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CD28 co-stimulation results in down-regulation of lymphotactin expression in human CD4(+) but not CD8(+) T cells via an IL-2-dependent mechanism.
Chemokines are key molecules in promoting leukocyte migration and, for some of them, T cell adhesion and activation. Lymphotactin, which is the unique known member of the C class of chemokines, is produced by and acts on T lymphocytes, but the requirement of co-stimulatory pathways such as CD28 for its expression is largely unknown. CD28 plays a dominant role in the amplification of T cell proliferation, survival and cytokine production. In this report, we demonstrate that human lymphotactin expression, at both the mRNA and protein levels, is optimally induced by CD3/TCR activation alone, whereas CD28 co-stimulation turns off this expression. This down-regulation is not attributable to secondary activation via CTLA-4, the alternative counter-receptor of B7 ligands. Only the CD4(+) and not the CD8(+) subset is directly affected by this negative regulation. Transcript destabilization can be ruled out as a mechanism by which CD28 down-regulates lymphotactin expression. However, such down-regulation can be partly induced by IL-2 and abrogated by blocking IL-2/ IL-2 receptor interaction. This particular profile of lymphotactin expression is not in line with the prevailing dogma of up-regulation of cytokine gene expression by CD28 co-stimulation, and represents a new CD28- mediated regulatory mechanism for lymphotactin expression.[1]References
- CD28 co-stimulation results in down-regulation of lymphotactin expression in human CD4(+) but not CD8(+) T cells via an IL-2-dependent mechanism. Olive, D., Cerdan, C. Eur. J. Immunol. (1999) [Pubmed]
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