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*
Department of Pathology, Harvard Medical School, and
Department of Cancer Immunology and AIDS, Dana Farber Cancer Institute, Boston, MA 02115
Dendritic cells (DC) are the most potent APCs and the principal
activators of naive T cells. We now report that chemokines can serve as
activating agents for immature DC. Murine bone marrow-derived DC
respond to the CC chemokine RANTES (10–100 ng/ml) by production of
proinflammatory mediators. RANTES induces rapid expression of
transcripts for the CXC chemokines KC and macrophage inflammatory
protein (MIP)-2, the CC chemokines MIP-1
and MIP-1
, and the
cytokines TNF- and IL-6. Synthesis of KC, IL-6, and TNF- proteins
were also demonstrated. After 4 h, autoinduction of RANTES transcripts
was observed. These responses are chemokine specific. Although DC
demonstrated weak responses to eotaxin, DC failed to respond to other
chemokines including KC, MIP-2, stromal-derived factor-1, MIP-1,
MIP-1, monocyte chemoattractant protein-1, T cell activation gene 3,
or thymus-derived chemotactic agent 4. In addition, RANTES treatment
up-regulated expression of an orphan chemokine receptor termed Eo1.
Chemokine induction was also observed after treatment of splenic DC and
neonatal microglia with RANTES, but not after treatment of thymocytes
or splenocytes depleted of adherent cells. TNF--treated DC lose
responsiveness to RANTES. DC from mice deficient for CCR1, CCR3, and
CCR5 respond to RANTES, indicating that none of these receptors are
exclusively used to initiate the chemokine cascade. RANTES-mediated
chemokine amplification in DC may prolong inflammatory responses and
shape the microenvironment, potentially enhancing acquired and innate
immune responses.
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