Ly49H signaling through DAP10 is essential for optimal natural killer cell responses to mouse cytomegalovirus infection

Mark T. Orr, Joseph C. Sun, David G.T. Hesslein, Hisashi Arase, Joseph H. Phillips, Toshiyuki Takai, Lewis L. Lanier

研究成果: Article査読

60 被引用数 (Scopus)

抄録

The activating natural killer (NK) cell receptor Ly49H recognizes the mouse cytomegalovi rus (MCMV) m157 glycoprotein expressed on the surface of infected cells and is required for protection against MCMV. Although Ly49H has previously been shown to signal via DAP12, we now show that Ly49H must also associate with and signal via DAP10 for optimal function. In the absence of DAP12, DAP10 enables Ly49H-mediated killing of m157- bearing target cells, proliferation in response to MCMV infection, and partial protection against MCMV. DAP10-defcient Ly49H + NK cells, expressing only Ly49H-DAP12 receptor complexes, are partially impaired in their ability to proliferate during MCMV infection, display diminished ERK1/2 activation, produce less IFN-γ upon Ly49H engagement, and demonstrate reduced control of MCMV infection. Deletion of both DAP10 and DAP12 completely abrogates Ly49H surface expression and control of MCMV infection. Thus, optimal NK cell-mediated immunity to MCMV depends on Ly49H signaling through both DAP10 and DAP12.

本文言語English
ページ(範囲)807-817
ページ数11
ジャーナルJournal of Experimental Medicine
206
4
DOI
出版ステータスPublished - 2009 4 13

ASJC Scopus subject areas

  • 医学(全般)

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