Evidence map›Paper›PMID 22855296›Full record

ReviewCurrent rheumatology reports2012

Managing macrophages in rheumatoid arthritis by reform or removal.

Jun Li, Hui-Chen Hsu, John D Mountz

Open access · greenAbstract readReview
In one paragraph

Review in Current rheumatology reports, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers.

0numbers the graph read from it
0cells of the map it votes in
86citing papers in PubMed
8.1field-weighted citation impact, top 2% 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

86 citing papers in PubMed, 147 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Article
  5. Article
  6. Nanoparticle Delivery Systems in Rheumatoid Arthritis: More Than Vehicles.Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2026
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Retinoic acid ameliorates rheumatoid arthritis by attenuating inflammation and modulating macrophage polarization through MKP-1/MAPK signaling pathway.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025
    Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article

26 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

3 authors at 2 institutions in 1 country.

Jun LiDivision of Clinical Immunology and Rheumatology, Department of Medicine, University of Alabama at Birmingham, SHEL Bldg., Suite 337, 1825 University Blvd., Birmingham, AL 35294-2182, USA. junliuab@uab.edu
Hui-Chen Hsu
John D Mountz
University of Alabama at Birmingham · USBirmingham VA Medical Center · US

Funding

ROS Modulation of Innate and Adaptive Immunity in RAP30AR048311 · NIAMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI MOUNTZ, JOHN D · 2001 to 2017
$9.5M
Suppression of pathogenic autoantibodies in lupus by inhibition of AIDR01AI071110 · NIAID · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI MOUNTZ, JOHN D · 2008 to 2018
$4.0M
Entry of antigen-presenting B cells into the follicle directed by IFNa and IL-17R01AI083705 · NIAID · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI HSU, HUI-CHEN · 2011 to 2015
$1.8M
Regulation of Migration of Autoreactive Germinal Centers and Precursor B CellsI01BX000600 · VA · BIRMINGHAM VA MEDICAL CENTER · PI MOUNTZ, JOHN D · 2009 to 2017
–
BLRD VA I01 BX000600NIAID NIH HHS 1R01AI083705NIAID NIH HHS R01 AI071110NIAID NIH HHS R01 AI071110-01A1NIAID NIH HHS R01 AI083705NIAMS NIH HHS P30 AR048311
6 · The paper itself

Abstract

Macrophages play a central role in the pathogenesis of rheumatoid arthritis (RA). There is an imbalance of inflammatory and antiinflammatory macrophages in RA synovium. Although the polarization and heterogeneity of macrophages in RA have not been fully uncovered, the identity of macrophages in RA can potentially be defined by their products, including the co-stimulatory molecules, scavenger receptors, different cytokines/chemokines and receptors, and transcription factors. In the last decade, efforts to understand the polarization, apoptosis regulation, and novel signaling pathways in macrophages, as well as how distinct activated macrophages influence disease progression, have led to strategies that target macrophages with varied specificity and selectivity. Major targets that are related to macrophage development and apoptosis include TNF-α, IL-1, IL-6, GM-CSF, M-CSF, death receptor 5 (DR5), Fas, and others, as listed in Table 1. Combined data from clinical, preclinical, and animal studies of inhibitors of these targets have provided valuable insights into their roles in the disease progression and, subsequently, have led to the evolving therapeutic paradigms in RA. In this review, we propose that reestablishment of macrophage equilibrium by inhibiting the development of, and/or eliminating, the proinflammatory macrophages will be an effective therapeutic approach for RA and other autoimmune diseases.

Indexed as

AnimalsAntirheumatic AgentsApoptosisArthritis, RheumatoidClinical Trials as TopicDisease Models, AnimalHumansMacrophage ActivationMacrophagesMiceMice, TransgenicSynovial MembraneTNF-Related Apoptosis-Inducing LigandAntirheumatic AgentsTNF-Related Apoptosis-Inducing Ligand

Identifiers

PMID22855296
PMCPMC3638732
OpenAlexW2047159240

What OpenQuestion holds

Textmetadata
LicenceTDM
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.