Research ArticleFibrosis

PD-1 up-regulation on CD4+ T cells promotes pulmonary fibrosis through STAT3-mediated IL-17A and TGF-β1 production

See allHide authors and affiliations

Science Translational Medicine  26 Sep 2018:
Vol. 10, Issue 460, eaar8356
DOI: 10.1126/scitranslmed.aar8356

eLetters is an online forum for ongoing peer review. Submission of eLetters are open to all. Please read our Terms of Service before submitting your own eLetter.

Compose eLetter

Plain text

  • Plain text
    No HTML tags allowed.
  • Web page addresses and e-mail addresses turn into links automatically.
  • Lines and paragraphs break automatically.
Author Information
First or given name, e.g. 'Peter'.
Your last, or family, name, e.g. 'MacMoody'.
Your email address, e.g. higgs-boson@gmail.com
Your role and/or occupation, e.g. 'Orthopedic Surgeon'.
Your organization or institution (if applicable), e.g. 'Royal Free Hospital'.
Statement of Competing Interests
CAPTCHA

This question is for testing whether or not you are a human visitor and to prevent automated spam submissions.

Image CAPTCHA
Enter the characters shown in the image.

Vertical Tabs

  • RE: PD-1 up-regulation on CD4+ T cells promotes pulmonary fibrosis through STAT3-mediated IL-17A and TGF-β1 production
    • Dr Dianne Sika-Paotonu, Associate Dean (Pacific)/Senior Lecturer Pathology & Molecular Medicine, Wellington School of Medicine & Health Sciences, University of Otago, New Zealand

    To the Editor,

    I read with interest the article authored by Celada L.J. et al (1) and entitled: “PD-1 upregulation on CD4+ T cells promotes pulmonary fibrosis through STAT3-mediated IL-17A and TGF-β1 production.”

    This series of experiments sought to obtain improved understanding of the preceding immune responses, and related interactions associated with collagen deposition in pulmonary fibrosis.

    The authors showed that PD-1 expressing CD4+T cells were producers of both IL-17A and TGF-β1 via increased STAT3 transcription-an essential transcription factor for Th17 cell development.

    Links were established using two disease model systems (1) Idiopathic Pulmonary Fibrosis (IPF) and (2) Sarcoidosis which connected the PD-1 expressing T cells, STAT3, IL-17A and the profibrotic component of pulmonary fibrosis.

    PD-1 and IL17A interactions had not been previously identified in the context of pulmonary fibrosis before with this work clearly highlighting the profibrotic role of PD-1 up-regulation, via increased STAT3 expression and subsequent production of TGF-β1 and IL-17A cytokines.

    As acknowledged by the authors, the impact of PD-1 on IL-10 induced inhibition of IL-17A production by CD4+ T cells is of significant interest and deserves further exploration.

    Distinctions in gene expression patterns observed within this study indicate that further validation using extra participant cohorts, and utilizing standardized gene expression...

    Show More
    Competing Interests: None declared.

Navigate This Article