Stepping Out of the Cytosol: AIMp1/p43 Potentiates the Link Between Innate and Adaptive Immunity

International Reviews of Immunology
D LiangWilliam K Decker

Abstract

As a structural component of the multi-aminoacyl tRNA synthetase (mARS) complex, AIMp1, also known as p43, hasn't until recently been recognized for its prominent immunological functions. Together with other nonenzymatic mARS structural components AIMp2/38 and AIMp3/p18, it participates in the machinery responsible for cell-cycle control and tumor suppression. Novel studies also show that AIMp1/p43 can be released by certain cancer cells under conditions of stress. Extracellularly, AIMp1 promotes the proliferation and migration of fibroblasts/endothelial cells and importantly, pro-inflammatory gene expression in monocytes/macrophages and dendritic cells. AIMp1/p43 deficiency is also correlated with spontaneous Type-2 airway hypersensitivity in mice, indicating a potential role in skewing toward T-helper type-1 (T(H)1) immunity. Vaccination strategies in which dendritic cells receive dual MHC class I and MHC class II antigens of homologous origins (i.e., that share overlapping class I and II binding epitopes) boost downstream T(H)1 immunity in a manner that appears to be wholly dependent upon dendritic cell AIMp1 release. Here we underscore the importance of AIMp1/p43 as a pro-inflammatory cytokine when it is released from cytos...Continue Reading

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Citations

Apr 17, 2020·FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology·Matthew M HalpertWilliam K Decker
Nov 30, 2018·Journal of Child Neurology·Andrea AccogliGeneviève Bernard
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Aug 21, 2020·The Journal of Biological Chemistry·Charlotta PregerHelena Persson

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