Evidence map›Paper›PMID 42605454›Full record

ArticleIranian journal of pathology2026

The Integrin Signature of Ankylosing Spondylitis: Divergent Regulation of CD29 and CD49b in HLA-B27-Positive Cohorts in Iraqi Patients.

Ahmed Ali Alshammari, Muslim Idan Mohsin

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Article in Iranian journal of pathology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

2 authors.

Ahmed Ali AlshammariDepartment of Pathological Analyses, Faculty of Science, University of Kufa, Kufa, Najaf Governorate, Iraq.ORCID https://orcid.org/0000-0002-8276-0825
Muslim Idan MohsinDepartment of Pathological Analyses, Faculty of Science, University of Kufa, Kufa, Najaf Governorate, Iraq.ORCID https://orcid.org/0009-0003-3274-3669

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background & Objective: Ankylosing spondylitis (AS) is a systemic inflammatory disorder where the HLA-B27 allele significantly influences disease severity. This study evaluated the molecular profiles of integrins CD29 and CD49b in peripheral blood mononuclear cells (PBMCs) to identify potential biomarkers associated with HLA-B27 status. Methods: In this cross-sectional study of an Iraqi cohort, 130 participants were recruited: 50 HLA-B27-positive (HLA+) radiographic AS patients, 50 HLA-B27-negative (HLA-) radiographic AS patients, and 30 healthy controls. Transcriptomic and proteomic expressions of CD29 and CD49b were quantified using qPCR and flow cytometry (mean fluorescence intensity, MFI). Hematological and biochemical profiles were also assessed. Results: CD29 mRNA was significantly upregulated in both patient groups, with a more pronounced median elevation in the HLA+ group (11-fold; P < 0.0001) than in the HLA- group (3-fold; P < 0.001). Surface CD29 protein significantly increased only in the HLA+ cohort (mean MFI approximately 3000; P < 0.0001). Conversely, CD49b mRNA was substantially suppressed, particularly in the HLA+ group (P < 0.0001). Correspondingly, a marked reduction in CD49b surface protein occurred in the HLA+ cohort (mean MFI approximately 300; P < 0.0001), whereas the HLA- group remained statistically comparable to controls. Additionally, the HLA- phenotype was characterized by significant granulocytosis (85%-90%) and more pronounced elevations in urea and ALT levels. Conclusion: These findings suggest a divergent regulation of CD29 and CD49b integrins associated with HLA-B27 status in Iraqi AS patients. While these integrins may serve as molecular indicators for disease stratification, longitudinal validation is required to confirm their clinical utility as diagnostic or therapeutic targets.

Indexed as

Ankylosing spondylitisCD29CD49bHLA-B27integrinsPBMCs

Identifiers

PMID42605454
PMCPMC13477783

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