# Peste des petits ruminants virus (PPRV) modulates caprine dendritic cell function and induces immunosuppression through IL-10 upregulation

## TL;DR

This study shows how Peste des petits ruminants virus affects goat immune cells, leading to weakened immune responses and increased susceptibility to infections.

## Contribution

The study reveals how PPRV alters dendritic cell function in goats through IL-10 upregulation, contributing to immunosuppression.

## Key findings

- PPRV infects goat monocytes but does not block their differentiation into dendritic cells.
- PPRV-infected dendritic cells show increased maturation markers and reduced phagocytic activity.
- PPRV infection impairs T cell proliferation by increasing IL-10 production and reducing DC-T cell conjugation.

## Abstract

Peste des petits ruminants (PPR) is a WOAH notifiable disease affecting sheep and goats, caused by Peste des petits ruminants virus (PPRV), a morbillivirus of the Paramyxoviridae family. Infection with PPRV leads to immunosuppression, creating conditions for opportunistic infections that can result in animal mortality. Although goats generally exhibit more severe clinical signs than sheep, the underlying mechanisms driving this species-specific difference remain poorly understood. Dendritic cells (DC), which play a pivotal role in initiating immune responses, are among the immune targets of PPRV in small ruminants. In this study, we examined the impact of PPRV on caprine immune cells, focusing on CD14+ monocytes and monocyte-derived dendritic cells (MoDC). Our findings indicate that PPRV infects goat monocytes without preventing their differentiation into DC. Infected MoDC displayed increased expression of maturation markers and reduced phagocytic activity, suggesting a transition toward an activated phenotype. However, mixed lymphocyte reaction assays revealed that PPRV-infected MoDCs have a diminished capacity to promote T cell proliferation. This impaired function was associated with elevated IL-10 production and reduced conjugation between DCs and T cells. Overall, PPRV infection induces an atypical maturation stage in goat MoDCs, characterized by partial activation but impaired antigen presentation. These findings demonstrate that PPRV-driven modulation of DC function contributes to the immunosuppression observed during PPRV infection in goats.