Photo Credit: Nemes Laszlo

The following is a summary of “Expansion of distinct peripheral blood myeloid cell subpopulations in patients with rheumatoid arthritis-associated interstitial lung disease,” published in the January 2024 issue of Allergy and Immunology by Poole et al.

The study aimed to discern distinct inflammatory and myeloid-derived suppressor cell (MDSC) subpopulations in rheumatoid arthritis-associated interstitial lung disease (RA-ILD), comparing them with rheumatoid arthritis (RA), idiopathic pulmonary fibrosis (IPF) without autoimmunity, and controls. Peripheral blood samples from 60 individuals (15/cohort) were examined using flow cytometry to identify myeloid cell subsets based on CD45, CD3, CD19, CD56, CD11b, HLA-DR, CD14, CD16, CD15, CD125, and CD33 markers. Subsets’ functionality was determined by assessing intracellular arginase-1 (Arg-1) and inducible nitric oxide synthase (iNOS) expression. 

Results revealed increased intermediate and nonclassical monocytes and decreased classical monocytes in RA, RA-ILD, and IPF versus controls. RA-ILD showed higher intermediate and lower classical monocytes compared to RA, distinct from IPF. Monocytic MDSCs were elevated in RA-ILD versus control and RA but not IPF. Conversely, granulocytic MDSCs showed no significant differences. Neutrophil increase and Arg-1 expression were common in IPF and RA-ILD patients. Eosinophils were uniquely expanded in RA-ILD. Across cohorts, iNOS was reduced in intermediate/nonclassical monocytes but increased in mMDSCs versus classical monocytes. In RA-ILD, iNOS+ mMDSCs were higher than in classic monocytes. 

The findings indicate significant modulation of myeloid cell subsets in RA-ILD, marked by the expansion of CD16+ monocytes, mMDSCs, and neutrophils, resembling IPF more than other RA patients. Notably, RA-ILD exhibited unique eosinophil expansion, potentially influencing disease pathogenesis and serving as a promising therapeutic target.

Source: sciencedirect.com/science/article/abs/pii/S1567576923016570