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Prepublished online as a Blood First Edition Paper on April 24, 2003; DOI 10.1182/blood-2002-07-2206.
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Blood, 1 September 2003, Vol. 102, No. 5, pp. 1745-1752
IMMUNOBIOLOGY
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,
Baldev Vasir,
Charles E. Larsen,
Dana Gabuzda,
Ellis Reinherz, and
Chester A. Alper
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.
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-1 (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 dendritic cells
and initiate innate and adaptive immune responses.
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