CD2 engagement induces dendritic cell activation: implications for immune surveillance and T-cell activation

Author:

Crawford Keith1,Stark Aleksandra1,Kitchens Betsy1,Sternheim Kerry1,Pantazopoulos Vassilios1,Triantafellow Ellen1,Wang Zhigang1,Vasir Baldev1,Larsen Charles E.1,Gabuzda Dana1,Reinherz Ellis1,Alper Chester A.1

Affiliation:

1. From The Center for Blood Research, Boston, MA; Departments of Cancer Immunology & AIDS and Adult Oncology, Dana-Farber Cancer Institute, Boston, MA; and the Departments of Medicine, Pathology, Pediatrics, and Neurology, Harvard Medical School, Boston, MA.

Abstract

Abstract 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 natural killer (NK) cells through its interaction with CD58. CD2 epitopes recognized by anti-T111, -T112, and -T113 monoclonal antibodies (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, because these molecules are already maximally expressed. However, both kinds of dendritic cells release interleukin-1β (IL-1β) 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 dendritic cells and initiate innate and adaptive immune responses.

Publisher

American Society of Hematology

Subject

Cell Biology,Hematology,Immunology,Biochemistry

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