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PGLYRP1/Tag7 的 N 端肽是 TREM-1 受体的新型配体。

N-Terminal Peptide of PGLYRP1/Tag7 Is a Novel Ligand for TREM-1 Receptor.

机构信息

Laboratory of Molecular Immunogenetics of Cancer, Institute of Gene Biology RAS, 111394 Moscow, Russia.

出版信息

Int J Mol Sci. 2022 May 20;23(10):5752. doi: 10.3390/ijms23105752.

DOI:10.3390/ijms23105752
PMID:35628562
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9144885/
Abstract

An investigation of innate immunity receptors sheds light on the mechanisms of inflammation and associated immune reactions. One of the key immune regulators is the TREM-1 receptor, which is involved in both inflammation and antitumor immune response. In this article, we have obtained a new ligand for the TREM-1 receptor. The peptide, named N3, is a part of the innate immune protein PGLYRP1/Tag7. It is responsible for activating the TREM-1 signaling pathway. Here, we have demonstrated that the N3 peptide acts like other TREM-1 receptor ligands: its binding results in a mild inflammation response and appearance of cytotoxic lymphocytes. We have shown that cytotoxic populations of lymphocytes in N3 peptide-treated PBMCs are similar to those treated with Tag7 or Hsp70. We also determined the part of the N3 peptide responsible for binding to TREM-1. The resulting peptide (N9) consists of nine amino acids and can be considered as a potential peptide that blocks TREM-1 signaling.

摘要

固有免疫受体的研究揭示了炎症和相关免疫反应的机制。关键的免疫调节剂之一是 TREM-1 受体,它参与炎症和抗肿瘤免疫反应。在本文中,我们获得了 TREM-1 受体的新配体。该肽名为 N3,是先天免疫蛋白 PGLYRP1/Tag7 的一部分。它负责激活 TREM-1 信号通路。在这里,我们已经证明 N3 肽的作用类似于其他 TREM-1 受体配体:它的结合导致轻度炎症反应和细胞毒性淋巴细胞的出现。我们已经表明,在 N3 肽处理的 PBMC 中,细胞毒性淋巴细胞群与用 Tag7 或 Hsp70 处理的细胞毒性淋巴细胞群相似。我们还确定了与 TREM-1 结合的 N3 肽的部分。得到的肽(N9)由九个氨基酸组成,可被视为一种潜在的肽,可阻断 TREM-1 信号。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c4b7/9144885/e156026db936/ijms-23-05752-g008a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c4b7/9144885/ab12f996d098/ijms-23-05752-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c4b7/9144885/e4bc0a2193ce/ijms-23-05752-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c4b7/9144885/4d7197d64b0a/ijms-23-05752-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c4b7/9144885/c47e584b1f9f/ijms-23-05752-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c4b7/9144885/0c228b744e2e/ijms-23-05752-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c4b7/9144885/88e1aec20939/ijms-23-05752-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c4b7/9144885/e156026db936/ijms-23-05752-g008a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c4b7/9144885/ab12f996d098/ijms-23-05752-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c4b7/9144885/2c71c09fe235/ijms-23-05752-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c4b7/9144885/e4bc0a2193ce/ijms-23-05752-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c4b7/9144885/4d7197d64b0a/ijms-23-05752-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c4b7/9144885/c47e584b1f9f/ijms-23-05752-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c4b7/9144885/0c228b744e2e/ijms-23-05752-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c4b7/9144885/88e1aec20939/ijms-23-05752-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c4b7/9144885/e156026db936/ijms-23-05752-g008a.jpg

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