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Venkataraman, C. et al.

Venkataraman, Justen, Zhao, Galbreath, Na,

Death receptor-6 regulates the development of pulmonary eosinophilia and airway inflammation in a mouse model of asthma.

Death receptor-6 ( DR6), a member of the death domain-containing TNFR superfamily, is highly expressed in lymphoid tissues and regulated upon lymphocyte activation. Targeted disruption of DR6 results in enhanced CD4(+) T cell proliferation and T helper 2 ( Th2) differentiation in vitro, whereas the in vivo role of DR6 in regulating Th2 cell differentiation and effector function remains largely unknown. In the current study, we used a Th2-skewed allergic airway inflammation model induced by ovalbumin ( OVA) sensitization and challenge to compare the inflammatory response in the lung of both wild type (WT) and DR6(-/-) mice. DR6(-/-) mice were protected from the development of airway inflammation as evidenced by attenuated eosinophil accumulation and reduced mucus-producing cells in the lining airways of allergen-challenged animals. Consistent with these observations, a profound reduction of Th2 cytokine production (IL-5 and IL-13) was detected in the bronchoalveolar lavage fluid (BAL). Furthermore, a significant increase in the frequency of IFN-gamma secreting cells was observed in the DR6(-/-) mouse lungs after OVA challenge, which may account for the reduced pulmonary Th2 cytokine production. These data point to a critical role of DR6 in regulating airway inflammation in the OVA-induced mouse model of asthma.[1]

References

Death receptor-6 regulates the development of pulmonary eosinophilia and airway inflammation in a mouse model of asthma. Venkataraman, C., Justen, K., Zhao, J., Galbreath, E., Na, S. Immunol. Lett. (2006) [Pubmed]

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