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Prepublished online as a Blood First Edition Paper on August 15, 2002; DOI 10.1182/blood-2002-03-0697.
Submitted March 6, 2002
Accepted August 7, 2002
Differential chemokine expression profiles in human peripheral blood T lymphocytes: dependence on T-cell coreceptor and calcineurin signaling
Anthony D Cristillo, Mirtha J Macri, and Barbara E Bierer*
National Institutes of Health, National Heart, Lung and Blood Institute, Bethesda, MD, USA
* Corresponding author; email: Barbara_Bierer{at}dfci.harvard.edu.
The chemokine superfamily consists of small (8-10 kDa) molecules that function to attract, selectively, different subsets of leukocytes. Binding of chemokines to their appropriate G-protein-coupled receptors is necessary for both primary immune responses and for homing of leukocytes to lymphoid tissues. Here, we have characterized the signaling pathways in primary T lymphocytes that regulate chemokine gene induction using an RNase protection assay (RPA). The dependence on stimulation via the coreceptor CD28 and sensitivity to the calcineurin inhibitors cyclosporine and tacrolimus were studied using purified human peripheral blood T cells (PBL). Lymphotactin (Ltn), macrophage inflammatory protein (MIP)-1 , and MIP-1ß were all rapidly induced and sensitive to cyclosporine treatment. At later time points, expression of MIP-1 and MIP-1ß, but not Ltn was restored despite inhibition of calcineurin activity. By contrast, the induction of interleukin (IL)-8 was more delayed and found to be cyclosporine-insensitive. The dependence on calcineurin activity of IP-10 mRNA induction depended on the specific T cell stimulation conditions, suggesting that IP-10 expression is modulated by both calcineurin-dependent and -independent signaling pathways. Differential chemokine expression profiles result from the engagement of T cell coreceptors and the requirement for, and dependence on, calcineurin phosphatase activity.
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