# CD45 and CD148 Are Critically Involved in Neutrophil Recruitment and Function During Inflammatory Arthritis in Mice

## TL;DR

This study shows that CD45 and CD148 play important roles in how neutrophils behave during inflammatory arthritis in mice.

## Contribution

The study reveals distinct regulatory roles of CD45 and CD148 in neutrophil recruitment and function during arthritis.

## Key findings

- CD45 is essential for neutrophil infiltration, cytokine release, and ROS production.
- CD148 deficiency delays arthritis onset and reduces ROS production without affecting neutrophil infiltration.
- CD45 and CD148 differentially regulate Src family kinase activation in neutrophils.

## Abstract

Neutrophils play a key role in autoimmune diseases like rheumatoid arthritis, contributing to tissue damage through rapid recruitment and activation. In this study, we investigated the regulatory properties of two receptor-like tyrosine phosphatases (RPTPs), CD45 and CD148, in inflammatory arthritis. Using an in vivo mouse model of K/BxN serum transfer-induced arthritis, we found that CD45 and CD148 feature distinct regulatory properties during inflammatory arthritis. CD45 is required for neutrophil infiltration, cytokine release, and reactive oxygen species production, whereas CD148 deficiency leads to a delayed onset of arthritis but unaltered overall neutrophil infiltration and reduced ROS production. Furthermore, we could demonstrate that activation of Src family kinases in neutrophils is differentially regulated by CD45 and CD148 in a stimulus-dependent manner. Summarizing, our results suggest that CD45 is positively involved, while CD148 is positively and negatively involved in neutrophil recruitment and function during inflammatory arthritis.