# Gene and Protein Profiles of CHI3L1 and CHI3L2 in Patients with Rheumatoid Arthritis

## TL;DR

This study examines how the proteins CHI3L1 and CHI3L2 change in rheumatoid arthritis patients before and after treatment, and how they relate to disease markers.

## Contribution

The study reveals distinct behaviors of CHI3L1 and CHI3L2 in response to different RA treatments and their correlations with disease activity.

## Key findings

- CHI3L1 and CHI3L2 plasma levels decreased after tofacitinib treatment but not after methotrexate.
- Strong correlations were found between CLPs and CRP and GUS7 markers.
- Gene expression of CLPs did not change significantly after either treatment.

## Abstract

Background/Objectives: Rheumatoid arthritis is an autoimmune disease that induces joint deformity and disability. There are great expectations for biomarkers that would predict the response to treatment. CHI3L1 and CHI3L2 are chitinase-like proteins (CLPs) which lack enzymatic activity. CHI3L1 is expressed by a variety of cells, while reports on CHI3L2 are limited. The aim of the current study is to evaluate gene and protein CHI3L1 and CHI3L2 expressions before and after treatment of patients with RA and to search for correlations with ultrasonography and conventional laboratory parameters. Methods: Twenty-four newly diagnosed RA patients (19 females and five males) were enrolled in the study. Fourteen patients were treated with tofacitinib (TOFA) and 10 patients with methotrexate (MTX) for twenty-four weeks. Conventional biochemical and immunological markers were examined at the start of the treatment and after the follow-up period. The activity of RA was assessed via the Disease Activity Score 28 (DAS28). Gene expression and protein analysis were performed. Results: Ultrasonographic and clinical laboratory parameters showed improvement after therapy in both groups. A decrease in plasma levels of CHI3L1 (p = 0.04 *) and CHI3L2 (p = 0.03 *) were found after treatment with TOFA. No changes in either protein level were detected after MTX therapy, nor were any differences discovered in the gene expression of CLPs after treatment with both therapeutics. Strong correlations between CRP, GUS7 and CLPs were also established. Conclusions: The similar dynamics of CLPs expression in naïve RA patients and their distinct interplay with disease-related parameters after therapy suggest that both proteins may display different functions in RA pathophysiology.