Lack of IL-4 receptor expression on T helper cells reduces T helper 2 cell polyfunctionality and confers resistance in allergic bronchopulmonary mycosis

Mucosal Immunol. 2012 May;5(3):299-310. doi: 10.1038/mi.2012.9. Epub 2012 Feb 15.

Abstract

T helper (Th)1 and Th2 cells play decisive roles in the regulation of resistance vs. susceptibility to pulmonary cryptococcosis. To study the function of interleukin (IL)-4 receptor (IL-4R) on Th cells in pulmonary cryptococcosis, we infected mice specifically lacking IL-4Rα on CD4(+) T cells (Lck(Cre)IL-4Rα(-/lox) mice) and IL-4Rα(-/lox) controls. Lck(Cre)IL-4Rα(-/lox) mice developed enhanced resistance accompanied by reduced pulmonary allergic inflammation and diminished production of the Th2 cytokines IL-4, IL-5, and IL-13 as compared with IL-4Rα(-/lox) mice. Polyfunctional antigen-specific Th2 cells producing simultaneously two or three Th2 cytokines were reduced in infected Lck(Cre)IL-4Rα(-/lox) mice, pointing to a critical role of polyfunctional Th2 cells for disease progression. Reduced Th2 polyfunctionality was associated with fewer pulmonary alternatively activated macrophages. This work is the first direct evidence for a critical contribution of the IL-4R on Th cells to Th2-dependent susceptibility during allergic bronchopulmonary mycosis. Moreover, the data demonstrate that the quality of the Th2 response has an impact on type 2 inflammation. The analysis of polyfunctional Th2 cells may be useful for monitoring the course of the disease.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cryptococcosis / complications
  • Cryptococcosis / immunology*
  • Cryptococcus neoformans / immunology*
  • Cryptococcus neoformans / pathogenicity
  • Cytokines / metabolism
  • Disease Susceptibility
  • Humans
  • Invasive Pulmonary Aspergillosis / etiology
  • Invasive Pulmonary Aspergillosis / immunology*
  • Lung / immunology
  • Lung / metabolism*
  • Lung / pathology
  • Macrophage Activation / genetics
  • Macrophages / immunology*
  • Mice
  • Mice, Inbred BALB C
  • Mice, Knockout
  • Mice, Transgenic
  • Receptors, Interleukin-4 / genetics
  • Receptors, Interleukin-4 / immunology
  • Receptors, Interleukin-4 / metabolism*
  • Th1 Cells / immunology
  • Th2 Cells / immunology*
  • Virulence

Substances

  • Cytokines
  • Receptors, Interleukin-4