Stepping Out of the Cytosol: AIMp1/p43 Potentiates the Link Between Innate and Adaptive Immunity
作者： D. Liang , M. M. Halpert , V. Konduri , W. K. Decker
DOI: 10.3109/08830185.2015.1077829
关键词: Acquired immune system 、 Epitope 、 Cytokine 、 Cell biology 、 Biology 、 Dendritic cell 、 Cancer cell 、 Inflammation 、 Immunity 、 MHC class I
摘要: 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 components AIMp2/38 and AIMp3/p18, it participates in machinery responsible cell-cycle control tumor suppression. Novel studies show that AIMp1/p43 can be released by certain cancer cells under conditions stress. Extracellularly, AIMp1 promotes proliferation migration fibroblasts/endothelial importantly, pro-inflammatory gene expression monocytes/macrophages dendritic cells. deficiency is correlated spontaneous Type-2 airway hypersensitivity mice, indicating potential role skewing toward T-helper type-1 (T(H)1) immunity. Vaccination strategies which receive dual MHC class I II antigens homologous origins (i.e., share overlapping binding epitopes) boost downstream T(H)1 immunity manner appears to wholly dependent upon cell release. Here we underscore importance cytokine when from cytosol extracellular space discuss future directions mechanisms regulate this process might better characterized, further elucidating link between innate adaptive
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