Responses

Download PDFPDF
Extended report
Prostaglandin I2 analogues enhance already exuberant Th17 cell responses in systemic sclerosis
Compose Response

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

PLEASE NOTE:

  • Responses are moderated before posting and publication is at the absolute discretion of BMJ, however they are not peer-reviewed
  • Once published, you will not have the right to remove or edit your response. Removal or editing of responses is at BMJ's absolute discretion
  • If patients could recognise themselves, or anyone else could recognise a patient from your description, please obtain the patient's written consent to publication and send them to the editorial office before submitting your response [Patient consent forms]
  • By submitting this response you are agreeing to our full [Response terms and requirements]

Vertical Tabs

Other responses

Jump to comment:

  • Published on:
    PGI2-induced Th17 cells differentiation in connective tissue disease: a comment
    • He Jianguo, MD
    • Other Contributors:
      • Zheng Yaguo, Xiong Changming

    Dear Editor

    We read with interest the study conducted by Truchetet and colleagues on the regulation of PGI2 in Th17 cells differentiation in systemic sclerosis (SSc). Actually, previous in vitro studies have found that synthetic PGI2 enhanced Th17 cells differentiation1. Zhou et al2 has also demonstrated that PGI2 induced Th17 cells differentiation through modulating the ratio of IL-23/IL-12 in a mouse model of experim...

    Show More
    Conflict of Interest:
    None declared.