Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2024 Jun 25;13(2):89985. doi: 10.5501/wjv.v13.i2.89985

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

©The Author(s) 2024. Published by Baishideng Publishing Group Inc. All rights reserved.

This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial.

PMC Copyright notice

Supposed mechanisms involved in the pathogenesis of arthritis caused by Chikungunya virus. The elevation in levels of pro-inflammatory chemokines induces T helper type 17 response polarization, leading to interleukin-17 expression and subsequent increase in receptor activator of nuclear factor kappa-Β ligand. Granzyme A released by natural killer cells and CD8+ T cells targets type IV collagen, contributing to progressive joint damage. Th17: T helper type 17; CCL4: C-C motif ligand 4; NK: Natural killer; LTCD8: CD8 T lymphocytes; LTCD4: CD4 T lymphocytes; RANKL: Receptor activator of nuclear factor kappa-Β ligand; MMP: Matrix metalloproteinases; IL: Interleukin; TNF: Tumor necrosis factor.