Evidence map›Paper›PMID 35595051›Full record

ReviewAutoimmunity reviews2022

Significance of IL-7 and IL-7R in RA and autoimmunity.

Anja Meyer, Prashant J Parmar, Shiva Shahrara

Open access · greenAbstract readReview
In one paragraph

Review in Autoimmunity reviews, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 1 pooled it
7.2field-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

38 citing papers in PubMed, 1 synthesis or guideline pooled it, 69 citations in OpenAlex.

  1. Identification ofFrontiers in immunology · 2026
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  3. Cytotoxic CD4Signal transduction and targeted therapy · 2026
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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.

Anja MeyerJesse Brown VA Medical Center, Chicago, IL, USA; Department of Medicine, Division of Rheumatology, the University of Illinois at Chicago, IL, USA.
Prashant J ParmarDepartment of Medicine, Division of Rheumatology, the University of Illinois at Chicago, IL, USA.
Shiva ShahraraJesse Brown VA Medical Center, Chicago, IL, USA; Department of Medicine, Division of Rheumatology, the University of Illinois at Chicago, IL, USA. Electronic address: shahrara@uic.edu.
Jesse Brown VA Medical Center · USUniversity of Illinois Chicago · US

Funding

Identifying a novel pathway that regulates RA immunometabolismR01AI167155 · NIAID · UNIVERSITY OF ILLINOIS AT CHICAGO · PI SHIVA SHAHRARA · 2022 to 2026
$2.9M
Engineering a unique antibody for patients with RAR41AI147697 · NIAID · ABWIZ BIO, INC. · PI MARUYAMA, TOSHIAKI, SHAHRARA, SHIVA · 2020 to 2021
$600k
Ligation of TLR7 promotes joint inflammation and bone loss in RA.I01BX002286 · VA · JESSE BROWN VA MEDICAL CENTER · PI SHAHRARA, SHIVA · 2015 to 2023
–
BLRD VA I01 BX002286CSRD VA I01 CX002565NIAID NIH HHS R01 AI167155NIAID NIH HHS R41 AI147697
6 · The paper itself

Abstract

While physiological levels of IL-7 are essential for T cell proliferation, survival and co-stimulation, its escalated concentration has been associated with autoimmune diseases such as Rheumatoid arthritis (RA). Expression of IL-7 and IL-7R in RA monocytes is linked to disease activity score and TNF transcription. TNF stimulation can modulate IL-7 secretion and IL-7R frequency in myeloid cells, however, only IL-7R transcription levels are downregulated in anti-TNF responsive patients. Elevated levels of IL-7 in RA synovial tissue and fluid are involved in attracting RA monocytes into the inflammatory joints and remodeling them into proinflammatory macrophages and mature osteoclasts. Further, IL-7 amplification of RA Th1 cell differentiation and IFNγ secretion, can directly prime myeloid IL-7R expression and thereby exacerbate IL-7-mediated joint inflammatory and erosive imprints. In parallel, IL-7 accentuates joint angiogenesis by expanding the production of proangiogenic factors from RA macrophages and endothelial cells. In preclinical models, blockade of IL-7 or IL-7R can effectively impair joint inflammation, osteoclast formation, and neovascularization primarily by impeding monocyte and endothelial cell infiltration as well as inhibition of pro-inflammatory macrophage and Th1/Th17 cell differentiation. In conclusion, disruption of IL-7/IL-7R signaling can uniquely intercept the crosstalk between RA myeloid and lymphoid cells in their ability to trigger neovascularization.

Indexed as

Arthritis, RheumatoidInterleukin-7AutoimmunityEndothelial CellsHumansSynovial FluidTumor Necrosis Factor InhibitorsInterleukin-7Tumor Necrosis Factor InhibitorsIL-7IL-7RMacrophagesRAT cells and autoimmunity

Identifiers

PMID35595051
PMCPMC9987213
OpenAlexW4280629587

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.