# Circulating CD16-Positive Monocyte-like Myeloid-Derived Suppressor Cells and Intermediate Monocytes Associated with Clinical and Immunological Complications in Pars Planitis Patients

## TL;DR

This study finds that certain immune cells, like CD16+ myeloid cells, are increased in patients with a specific eye condition called pars planitis, linking them to disease severity.

## Contribution

The first study to evaluate circulating myeloid cell subpopulations in pars planitis patients, revealing their association with clinical and immunological severity.

## Key findings

- PP patients with cystoid macular edema have higher CD16+ IDO-expressing MDSCs and intermediate monocytes compared to healthy controls.
- Increased CD16+ myeloid cells correlate with upregulated Th1/Th17 and downregulated Treg in PP patients.
- IDO expression is dysregulated in MDSCs, particularly in CD16− subsets, in cystoid macular edema patients.

## Abstract

Recently, we observed that pars planitis (PP) patients present alterations in peripheral blood (PB) Th17/Treg associated with dysregulation in the Th1 response. Yet, little is known about the systemic distribution of myeloid cells, which drive the recruitment and differentiation of the adaptive effectors toward pathogenic inflammatory Th1 and Th17 as well as regulatory lymphocytes in PP. Although myeloid populations in patients with uveitis have previously been addressed, the data did not provide an exact description of PP patients. Using flow cytometry, we evaluated monocyte and IDO-expressing monocyte-like myeloid-derived suppressor cell (MDSC) subpopulations in PB samples from 15 patients with different courses of PP (cystoid macular edema and non-macular edema subgroups; CME and nCME, respectively) and 17 healthy controls (HCs) in relation to the Th1, Th17, and immunoregulatory subsets. We observed that only PP patients from the CME subgroup presented a significantly higher fraction of CD16+ IDO-expressing MDSCs and intermediate CD14highCD16+ monocytes compared to the HCs; this corresponded with relative up-regulation of Th1 and Th17, and down-regulation of Treg. In addition, alongside the increased percentage of IDO-expressing CD16+ MDSCs, the MDSC compartment displayed an inappropriate level of IDO (more pronounced in the CD16− subset) only in CME patients. At the same time, the fraction of CD16− myeloid cells did not differ significantly among the patient cohorts and healthy participants. Our study is the first to evaluate subpopulations of circulating myeloid cells in PP patients and indicates that an increased fraction of CD16+ myeloid cells might reflect the immunological and clinical severity of PP.