Single-cell eQTL Mendelian randomization reveals the monocyte-associated PRKCB–CTSL axis as a candidate regulatory pathway and potential therapeutic target in rheumatoid arthritis - Scorecard - MDSpire
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Single-cell eQTL Mendelian randomization identifies a monocyte-linked PRKCB–CTSL pathway as a potential regulatory mechanism and therapeutic target in rheumatoid arthritis

  • By

  • Pengli Wang

  • Guohang Shen

  • Wenhua Liao

  • Ruoyan Wang

  • Li Zhang

  • Mingjia Zhao

  • Dong Zhang

  • Nanxiang Huang

  • Yupei Dai

  • October 19, 2026

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Clinical Scorecard: Single-cell eQTL Mendelian randomization identifies a monocyte-linked PRKCB–CTSL pathway as a potential regulatory mechanism and therapeutic target in rheumatoid arthritis

At a Glance

CategoryDetail
ConditionRheumatoid arthritis (RA), a chronic autoimmune disorder marked by sustained synovial inflammation and progressive destruction of cartilage and bone.
Key MechanismsThe study examines cell-type-specific genetic regulation of gene expression and its association with RA susceptibility, focusing on a monocyte-linked PRKCB–CTSL pathway identified in the title as a potential regulatory mechanism and therapeutic target.
Target PopulationThe analyses use RA GWAS summary statistics and cis-eQTL data from 17 immune-cell populations; no clinical patient cohort is described in the supplied excerpt.
Care SettingResearch context: integrated genetic, transcriptomic, computational, and in vitro analyses; the supplied excerpt does not describe a clinical care setting.

Key Highlights

  • The study integrated cell-type-specific cis-eQTL data from 17 immune-cell populations with RA GWAS summary statistics.
  • Mendelian randomization estimates assessed associations between genetically predicted expression of individual eGenes in defined immune-cell populations and RA susceptibility.
  • The broader analysis combined transcriptomic, WGCNA, machine-learning, single-cell, virtual perturbation, drug-screening, and in vitro approaches.
  • The article title identifies a monocyte-linked PRKCB–CTSL pathway as a potential regulatory mechanism and therapeutic target; the supplied excerpt does not provide detailed validation results.

Guideline-Based Recommendations

Diagnosis

    Management

      Monitoring & Follow-up

        Risks

          Patient & Prescribing Data

          No patient-level prescribing or treatment cohort details are provided in the supplied excerpt.

          The study examines candidate therapeutic targets and drug-screening analyses, but the supplied excerpt does not report a specific drug, dose, or prescribing recommendation.

          Clinical Best Practices

          • Interpret the reported work as a research analysis of genetically prioritized RA-associated expression traits, not as a clinical diagnostic or treatment guideline.
          • The methods specify genome-wide significant cis-eQTL instruments (P < 5 × 10⁻⁸) and linkage-disequilibrium clumping (r² < 0.001; window > 1,000 kb).
          • For exposures with one qualifying instrument, the study used the Wald ratio; for exposures with multiple independent instruments, it used inverse-variance weighting and, when instrument counts allowed, MR-Egger and weighted-median analyses.

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