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Published on: June 16, 2019
The synthetic peptide, His-Phe-Tyr-Leu-Pro-Met, is a chemoattractant for Jukat T cells
1Division of Molecular and Life Sciences, Pohang University of Science and Technology, Korea.
Abstract:
His-Phe-Tyr-Leu-Pro-Met (HFYLPM) is a synthetic peptide that stimulates Jurkat T cells resulting in intracellular calcium ([Ca2+]i) increase in a pertussis toxin (PTX)-sensitive manner. We have examined the physiological role of the peptide in T cell activity by comparative investigation of intracellular signaling pathways accompanied with HFYLPM-induced T cell chemotaxis with a well-known chemokine, stromal cell-derived factor-1 (SDF-1)-induced signalings. Wortmannin and genistein inhibited both of HFYLPM- and SDF-1-induced Jurkat T cell chemotaxis indicating that phosphoinositide-3-kinase and tyrosine kinase activity were required for the processes. However, U-73122 and BAPTA/AM preferentially blocked HFYLPM- but not SDF-1-induced T cell chemotaxis. It indicates that phospholipase C/calcium signaling is necessary for only chemotaxis by HFYLPM. One of the well-known cellular molecules involving chemotaxis, extracellular signal-regulated protein kinase (ERK), was activated by SDF-1 but not by HFYLPM ruling out a possible role of ERK on the peptide-mediated chemotaxis. These results indicate that the synthetic peptide, HFYLPM, stimulates T cell chemotaxis showing unique signaling and provide a useful tool for the study of T cell activation mechanism.
Insights
The synthetic peptide His-Phe-Tyr-Leu-Pro-Met (HFYLPM) uniquely stimulates T cell chemotaxis via phospholipase C/calcium signaling, distinct from chemokine pathways. This peptide offers a novel tool for studying T cell activation mechanisms.
Area of Science:
- Immunology
- Cell Biology
- Biochemistry
Background:
- T cell activation is crucial for immune responses.
- Chemokines like stromal cell-derived factor-1 (SDF-1) are key regulators of T cell migration.
- Understanding novel signaling pathways in T cell activation is essential.
Purpose of the Study:
- To investigate the signaling pathways involved in His-Phe-Tyr-Leu-Pro-Met (HFYLPM)-induced T cell chemotaxis.
- To compare HFYLPM-induced signaling with that of SDF-1.
- To determine the physiological role of HFYLPM in T cell activity.
Main Methods:
- Comparative analysis of intracellular signaling pathways in Jurkat T cells.
- Assessment of T cell chemotaxis using inhibitors like wortmannin, genistein, U-73122, and BAPTA/AM.
- Measurement of intracellular calcium ([Ca2+]i) increase and extracellular signal-regulated protein kinase (ERK) activation.
Main Results:
- HFYLPM and SDF-1 both induce Jurkat T cell chemotaxis requiring phosphoinositide-3-kinase and tyrosine kinase activity.
- HFYLPM-induced chemotaxis is uniquely dependent on phospholipase C/calcium signaling, unlike SDF-1.
- HFYLPM does not activate ERK, whereas SDF-1 does, indicating distinct signaling mechanisms.
Conclusions:
- The synthetic peptide HFYLPM stimulates T cell chemotaxis through a unique signaling pathway involving phospholipase C and calcium.
- HFYLPM-mediated T cell activation differs significantly from SDF-1-induced signaling.
- HFYLPM serves as a valuable research tool for elucidating T cell activation mechanisms.
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