Evidence map›Paper›PMID 26284069›Full record

ReviewFrontiers in immunology2015

T Cell Migration in Rheumatoid Arthritis.

Mario Mellado, Laura Martínez-Muñoz, Graciela Cascio, Pilar Lucas, José L Pablos, José Miguel Rodríguez-Frade

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 164 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
164citing papers in PubMed, 5 pooled it
15.4field-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

164 citing papers in PubMed, 5 syntheses or guidelines pooled it, 285 citations in OpenAlex.

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  11. JAK/STAT inhibition reprograms T cell activation and metabolism in inflammatory arthritis patients.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
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104 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

6 authors at 1 institution in 1 country.

Mario MelladoDepartment of Immunology and Oncology, Centro Nacional de Biotecnología, Consejo Superior de Investigaciones , Madrid , Spain.
Laura Martínez-MuñozDepartment of Immunology and Oncology, Centro Nacional de Biotecnología, Consejo Superior de Investigaciones , Madrid , Spain.
Graciela CascioDepartment of Immunology and Oncology, Centro Nacional de Biotecnología, Consejo Superior de Investigaciones , Madrid , Spain.
Pilar LucasDepartment of Immunology and Oncology, Centro Nacional de Biotecnología, Consejo Superior de Investigaciones , Madrid , Spain.
José L PablosGrupo de Enfermedades Inflamatorias y Autoinmunes, Instituto de Investigación Sanitaria Hospital , Madrid , Spain.
José Miguel Rodríguez-FradeDepartment of Immunology and Oncology, Centro Nacional de Biotecnología, Consejo Superior de Investigaciones , Madrid , Spain.
Centro Nacional de Biotecnología · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rheumatoid arthritis (RA) is an autoimmune disease characterized by chronic inflammation in joints, associated with synovial hyperplasia and with bone and cartilage destruction. Although the primacy of T cell-related events early in the disease continues to be debated, there is strong evidence that autoantigen recognition by specific T cells is crucial to the pathophysiology of rheumatoid synovitis. In addition, T cells are key components of the immune cell infiltrate detected in the joints of RA patients. Initial analysis of the cytokines released into the synovial membrane showed an imbalance, with a predominance of proinflammatory mediators, indicating a deleterious effect of Th1 T cells. There is nonetheless evidence that Th17 cells also play an important role in RA. T cells migrate from the bloodstream to the synovial tissue via their interactions with the endothelial cells that line synovial postcapillary venules. At this stage, selectins, integrins, and chemokines have a central role in blood cell invasion of synovial tissue, and therefore in the intensity of the inflammatory response. In this review, we will focus on the mechanisms involved in T cell attraction to the joint, the proteins involved in their extravasation from blood vessels, and the signaling pathways activated. Knowledge of these processes will lead to a better understanding of the mechanism by which the systemic immune response causes local joint disorders and will help to provide a molecular basis for therapeutic strategies.

Indexed as

cell migrationchemokinescytokinesinflammationrheumatoid arthritis

Identifiers

PMID26284069
PMCPMC4515597
OpenAlexW2169868751

What OpenQuestion 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 OpenQuestion graph.