Causal relationship between immune cells and idiopathic pulmonary fibrosis based on Mendelian randomization analysis

Author:

Gong peng1,Lu yimin1,Li man1,Li xiaobo1,Carla Cristina Janjacomo2

Affiliation:

1. Shanxi University of Traditional Chinese Medicine

2. Faculdade EBRAMEC - Brazilian College of Chinese Medicine

Abstract

Abstract Context: Idiopathic pulmonary fibrosis (IPF) is a progressive and irreversible interstitial lung disease (ILD) characterized by respiratory disease with a pathogenesis closely linked to collagen fibrin deposition and autoimmunity, although the mechanism of action is unclear. The immune system is a diverse and complex system that employs its own defense functions to maintain homeostasis. The lungs are connected to the outside world, and immune cells play an important role. Therefore, the interaction between immune cells and the lungs is decisive for IPF disease progression and treatment. However, studies on immune cells have limitations, and there are no concrete conclusions at present, limiting to some extent the development of immunology in IPF. To identify immune cells associated with IPF, the relationship between immune cells and IPF was explored based on the Mendelian randomization (MR) method. Materials and Methods This study utilized two-sample Mendelian randomization analysis to confirm the causal relationship between immune cells and IPF. Based on the GWAS database and the immune cell database, MR analysis was performed using R software to explore the causal relationship between 731 immune cells and IPF, mainly through inverse variance weighting (IVW). Finally, the reliability of the results was analyzed, and scatterplots, forest plots and funnel plots were drawn using MR_heterogeneity, horizontal pleiotropy and leave-one-out analysis. Results The MR analysis identified 6 immune panels and 23 immune traits that were causally associated with IPF. including B-cell panel, myeloid cell panel, monocyte panel, maturation stages of T-cell panel, TBNK panel, and Treg panel. However, there was no significant causal relationship between IPF disease and immune traits, and the immune traits that increased IPF included the following (p < 0.05), (see Table 1). Conclusion: This study demonstrated a causal link between immune cells and IPF by genetic database and two-sample MR analysis, mainly by Sw mem% B cell, IgD- CD38dim% B cell, CD25 on CD4 Treg, CD45RA+ CD28- CD8br% T-cell and CD45RA+ CD28- CD8br AC modulation of immune expression occurs in idiopathic pulmonary fibrosis. This provides a theoretical.

Publisher

Research Square Platform LLC

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