UV inhibits allergic airways disease in mice by reducing effector CD4 T cells

Clin Exp Allergy. 2010 May;40(5):772-85. doi: 10.1111/j.1365-2222.2010.03469.x. Epub 2010 Mar 4.

Abstract

Background: In human asthma, and experimental allergic airways disease in mice, antigen-presenting cells and CD4(+) effector cells at the airway mucosa orchestrate, and CD4(+)CD25(+) regulatory T cells attenuate, allergen immunity. UV irradiation of skin before sensitization with ovalbumin (OVA) causes significantly reduced asthma-like responses in respiratory tissues.

Objective: To determine whether UV-induced changes in CD11c(+) cells, CD4(+)CD25(+) effector cells or CD4(+)CD25(+) regulatory cells in the trachea and airway draining lymph nodes (ADLNs) were responsible for reduced allergic airways disease.

Methods: The phenotype and function of CD11c(+) cells and CD4(+)CD25(+) cells in the trachea and ADLNs of UV- and non-irradiated, OVA-sensitized mice was examined 24 h after a single exposure to aerosolized OVA.

Results: No changes in the function of CD11c(+) cells from UV-irradiated mice were observed. CD4(+)CD25(+) cells from UV-irradiated, OVA-sensitized mice harvested 24 h after OVA aerosol proliferated less in response to OVA in vitro and were unable to suppress the proliferation of OVA-sensitized responder cells. This result suggested reduced activation of effector T cells in the airway mucosa of UV-irradiated, OVA-sensitized mice. To exclude regulatory cells of any type, there was similar proliferation in vivo to aerosolized OVA by CFSE-loaded, OVA-TCR-specific CD4(+) cells adoptively transferred into UV- and non-irradiated, OVA-sensitized mice. In addition, there was no difference in the expression of regulatory T cell markers (Foxp3, IL-10, TGF-beta mRNA). To examine effector T cells, ADLN cells from UV-irradiated, OVA-sensitized and -challenged mice were cultured with OVA. There was reduced expression of the early activation marker CD69 by CD4(+)CD25(+) cells, and reduced proliferation in the absence of the regulatory cytokine, IL-10.

Conclusion: Reduced allergic airways disease in UV-irradiated mice is due to fewer effector CD4(+)CD25(+) cells in the trachea and ADLNs, and not due to UV-induced regulatory cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Allergens / administration & dosage
  • Allergens / immunology
  • Animals
  • Antigens, CD / biosynthesis
  • Antigens, Differentiation, T-Lymphocyte / biosynthesis
  • Asthma / immunology*
  • CD11c Antigen / metabolism
  • Cell Proliferation
  • Cells, Cultured
  • Down-Regulation
  • Female
  • Interleukin-2 Receptor alpha Subunit / metabolism
  • Lectins, C-Type / biosynthesis
  • Lymph Nodes / radiation effects
  • Mice
  • Mice, Inbred BALB C
  • Mice, Transgenic
  • Ovalbumin / administration & dosage
  • Ovalbumin / immunology
  • Skin / immunology
  • Skin / radiation effects*
  • T-Lymphocytes, Regulatory / immunology
  • T-Lymphocytes, Regulatory / radiation effects*
  • Trachea / immunology
  • Trachea / radiation effects
  • Ultraviolet Rays*

Substances

  • Allergens
  • Antigens, CD
  • Antigens, Differentiation, T-Lymphocyte
  • CD11c Antigen
  • CD69 antigen
  • Il2ra protein, mouse
  • Interleukin-2 Receptor alpha Subunit
  • Lectins, C-Type
  • Ovalbumin