한빛사논문
- 조회3,933
Abstract
Jae-Kwang Yoo1,2, Carole L. Galligan1,2, Carl Virtanen3, and Eleanor N. Fish1,2
1Toronto General Research Institute, University Health Network, Toronto, Ontario M5G 2M1, Canada
2Department of Immunology, University of Toronto, Toronto, Ontario M5S 1A8, Canada
3Microarray Centre, University Health Network, Toronto, Ontario M5G 1L7, Canada
CORRESPONDENCE Eleanor N. Fish
Abstract
Antiinfluenza type 2 (T2) immunity contributes to both immunopathology and immunoprotection, yet the underlying mechanisms modulating T2 immunity remain ill defined. We describe a novel mouse antigen (Ag)-presenting cell (APC), designated late-activator APC (LAPC). After pulmonary influenza A (H1N1) virus infection, LAPCs enter the lungs, capture viral Ag, and subsequently migrate to the draining lymph node (DLN) and spleen, with delayed kinetics relative to dendritic cells (DCs). In the DLN, influenza virus-activated LAPCs present Ag and selectively induce T helper type 2 (Th2) effector cell polarization by cell-cell contact-mediated modulation of GATA-3 expression. In adoptive transfer experiments, influenza virus-activated LAPCs augmented Th2 effector T cell responses in the DLN, increased production of circulating antiinfluenza immunoglobulin, and increased levels of T2 cytokines in bronchoalveolar lavage fluid in recipient influenza virus-infected mice. LAPC-recipient mice exhibited exacerbated pulmonary pathology, with delayed viral clearance and enhanced pulmonary eosinophilia. Collectively, our results identify and highlight the importance of LAPCs as immunomodulators of T2 immunity during influenza A virus infection.
Footnotes
Submitted: 23 June 2009
Accepted: 12 May 2010
논문정보
- Research article
- 2010년 06월 (BRIC 등록일 )
- 국외 연구진
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