Development of Th1-type immune responses requires the type I cytokine receptor TCCR

Qi Chen, Nico Ghilardi, Hua Wang, Thad Baker, Ming-Hong Xie, Austin Gurney, Iqbal S. Grewal and Frederic J. de Sauvage ()
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Qi Chen: Departments of Molecular Oncology
Nico Ghilardi: Departments of Molecular Oncology
Hua Wang: Departments of Molecular Oncology
Thad Baker: Departments of Molecular Oncology
Ming-Hong Xie: Genentech, Inc.
Austin Gurney: Genentech, Inc.
Iqbal S. Grewal: Departments of Molecular Oncology
Frederic J. de Sauvage: Departments of Molecular Oncology

Nature, 2000, vol. 407, issue 6806, 916-920

Abstract: Abstract On antigen challenge, T-helper cells differentiate into two functionally distinct subsets, Th1 and Th2, characterized by the different effector cytokines that they secrete1. Th1 cells produce interleukin (IL)-2, interferon-γ (IFN-γ) and lymphotoxin-β, which mediate pro-inflammatory functions critical for the development of cell-mediated immune responses, whereas Th2 cells secrete cytokines such as IL-4, IL-5 and IL-10 that enhance humoral immunity1,2. This process of T-helper cell differentiation is tightly regulated by cytokines. Here we report a new member of the type I cytokine receptor family, designated T-cell cytokine receptor (TCCR). When challenged in vivo with protein antigen, TCCR-deficient mice had impaired Th1 response as measured by IFN-γ production. TCCR-deficient mice also had increased susceptibility to infection with an intracellular pathogen, Listeria monocytogenes. In addition, levels of antigen-specific immunoglobulin-γ2a, which are dependent on Th1 cells, were markedly reduced in these mice. Our results demonstrate the existence of a new cytokine receptor involved in regulating the adaptive immune response and critical to the generation of a Th1 response.

Date: 2000
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DOI: 10.1038/35038103

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