The relevance of lymphoid cell migration to immunodeficiency syndromes

J. B. Hay, N. J. Abernethy, A. N. Kalaaji, G. F. Teare, P. Borron

Research output: Contribution to journalArticlepeer-review

2 Scopus citations

Abstract

It has been known for some time that antigen stimulation can alter lymphocyte traffic patterns and that viruses are particularly potent in this respect; such alterations may be a consequence of host-derived factors. The retention of lymphocytes in lymph nodes can be sustained for several hours with locally administered interferon (IFN)α. The extravasation of lymphocytes from blood into non-lymphoid tissues can be induced in the skin with IFNγ and particularly tumor necrosis factor (TNF)α. Recent evidence supports the concept that the migratory capacity of CD4+ cells differs from the capacity of CD8+ cells. Agents (cytokines?) which differentially affect the traffic of these two sub-sets have not yet been described but such a possibility has not been adequately tested. Several new molecules have been defined which alter the interactions between lymphoctyes and blood vascular endothelial cells, and these may be important in the critical adhesive event in lymphocyte traffic. In both rat and sheep, it has been possible to cultivate post-capillary endothelial cells from lymphoid tissue, and this may be a helpful approach to studying the mechanisms and molecules involved in adhesion. New cell tracking dyes recently available (Zynaxis Cell Science) permit more significant, longterm studies on the life span of lymphocyte sub-sets and their migratory status. In our experiments, labeled lymphocytes can be followed in vivo for over 30 days. Traffic alterations may explain some of the abnormalities in immunodeficiency states.

Original languageEnglish (US)
Pages (from-to)64-72
Number of pages9
JournalLymphology
Volume23
Issue number2
StatePublished - 1990

ASJC Scopus subject areas

  • Immunology and Allergy
  • Hematology

Fingerprint

Dive into the research topics of 'The relevance of lymphoid cell migration to immunodeficiency syndromes'. Together they form a unique fingerprint.

Cite this