Primate Monocytes - CD14, CD16 - Ziegler-Heitbrock

The imbalance of circulating PD-L1-expressing non-classical/ classical monocytes is involved in immunocompromised host related pulmonary opportunistic infection.

Abstract

The application of biological therapy and glucocorticoids in Auto-immune diseases (AID) patients will cause immunocompromised host (ICH) prone to infection. And monocytes play a key role in both innate and adaptive immune responses. We aimed to investigate the changes of circulating monocyte subsets in AID or AID-ICH patients with pulmonary infection. The subgroups and PD-L1 expression of monocytes were measured by flow cytometry in healthy individuals (HC), new-onset AID patients (AID cohort) and AID-ICH patients with pulmonary opportunistic infection (AID-ICH cohort). Flow cytometry analysis was used to determine the distribution of monocyte subsets, including classical monocytes (CL, CD14++CD16-), intermediate monocytes (ITM, CD14++CD16+) and non-classical monocytes (NC, CD14+/-CD16++), as well as the dynamic change of PD-L1 + cluster among monocyte subsets. Among total monocyte, AID-ICH displayed decreased CL subset along with increased NC subset compared to HCs and AID. Regarding PD-L1 + monocytes, although CL subset constituted the majority of that in HCs, AIDs and AID-ICHs, imbalance of NC/CL within PD-L1 + monocytes was only noticed in AID-ICHs (P < 0.05). Furthermore, when AID subjects were developed into immunocompromised status (ICH), PD-L1 + cluster in CL was minorly decreased (P > 0.05). Clinically, the lower ratio of PD-L1 + cluster among CL subset (P < 0.05) and the less differentiated CL in PD-L1 + monocytes (P < 0.05) was more likely to leaded to disease progression. The imbalance of circulating NC/CL subset was remarkable in immunocompromised host with pulmonary opportunistic infection, especially involvement of PD-L1+ cluster, which served as a potential biomarker in clinical practice.