ArticleJournal of clinical laboratory analysis2025
Exploring the Causal Relationship Between Immune Cells and Idiopathic Pulmonary Fibrosis: A Mendelian Randomization Analysis.
Article in Journal of clinical laboratory analysis, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 2 of them syntheses that pooled 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.
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.
Who cites it
2 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Risk factors for pulmonary complications in systemic lupus erythematosus: a meta-analysis of infectious pneumonia and interstitial lung disease.Frontiers in immunology · 2026Pooled it
- Correlation does not equal causation: the imperative of causal inference in machine learning models for immunotherapy.Frontiers in immunology · 2025Pooled it
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
backgroundIdiopathic pulmonary fibrosis (IPF) is a progressive and irreversible interstitial lung disease with a complex pathogenesis involving multiple immune cells. This study investigates the relationship between immune cells and IPF using Mendelian randomization (MR) analysis.
methodsA two-sample MR analysis was performed using genome-wide association studies (GWAS) and immune cell databases by R software. We analyzed data from 1028 European individuals with IPF, focusing on 731 immune traits. The primary method of analysis was inverse variance weighting (IVW), supplemented with sensitivity analyses, including MR-Egger regression and MR-PRESSO, to detect and correct for pleiotropy.
resultsThe MR analysis identified six immune panels and 23 immune traits significantly associated with IPF, including five traits that increase and 18 traits that decrease IPF risk. Notable traits increasing IPF risk included switched memory B-cells (OR = 1.27, p = 0.0029) and IgD- CD38dim B-cells (OR = 1.08, p = 0.0449). Traits associated with a reduced IPF risk included central memory CD4+ T-cells (%CD4+, OR = 0.96, p = 0.0489), CD20 on naive-mature B-cells (OR = 0.94, p = 0.0499), and CD33br HLA-DR+ absolute count (AC) (OR = 0.93, p = 0.0489). There was no significant causal relationship between IPF disease and some immune traits (p > 0.05).
conclusionThis study suggests a potential causal link between specific immune cell traits and the development of IPF, providing new insights into the disease's immunological mechanisms. Future research should focus on validating these findings in larger, more diverse populations to inform drug development and therapeutic strategies.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.