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CCL27/PESKY: a novel paradigm for chemokine function
Robert J B Nibbs1, Gerard J Graham
1The Beatson Institute for Cancer Research, Cancer Research UK Beatson Laboratories, Garscube Estate, Switchback Road, Bearsden, Glasgow, G61 1BD, UK. r.nibbs@beatson.gla.ac.uk
Expert Opinion on Biological Therapy
|April 30, 2003
Summary
CC chemokine ligand 27 (CCL27) has dual roles. It attracts T cells to skin and, as PESKY, enhances cell motility by altering the cytoskeleton and modulating transcription.
Area of Science:
- Immunology
- Cell Biology
- Molecular Biology
Background:
- Chemokines regulate leukocyte migration, crucial for immune responses.
- CC chemokine ligand 27 (CCL27) and its receptor CC chemokine receptor 10 (CCR10) are implicated in T cell homing to the skin.
- Alternative splicing of CCL27 produces a nuclear form, PESKY, with unknown functions.
Purpose of the Study:
- To review the novel functions of CCL27 beyond leukocyte trafficking.
- To elucidate the mechanisms by which nuclear CCL27/PESKY influences cellular processes.
- To discuss the implications of these dual roles in cutaneous inflammation.
Main Methods:
- Review of existing literature on CCL27, CCR10, and related cellular pathways.
- Analysis of studies investigating alternative splicing and nuclear localization of CCL27.
- Examination of research on actin cytoskeleton regulation and transcriptional modulation.
Main Results:
- CCL27 attracts memory T cells to the skin via CCR10.
- Alternative splicing yields nuclear PESKY, which disrupts actin stress fibers and enhances cell motility.
- Secreted CCL27 can internalize via CCR10, enter the nucleus, and modulate transcription.
Conclusions:
- CCL27 exhibits unprecedented dual functions: extracellularly as a chemokine and intracellularly as a nuclear protein.
- Nuclear CCL27/PESKY directly impacts cell morphology and motility through cytoskeletal rearrangement and transcriptional control.
- These findings reveal novel mechanisms in immune cell behavior and cutaneous inflammation, warranting further investigation.