Regulation of T lymphocyte trafficking into lymph nodes during an immune response by the chemokines macrophage inflammatory protein (MIP)-1α and MIP- 1β

Nicodemus Tedla, Hong Wei Wang, H. Patrick McNeil, Nick Di Girolamo, Taline Hampartzoumian, Denis Wakefield, Andrew Lloyd*

*Corresponding author for this work

Research output: Contribution to journalArticle

105 Citations (Scopus)

Abstract

By virtue of their target cell specificity, chemokines have the potential to selectively recruit leukocyte subpopulations into sites of inflammation. Their role in regulation oft 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)-1α and MIP-1β mRNAs and proteins. Mast cells accumulating in the nodes during DNFB sensitization were the predominant source of MIP-1β, whereas MIP-1α 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, β-chemokines regulate T lymphocyte emigration from the circulation into lymph nodes during an immune response and contribute significantly to the immunologic outcome.

Original languageEnglish
Pages (from-to)5663-5672
Number of pages10
JournalJournal of Immunology
Volume161
Issue number10
Publication statusPublished - 15 Nov 1998
Externally publishedYes

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