Skip NavigationSkip to Content
Return Return to Search Results

A novel role for IL-22R1 as a driver of inflammation

  1. Author:
    Savan, R.
    McFarl, A. P.
    Reynolds, D. A.
    Feigenbaum, L.
    Ramakrishnan, K.
    Karwan, M.
    Shirota, H.
    Klinman, D. M.
    Dunleavy, K.
    Pittaluga, S.
    Anderson, S. K.
    Donnelly, R. P.
    Wilson, W. H.
    Young, H. A.

  2. Author Address

    [Savan, Ram; McFarland, Adelle P.; Reynolds, Della A.; Ramakrishnan, Karthika; Shirota, Hidekazu; Klinman, Dennis M.; Anderson, Stephen K.; Young, Howard A.] Ctr Canc Res, Canc & Inflammat Program, Frederick, MD 21702 USA. [Feigenbaum, Lionel; Karwan, Megan] NCI, Lab Anim Sci Program, SAIC Frederick Inc, Frederick, MD 21701 USA. [Dunleavy, Kieron; Wilson, Wyndham H.] NCI, Metab Branch, Lymphoma Therapeut Sect, Ctr Canc Res, Bethesda, MD 20892 USA. [Pittaluga, Stefania] NCI, Pathol Lab, Hematopathol Sect, Ctr Canc Res, Bethesda, MD 20892 USA. [Donnelly, Raymond P.] US FDA, Div Therapeut Prot, Ctr Drug Evaluat & Res, Bethesda, MD 20014 USA.;Young, HA, Ctr Canc Res, Canc & Inflammat Program, POB B,Bldg 560, Frederick, MD 21702 USA.;savanr@mail.nih.gov YoungHow@mail.nih.gov
    1. Year: 2011
    2. Date: Jan
  2. Journal: Blood
    1. 117
    2. 2
    3. Pages: 575-584
  4. Type of Article: Article
  5. ISSN: 0006-4971
  1. Abstract:

    The interleukin (IL)-22R1 chain of the heterodimeric IL-22 receptor is not expressed on normal leukocytes, but this receptor is expressed on T cells from anaplastic lymphoma kinase-positive (ALK(+)) anaplastic large cell lymphoma (ALCL) patients. To investigate the consequences of aberrant expression of this receptor on lymphocytes, we generated transgenic mice that express IL-22R1 on lymphocytes. The health of these animals progressively deteriorated at 8 to 12 weeks of age, as they displayed respiratory distress, rough coat and sluggish movement, and subsequent lethality due to multiorgan inflammation. The IL-22R1 transgenic animals developed neutrophilia that correlated with increased levels of circulating IL-17 and granulocyte colony-stimulating factor. In addition, these mice had increased serum IL-22 levels, suggesting that T cells expressing IL-22R1 generate IL-22 in a positive autoregulatory loop. As a result of the mouse model findings, we analyzed circulating cytokine levels in ALK(+)ALCL patients and detected elevated levels of IL-22, IL-17, and IL-8 in untreated patient samples. Importantly, IL-22 and IL-17 were undetectable in all patients who were in complete remission after chemotherapy. This study documents a previously unknown role of IL-22R1 in inflammation and identifies the involvement of IL-22R1/IL-22 in ALK(+)ALCL. (Blood. 2011;117(2):575-584)

    See More

  1. Keywords:

External Sources

  1. View Full Text
  2. DOI: 10.1182/blood-2010-05-285908
  3. View record in Web of Science®
  4. WOS: 000286178700027

Library Notes

  1. Fiscal Year: FY2010-2011
NCI at Frederick

You are leaving a government website.

This external link provides additional information that is consistent with the intended purpose of this site. The government cannot attest to the accuracy of a non-federal site.

Linking to a non-federal site does not constitute an endorsement by this institution or any of its employees of the sponsors or the information and products presented on the site. You will be subject to the destination site's privacy policy when you follow the link.

ContinueCancel