Open AccessDendritic Cell Surface Calreticulin Is a Receptor for NY-ESO-1: Direct Interactions between Tumor-Associated Antigen and the Innate Immune System
Author(s) -
Gang Zeng,
Michael E. Aldridge,
Xiaoli Tian,
Daniel Seiler,
Xiaolong Zhang,
Yusheng Jin,
Jianyu Rao,
Weidong Li,
Dequan Chen,
Marlyn P. Langford,
Chris Duggan,
Arie S. Belldegrun,
Steven M. Dubinett
Publication year - 2006
Publication title -
the journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.737
H-Index - 372
eISSN - 1550-6606
pISSN - 0022-1767
DOI - 10.4049/jimmunol.177.6.3582
Subject(s) - calreticulin , immune system , immunogenicity , acquired immune system , biology , immunoprecipitation , innate immune system , antigen , microbiology and biotechnology , cd8 , dendritic cell , antigen presentation , immunogenic cell death , immunology , t cell , antibody , immunotherapy , endoplasmic reticulum
How the immune system recognizes endogenously arising tumors and elicits adaptive immune responses against nonmutated tumor-associated Ags is poorly understood. In search of intrinsic factors contributing to the immunogenicity of the tumor-associated Ag NY-ESO-1, we found that the NY-ESO-1 protein binds to the surface of immature dendritic cells (DC), macrophages, and monocytes, but not to that of B cells or T cells. Using immunoprecipitation coupled with tandem mass spectrometry, we isolated DC surface calreticulin as the receptor for NY-ESO-1. Calreticulin Abs blocked NY-ESO-1 binding on immature DC and its cross-presentation to CD8+ T cells in vitro. Calreticulin/NY-ESO-1 interactions provide a direct link between NY-ESO-1, the innate immune system, and, potentially, the adaptive immune response against NY-ESO-1.
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