Loss of PKC lambda/iota impairs Th2 establishment and allergic airway inflammation in vivo. Academic Article uri icon

Overview

abstract

  • The differentiation of T cells along different lineages is central to the control of immunity. Here we have used a conditional gene knockout system to delete PKC lambda/iota selectively in activated T cells. With this system we have demonstrated that PKC lambda/iota is necessary for T-helper cell (Th2) cytokine production and optimal T-cell proliferation and allergic airway inflammation in vivo. Our data demonstrate that the activation of the transcription factors nuclear factor of activated T cells and NF-kappaB is impaired in PKC lambda/iota-deficient activated T cells. In addition, we present genetic knockout evidence in ex vivo experiments with primary T cells that PKC lambda/iota is critical for the control of cell polarity during T-cell activation. Therefore PKC lambda/iota emerges as a critical regulator of Th 2 activation.

publication date

  • January 14, 2009

Research

keywords

  • Hypersensitivity
  • Inflammation
  • Isoenzymes
  • Protein Kinase C
  • Respiratory System
  • Th2 Cells

Identity

PubMed Central ID

  • PMC2633554

Scopus Document Identifier

  • 59049090061

Digital Object Identifier (DOI)

  • 10.1073/pnas.0805907106

PubMed ID

  • 19144923

Additional Document Info

volume

  • 106

issue

  • 4