# Intact lymph node homing and CD8+ T-cell priming abilities of Sprouty2-deficient dendritic cells

## TL;DR

This study shows that dendritic cells lacking Sprouty2 still function normally in immune responses, including migration and activating T-cells.

## Contribution

The study reveals that Sprouty2 is not essential for dendritic cell immune functions, despite its role in other cell types.

## Key findings

- Sprouty2-deficient dendritic cells show normal differentiation and migration abilities.
- These cells maintain effective lymph node homing and CD8+ T-cell activation during viral infection.
- Sprouty2 absence does not impair dendritic cell-mediated immune responses.

## Abstract

Sprouty2 (Spry2) acts as a modulator of the MAPK-ERK signaling pathway by exerting both positive and negative regulation in a highly context- and cell type-specific manner. While its role in controlling the migration of non-immune cells in growth factor-dependent contexts is well established and continuously expanding, its function as a modulator of immune cell responses has only recently begun to emerge. Spry2 appears to critically and differentially influence B- and T-cell responses, consistent with its cell type-specific nature. However, its role in dendritic cells (DCs) remains unexplored. DCs serve as the cellular link between innate and adaptive immunity, and hence, DCs rely on their ability to navigate through different tissues and migrate to distinct target locations to initiate and coordinate effective immune responses. In the present study, we show that Spry2 expression is regulated during bone marrow-derived (BM)DC maturation and established a CD11c-specific Spry2 knockout mouse model to analyze the in vitro and in vivo immune functions of Spry2-deficient DCs. Unexpectedly, we found that its complete absence does not alter essential DC immune functions. Spry2-deficient DCs display intact DC differentiation in vitro and in vivo, efficient CCR7-driven migration and effective lymph node homing in vivo. Furthermore, we demonstrate that Spry2-deficient DCs retain an unaltered ability to stimulate CD8+ T-cell activation and proliferation, ultimately resulting in normal CD8+ T-cell effector differentiation during acute viral infection. Collectively, our findings shed light on the function of Spry2 in DCs, thereby extending and reinforcing current knowledge of its diverse immunomodulatory functions.