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Vasoactive intestinal peptide (VIP) is chemoattractant for resting, mouse T cells by upregulating the epidermal growth factor receptor (EGFR) pathway
Author(s) -
Wanjara Steve Biko,
Dorsam Glenn P
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.765.3
Subject(s) - downregulation and upregulation , vasoactive intestinal peptide , biology , microbiology and biotechnology , receptor , signal transduction , epidermal growth factor receptor , gut flora , epidermal growth factor , t cell , immune system , immunology , neuropeptide , biochemistry , gene
Effective immune protection against enteric pathogens is critical for the survival of the mammalian host. The human gut is home to nearly 100 trillion microorganisms consisting of ≈1000 distinct bacterial species, some of which are life‐threatening if they escape the gut lumen. Recruitment of peripheral, naïve T Lymphocytes to the gut replenishes this organ with regulatory T cells and folicular helper T cells, as well as assisting in B cell activation within specilizaed gut‐lymphoid regions, called Peyer's Patches. A potent T cell chemoattractant, called vasoactive intestinal peptide (VIP), is secreted by a dense network of nerves innervating the gut. Importantly, the removal of VIP receptors expressed on T cells causes a drastic reduction in recruited gut T cells supporting a role for this signaling axis in T cell trafficking to this organ. However, the molecular mechanism controlling T cell homing to the gut by VIP is presently unknown. We hypothesized that VIP signaling upregulates an epidermal growth factor receptor (EGFR) signaling pathway, based on a previously published global microarray study by our laboratory. Using primary, resting mouse CD4 T cells, we tested whether a coordinated upregulation of this EGFR pathway occurred by qRT‐PCR. This analysis showed a rapid, transient and coordinated upregulation of the EGFR pathway ≤ 2.5 hours post‐exogenous VIP treatment. Collectively, we conclude that VIP signaling initiates a chemoattractant cellular program through the coordinated upregulation of the EGFR pathway. Future research will be required to directly test whether this mechanism controls resting T cell trafficking to the gut.