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Prepublished online as a Blood First Edition Paper on April 24, 2003; DOI 10.1182/blood-2002-07-2206.

Submitted July 26, 2002
Accepted March 3, 2003
CD2 engagement induces dendritic cell activation: implications for immune surveillance and T-cell activation
Keith Crawford, Aleksandra Stark, Betsy Kitchens, Kerry Sternheim, Vassilios Pantazopoulos, Ellen Triantafellow, Zhigang Wang, Beldav Vasir, Charles E Larsen, Dana Gabuzda, Ellis Reinherz, and Chester A Alper*
The Center for Blood Research, Boston, MA, USA; Department of Pediatics, Harvard Medical School, Boston, MA, USA
Departments of Cancer Immunology & AIDS, Dana -Farber Cancer Institute, Boston, MA, USA
Department of Adult Oncology, Dana -Farber Cancer Institute, Boston, MA, USA
Department of Pathology, Harvard Medical School, Boston, MA, USA
Department of Neurology, Harvard Medical School, Boston, MA, USA
Department of Medicine, Harvard Medical School, Boston, MA, USA
Department of Pediatics, Harvard Medical School, Boston, MA, USA
* Corresponding author; email: alper{at}cbr.med.harvard.edu.
We have shown previously that primary dendritic cells and monocytes express equal levels of CD14 but are distinguishable by the presence of CD2 on dendritic cells. CD2 is known to mediate the activation of T and NK cells through its interaction with CD58. CD2 epitopes recognized by anti-T111, -T112 and -T113 mAbs are present on dendritic cells. Here we show that CD2 engagement significantly increases class II, costimulatory (CD40, CD80, CD86), adhesion (CD54, CD58), and CCR7 molecule expression on primary dendritic cells. Conversely, minimal or no change in the expression of the above antigens occurs on monocyte-derived dendritic cells, since these molecules are already maximally expressed. However, both kinds of dendritic cells release IL-1 and IL-12 after CD2 engagement. Lastly, interference with dendritic cell CD2-T cell CD58 engagement decreases naive CD4+CD45RA+ T cell proliferation. Collectively, our results suggest another role of the CD2-CD58 pathway that allows nonimmune and immune cells to interact directly with dendrictic cells and initiate innate and adaptive immune responses.

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