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and MIP-1ß1
Inflammation Research Unit, School of Pathology, University of New South Wales, Sydney, Australia
By virtue of their target cell specificity, chemokines have the
potential to selectively recruit leukocyte subpopulations into sites of
inflammation. Their role in regulation of T lymphocyte traffic into
lymph nodes during the development of an immune response has not
previously been explored. The sensitization phase of contact
hypersensitivity induced by the hapten, dinitrofluorobenzene (DNFB) in
the mouse was used as a model of T lymphocyte trafficking in response
to antigenic stimulation. Rapid accumulation of CD8+ and
CD4+ T cells in the draining lymph nodes was closely
associated with strongly enhanced expression of macrophage inflammatory
protein (MIP)-1
and MIP-1ß mRNAs and proteins. Mast cells
accumulating in the nodes during DNFB sensitization were the
predominant source of MIP-1ß, whereas MIP-1 was expressed by
multiple cell types. Neutralization of these chemokines profoundly
inhibited T lymphocyte trafficking into lymph nodes and altered the
outcome of a subsequent challenge to DNFB. Thus, ß-chemokines
regulate T lymphocyte emigration from the circulation into lymph nodes
during an immune response and contribute significantly to the
immunologic outcome.
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