# Rituximab in Connective Tissue Disease-Associated Interstitial Lung Disease: From Immunopathogenesis to Therapeutic Implications

## TL;DR

This review explores how B cells contribute to lung disease in connective tissue disorders and how the drug Rituximab may help by targeting these cells.

## Contribution

The paper provides a comprehensive overview of Rituximab's mechanisms and clinical potential in treating CTD-ILD.

## Key findings

- B cells contribute to CTD-ILD through autoimmunity, inflammation, and fibrosis.
- Rituximab depletes B cells and shows promise as a treatment for CTD-ILD.
- The drug's therapeutic effects are linked to its multifaceted mode of action on B cells.

## Abstract

Connective tissue disease-associated interstitial lung disease (CTD-ILD) comprises a heterogeneous group of immune-mediated pulmonary disorders with significant morbidity and mortality. The pathogenesis involves complex interactions of autoimmunity, chronic inflammation, and fibrosis. B cells play a central role in these processes through antigen presentation, autoantibody production, cytokine secretion, and the formation of ectopic lymphoid tissue within the lung parenchyma. Rituximab (RTX)—a chimeric anti-CD20 monoclonal antibody—depletes B cells and has emerged as a promising therapeutic agent for CTD-ILD. This review comprehensively presents the immunopathogenic mechanisms underlying CTD-ILD, elaborating on the multifaceted mode of action of RTX and summarizing the evolving clinical evidence.