway but the molecular mechanisms involved. In B cells, this task is complicated by the cross-talk between the B cell receptor, toll-like receptors (TLR), and cytokine signaling molecules, which contribute to both GC and EF responses. While risk variants that affect the function of dendritic cells and T follicular helper cells are likely to primarily influence GC responses, it will be important to discover whether some risk variants in the interferon and TLR pathways preferentially influence EF responses. Identifying the pathways of autoreactive PC differentiation in SLE may help us to understand patient heterogeneity and thereby guide precision therapy.

Indexed as

AnimalsAutoantibodiesB-LymphocytesCell DifferentiationCytokinesGenetic Predisposition to DiseaseGerminal CenterHumansLupus Erythematosus, SystemicMolecular Targeted TherapyPlasma CellsReceptor Cross-TalkReceptors, Antigen, B-CellSignal TransductionToll-Like ReceptorsAutoantibodiesCytokinesReceptors, Antigen, B-CellToll-Like ReceptorsautoantibodiesB cellsplasma cellssystemic lupus erythematosustolerance

Identifiers

PMID29556239
PMCPMC5845388

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.