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Related Experiment Video

Updated: Jan 25, 2026

Imaging Features of Systemic Sclerosis-Associated Interstitial Lung Disease

Imaging Features of Systemic Sclerosis-Associated Interstitial Lung Disease

Published on: June 16, 2020

Interleukin-17 pathways in systemic sclerosis-associated fibrosis.

Sakir Ahmed¹, Durga Prasanna Misra², Vikas Agarwal³

¹Department of Clinical Immunology and Rheumatology, Kalinga Institute of Medical Sciences (KIMS), KIIT University, Bhubaneswar, 751024, India.

Rheumatology International

|May 11, 2019

Summary

Fibrosis, a key feature of systemic sclerosis (SSc), involves complex pathways. Understanding novel targets like Interleukin-17 (IL-17) and its related molecules is crucial for developing effective antifibrotic therapies.

Keywords:

Fibrosis Interleukin 17 STAT3 Systemic sclerosis T helper 17

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Area of Science:

Immunology
Pathology
Molecular Biology

Background:

Fibrosis, characterized by unregulated tissue repair, impairs organ function and is central to systemic sclerosis (SSc).
Previous therapeutic targets for SSc, including TGF-β and IL-6, have shown limited success.
Emerging evidence links Interleukin-17 (IL-17) and its downstream pathways to fibrosis across multiple organs.

Purpose of the Study:

To review the current understanding of fibrotic mechanisms in SSc.
To highlight the role of IL-17 and newly identified signaling molecules in fibrosis.
To emphasize the need for further research into these pathways for therapeutic development.

Main Methods:

Literature review of studies on fibrosis, SSc, and related molecular pathways.
Analysis of evidence linking IL-17, PD-1, SHP2, STAT3, Ras/Erk, mTOR, and complement components to fibrotic processes.
Synthesis of data from patient cohorts and animal models of SSc.

Main Results:

IL-17 and its downstream effectors are strongly implicated in the initiation and progression of fibrosis in SSc.
Novel molecules such as Programmed Death-protein1 (PD-1) and SHP2, alongside STAT3, Ras/Erk, mTOR, and complement, are involved in fibrotic pathogenesis.
These pathways exhibit complex interactions, redundancies, and potential for off-target effects.

Conclusions:

IL-17 and associated molecular pathways represent promising targets for antifibrotic therapies in SSc.
A comprehensive understanding of the interplay between these newly identified molecules and IL-17 is essential.
Further elucidation of these complex biological networks is required to optimize therapeutic strategies for modulating fibrosis.