2013/01/24 by Naveen Sharma, Ajay Suresh Akhade, Ayub Qadri · 1 citation
Immunology and Microbiology · Biochemistry, Genetics and Molecular Biology · #Immune Response and Inflammation #Immune Cell Function and Interaction #Sphingolipid Metabolism and Signaling
paper · doi:10.1189/jlb.0712328
openalex publication_date 2013/01/24 · openalex created_date 2025/10/10 · openalex updated_date 2026/05/21
T cells produce a number of cytokines and chemokines upon stimulation with TLR agonists in the presence or absence of TCR signals. Here, we show that secretion of neutrophil chemoattractant CXCL8 from human T cell line Jurkat in response to stimulation with TLR agonists is reduced when cell stimulation is carried out in presence of serum. Serum does not, however, inhibit TCR-activated secretion of CXCL8 nor does it down-regulate TLR-costimulated IL-2 secretion from activated T cells. The molecule that can mimic the ability to bring about suppression in CXCL8 from TLR-activated T cells is serum-borne bioactive lipid, S1P. Serum and S1P-mediated inhibition require intracellular calcium. S1P also suppresses CXCL8 secretion from peripheral blood-derived human T cells activated ex vivo with various TLR ligands. Our findings reveal a previously unrecognized role for S1P in regulating TLR-induced CXCL8 secretion from human T cells.