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Helminth-derived peptide GK-1 induces Myd88-dependent pro-inflammatory signaling events in bone marrow-derived antigen-presenting cells.

Abstract：

:GK-1 is an immunomodulatory, 18-aa-long peptide that has been proved to promote the activation of mouse peritoneal macrophages and LPS-pulsed mouse bone marrow-derived dendritic cells (BM-DCs). This study is aimed to explore the mechanisms underlying the activation of these antigen-presenting cells (APCs) by GK-1. In our study, GK-1 up-regulated in vitro the expression of CD86 and CD40, and it increased the secretion of NO in bone marrow-derived macrophages (BMDMs). In BM-DCs, GK-1 upregulated the expression of MHC class II and CD86. Additionally, GK-1 was found to be involved in the phosphorylation of MAPK p38, JNK and ERK 1/2 and in Myd88-dependent activation of NF-κB in both antigen-presenting cell types. In vivo, GK-1 increased the secretion of IL-15, CCL2, and IL-6 through a Myd88-dependent mechanism. This study demonstrated that GK-1 promotes the activation and effector activity of APCs through a mechanism dependent on Myd88, probably involving a Toll-like receptor as a target.

journal_name

Mol Immunol

journal_title

Molecular immunology

authors

Montero L,Cervantes-Torres J,Sciutto E,Fragoso G

doi

10.1016/j.molimm.2020.09.015

subject

Has Abstract

pub_date

2020-12-01 00:00:00

pages

22-32

eissn

0161-5890

issn

1872-9142

pii

S0161-5890(20)30491-0

journal_volume

128

pub_type

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