Evidence map›Paper›PMID 37807647›Full record

ArticleCurrent molecular medicine2024

Expression of Transcriptional Factors of T Helper Differentiation (T-bet, GATA-3, RORγt, and FOXP3), MIF Receptors (CD44, CD74, CXCR2, 4, 7), and Th1, Th2, and Th17 Cytokines in PBMC from Control Subjects and Rheumatoid Arthritis Patients.

Darbi Alfredo Zerpa-Hernández, Mariel García-Chagollán, Gabriela Athziri Sánchez-Zuno, Samuel García-Arellano, Jorge Hernández-Bello, Luis Alexis Hernández-Palma, Sergio Cerpa-Cruz, Gloria Martinez-Bonilla, Ferdinando Nicoletti, José Francisco Muñoz-Valle

Abstract read
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In one paragraph

Article in Current molecular medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.3field-weighted citation impact, top 34% 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

4 citing papers in PubMed, 2 citations in OpenAlex.

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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

10 authors at 3 institutions in 2 countries.

Darbi Alfredo Zerpa-HernándezInstituto de Investigación en Ciencias Biomédicas, Universidad de Guadalajara, Jalisco 44340, México.
Mariel García-ChagollánInstituto de Investigación en Ciencias Biomédicas, Universidad de Guadalajara, Jalisco 44340, México.
Gabriela Athziri Sánchez-ZunoInstituto de Investigación en Ciencias Biomédicas, Universidad de Guadalajara, Jalisco 44340, México.
Samuel García-ArellanoInstituto de Investigación en Ciencias Biomédicas, Universidad de Guadalajara, Jalisco 44340, México.
Jorge Hernández-BelloInstituto de Investigación en Ciencias Biomédicas, Universidad de Guadalajara, Jalisco 44340, México.
Luis Alexis Hernández-PalmaInstituto de Investigación en Ciencias Biomédicas, Universidad de Guadalajara, Jalisco 44340, México.
Sergio Cerpa-CruzServicio de Reumatología, O.P.D. Hospital Civil de Guadalajara "Fray Antonio Alcalde", Jalisco 44280, Mexico.
Gloria Martinez-BonillaServicio de Reumatología, O.P.D. Hospital Civil de Guadalajara "Fray Antonio Alcalde", Jalisco 44280, Mexico.
Ferdinando NicolettiDepartment of Biomedical and Biotechnological Sciences, University of Catania, 95123 Catania, Italy.
José Francisco Muñoz-ValleInstituto de Investigación en Ciencias Biomédicas, Universidad de Guadalajara, Jalisco 44340, México.
Universidad de Guadalajara · MXHospital Civil de Guadalajara · MXUniversity of Catania · IT

Funding

National Council of Science and Technology (CONACYT) A1-S-8774
6 · The paper itself

Abstract

introductionThe macrophage migration inhibitory factor (MIF) plays a pivotal role in the development of rheumatoid arthritis (RA). Previous research indicates that MIF can trigger the expression of cytokine profiles associated with Th1, Th2, and Th17 responses in peripheral blood mononuclear cells (PBMC) from both RA patients and control subjects (CS). Despite these, few studies to date precisely elucidate the molecular mechanisms involved. The present study aimed to associate the expression of Th differentiation TF (T-bet, GATA-3, RORγt) with MIF receptors (CD44, CD74, CXCR2, 4, 7) and Th1, Th2, and Th17 cytokines in PBMC from CS and RA patients.

methodPBMC from both groups was cultured for 24 h. The expression of the canonical and non-canonical MIF receptors and the TF was determined by flow cytometry. Additionally, multiplex bead analysis was employed to assess the levels of cytokines in the culture supernatants. The findings revealed that T CD4+ lymphocytes in the CS group exhibited a heightened expression of CD74 (p<0.05), whereas RA patients displayed an elevated expression of CXCR7 (p<0.001). Furthermore, T CD4+ lymphocytes from RA patients exhibited greater expression of GATA3, RORγt, and FOXP3, along with elevated levels of pro-inflammatory cytokines compared to the CS group (p<0.001).

resultThese results indicate that CD74 is more prominently expressed in PBMC from the CS group, whereas CXCR7 is more expressed in PBMC from RA patients.

conclusionWe also noted an increased secretion of Th17 profile cytokines in RA, potentially influenced by the activation of FOXP3 via CD74 and RORγt through CXCR7 using the endocytic pathway.

Indexed as

Arthritis, RheumatoidCell DifferentiationReceptors, ImmunologicT-Lymphocytes, Helper-InducerTranscription FactorsAdultAgedCell MembraneCells, CulturedFemaleHumansLeukocytes, MononuclearMaleMiddle AgedTh17 CellsTh1 Cellsmacrophage migration inhibitory factor receptorReceptors, ImmunologicTranscription FactorsCD44CD74CXCRcytokines.MIFRheumatoid arthritistranscription factor

Identifiers

PMID37807647
OpenAlexW4387440516

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Registered trials

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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.