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* Department of Immunology, DNAX Research, Palo Alto, CA 94304; and
Schering Plough Research Institute, Kenilworth, NJ 07033
Tumor necrosis factor is a proinflammatory cytokine that induces
directly many of the components required for inflammation to proceed
rapidly. We show in this study that the interplay between TNF and
chemokines, now recognized to be essential for normal secondary
lymphoid tissue development, is also a feature of CNS inflammation, and
that the two apparently dissimilar biological processes share many
properties. Thus, induction of seven chemokines, including T cell
activation gene 3 (TCA3), monocyte chemoattractant protein-1, and
IFN-
-inducible protein-10 within the CNS during experimental
autoimmune encephalomyelitis fails to occur early in the inflammatory
process in TNF-deficient mice, despite local expression of monokines
and IFN-. The critical source of TNF in CNS inflammation is the
infiltrating hemopoietic cell, and, in its absence, chemokine
expression by irradiation-resistant CNS-resident cells fails. The CCR8
ligand, TCA3, is shown to be produced predominantly by resident
microglia of the CNS in response to TNF. Using CCR8-/-
mice, evidence is provided that TCA3-CCR8 interactions contribute to
rapid-onset CNS inflammation. Thus, through TNF production, the
hemopoietic compartment initiates the signals for its own movement into
tissues, although the tissue ultimately defines the nature of that
movement. Chemokines are a major, although not exclusive, mechanism by
which tissues regulate leukocyte movement in response to
TNF.
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