The impact of Meth A fibrosarcoma derived EMAP II on dendritic cell migration

Haridas, Seema; Bowers, Mary Lou; Tusano, Jackie; Mehojah, Justin; Kirkpatrick, Megan; Burnham, D. Kim

doi:10.1016/j.cyto.2008.09.002

Cited by 5 publications

(5 citation statements)

References 29 publications

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“…It was later found to possess cytokine activity including angiostatic or pro-apoptotic functions (Murray et al, 2004;Haridas et al, 2008). In this study, our data shows that AIMP1-(101-192) is a binding site for CD23 and induces TNF-a secretion.…”

Section: Aimp1 But Not Emap II Induces Tnf-a Secretion Via Cd23mentioning

confidence: 50%

Identification of CD23 as a functional receptor for the proinflammatory cytokine AIMP1/p43

Kwon¹,

Park²,

Kim³

et al. 2012

Journal of Cell Science

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SummaryAminoacyl-tRNA-synthetase-interacting multifunctional protein 1 (AIMP1/p43) can be secreted to trigger proinflammatory molecules while it is predominantly bound to a cytoplasmic macromolecular protein complex that contains several different aminoacyl-tRNA synthetases. Although its activities as a secreted signaling factor have been well characterized, the functional receptor for its proinflammatory activity has not yet identified. In this study, we have identified the receptor molecule for AIMP1 that mediates the secretion of TNF-a from THP-1 monocytic cells and primary human peripheral blood mononuclear cells (PBMCs). In a screen of 499 soluble receptors we identified CD23, a known low-affinity receptor for IgE, as a high affinity binding partner of AIMP1. We found that downregulation of CD23 attenuated AIMP1-induced TNF-a secretion and AIMP1 binding to THP-1 and PBMCs. We also observed that in THP-1 and PBMCs, AIMP1-induced TNF-a secretion, mediated by CD23, involved activation of ERK1/2. Interestingly, endothelial monocyte activating polypeptide II (EMAP II), the Cterminal fragment of AIMP1 that is also known to work as a proinflammatory cytokine, was incapable of binding to CD23 and of activating ERK1/2. Therefore, identification of CD23 not only explains the inflammatory function of AIMP1 but also provides the first evidence by which the mode of action of AIMP1 can be distinguished from that of its C-terminal domain, EMAP II.

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Section: Aimp1 But Not Emap II Induces Tnf-a Secretion Via Cd23mentioning

confidence: 50%

Identification of CD23 as a functional receptor for the proinflammatory cytokine AIMP1/p43

Kwon¹,

Park²,

Kim³

et al. 2012

Journal of Cell Science

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“…Reported HsEMAPII effects include chemotactic attraction of monocytes, dendritic cells and endothelial cells, induction of apoptosis in lymphocytes, and TNF-α production by monocytes/macrophages [30], [53], [54]. In contrast, EELP attracts human endothelial cells but not human monocytes, and this cellular specificity depends on the sequence of the signaling peptide of this protein.…”

Section: Discussionmentioning

confidence: 99%

Entamoeba lysyl-tRNA Synthetase Contains a Cytokine-Like Domain with Chemokine Activity towards Human Endothelial Cells

et al. 2011

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Immunological pressure encountered by protozoan parasites drives the selection of strategies to modulate or avoid the immune responses of their hosts. Here we show that the parasite Entamoeba histolytica has evolved a chemokine that mimics the sequence, structure, and function of the human cytokine HsEMAPII (Homo sapiens endothelial monocyte activating polypeptide II). This Entamoeba EMAPII-like polypeptide (EELP) is translated as a domain attached to two different aminoacyl-tRNA synthetases (aaRS) that are overexpressed when parasites are exposed to inflammatory signals. EELP is dispensable for the tRNA aminoacylation activity of the enzymes that harbor it, and it is cleaved from them by Entamoeba proteases to generate a standalone cytokine. Isolated EELP acts as a chemoattractant for human cells, but its cell specificity is different from that of HsEMAPII. We show that cell specificity differences between HsEMAPII and EELP can be swapped by site directed mutagenesis of only two residues in the cytokines' signal sequence. Thus, Entamoeba has evolved a functional mimic of an aaRS-associated human cytokine with modified cell specificity.

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“…EMAP II's role in cancer is not known. Some reports have shown that EMAP II is a tumor suppressor [ 27 , 30 , 76 – 78 ]. On the other hand, previous studies have indicated that EMAP II protein expression was identified in tumor cells [ 32 , 33 , 45 , 47 ].…”

Section: Discussionmentioning

confidence: 99%

EMAP II Expression Is Increased on Peripheral Blood Cells from Non-Hodgkin Lymphoma

Saber

2022

Journal of Immunology Research

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Tumor immune evasion is a lineament of cancer. Endothelial monocyte activating polypeptide-II (EMAP II) has been assumed to impact tumor immune escape significantly. EMAP II was first reported in the murine methylcholanthrene A-induced fibrosarcoma supernatant and identified as a tumor-derived cytokine. This study evaluated EMAP II expression in peripheral blood cells and its association with treatment outcome, lactate dehydrogenase (LDH) levels, and clinical criteria in non-Hodgkin’s lymphoma (NHL) patients. EMAP II expression on different blood cells obtained from the peripheral blood of 80 NHL patients was evaluated by two-color flow cytometry. The study reported that EMAP II expression was significantly increased in peripheral blood cells in patients with NHL compared to normal volunteers ( P < 0.001 ). Additionally, EMAP II expression levels on blood cells decreased in complete remission (CR) while they increased in relapse. This study showed coexpression of EMAP II and CD36 on peripheral lymphocytes in NHL patients but not in healthy controls ( P < 0.001 ). EMAP II expression on blood cells was associated with increased serum LDH levels. Furthermore, the percentages of EMAP II+/CD36+ peripheral lymphocytes were significantly higher in relapse than in CR and healthy controls. Analyses revealed that higher percentages of EMAP II+CD36+ cells were positively correlated with hepatomegaly, splenomegaly, and an advanced (intermediate and high risk) NHL stage. The results assume that EMAP II might be involved in NHL development and pathogenesis.

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The impact of Meth A fibrosarcoma derived EMAP II on dendritic cell migration

Cited by 5 publications

References 29 publications

Identification of CD23 as a functional receptor for the proinflammatory cytokine AIMP1/p43

Identification of CD23 as a functional receptor for the proinflammatory cytokine AIMP1/p43

Entamoeba lysyl-tRNA Synthetase Contains a Cytokine-Like Domain with Chemokine Activity towards Human Endothelial Cells

EMAP II Expression Is Increased on Peripheral Blood Cells from Non-Hodgkin Lymphoma

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