17. Interleukin 10

  1. Kenji Izuhara MD, PhD2,
  2. Stephen T. Holgate MD, DSc, FMedSci3 and
  3. Marsha Wills-Karp PhD4
  1. Whitney W. Stevens PhD,
  2. Larry Borish MD and
  3. John W. Steinke PhD

Published Online: 27 JUL 2011

DOI: 10.1002/9781444346688.ch17

Inflammation and Allergy Drug Design

Inflammation and Allergy Drug Design

How to Cite

Stevens, W. W., Borish, L. and Steinke, J. W. (2011) Interleukin 10, in Inflammation and Allergy Drug Design (eds K. Izuhara, S. T. Holgate and M. Wills-Karp), Wiley-Blackwell, Oxford, UK. doi: 10.1002/9781444346688.ch17

Editor Information

  1. 2

    Department of Biomolecular Sciences, Division of Medical Biochemistry, Saga Medical School, Nabeshima, Saga, Japan

  2. 3

    School of Medicine, Allergy and Inflammation Research, Southampton General Hospital, University Medicine, Southampton, UK

  3. 4

    Division of Immunology, Cincinnati Children's Medical Center, Cincinnati, OH, USA

Author Information

  1. Asthma and Allergic Disease Center, Carter Immunology Center, University of Virginia Health Systems, Charlottesville, VA, USA

Publication History

  1. Published Online: 27 JUL 2011
  2. Published Print: 13 AUG 2011

ISBN Information

Print ISBN: 9781444330144

Online ISBN: 9781444346688



  • interleukin 10 (IL-10), immunoregulatory cytokine - with multiple biologic effects on cell types;
  • IL-10, inhibiting major histocompatibility complex (MHC) class II expression - on APCs and dendritic cells (DCs);
  • interleukin 10 signaling - binding to heterodimer receptor complex, IL-10 receptor 1 and IL-10R2 chains;
  • sources of interleukin 10 - immature DCs and B cells, major sources of IL-10 in humans;
  • dendritic cells/M2 macrophages - IL-10, by innate immune cells, as macrophage;
  • interleukin 10, and CD4+ lymphocytes - regulatory T lymphocyte families, nTreg , iTreg and Th3 cells;
  • IL-10, identified - as a Th2 lymphocyte product;
  • immunotherapy mechanisms, and interleukin 10 - immune deviation from Th2, toward a Th1-like response;
  • expression of IL-10, central to maintenance - of immune nonresponsiveness to allergens;
  • potential utility of direct IL-10 administration - as asthma therapeutic


Interleukin 10 (IL-10) is a potent cytokine synthesis inhibitor, that prevents the production of interferon γ by T helper 1 (Th1) lymphocytes, IL-4 and IL-5 by Th2 lymphocytes, and IL-1ß, IL-12, and tumor necrosis factor α (TNF-α) by mononuclear phagocytes. IL-10 inhibits the function of antigen-presenting cells and diminished IL-10 expression contributes to a milieu in which immune responses develop. IL-10 is primarily produced by immature dendritic cells, tolerance-inducing (M2) mononuclear phagocytes, and regulatory T cells. In allergy, IL-10 inhibits eosinophil survival, mast cell development, and, with uncommitted B cells, e transcript expression. IL-10 is central to the maintenance of the immune non-responsiveness to allergens observed in unaffected individuals and, similarly, induction of IL-10-producing lymphocytes is central to the restoration of the healthy state that occurs in association with immunotherapy. In theory, pharmacologic IL-10 could reproduce the “immune-ignorant” state of nonallergic individuals and would recapitulate one of the central mechanisms of immunotherapy.