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Last update 08 May 2025

TREML2

Last update 08 May 2025

Basic Info

Synonyms

C6orf76, dJ238O23.1, FLJ13693

+ [6]

Introduction

Cell surface receptor that may play a role in the innate and adaptive immune response. Acts as a counter-receptor for CD276 and interaction with CD276 on T-cells enhances T-cell activation.

Drugs associated with TREML2

GENA-105S05

Target

TREML2

Mechanism

TREML2 antagonists

Active Org.

Genome & Co.

Originator Org.

Genome & Co.

Active Indication

Neoplasms

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

CN115873109

Patent Mining

Target

TREML2

Mechanism-

Active Org.

Research Institute of Artificial Intelligence Biomedical Technology, Nanjing University [+1]

Originator Org.

Research Institute of Artificial Intelligence Biomedical Technology, Nanjing University [+1]

Active Indication

Cardiovascular Diseases [+2]

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with TREML2

100 Translational Medicine associated with TREML2

0 Patents (Medical) associated with TREML2

106

Literatures (Medical) associated with TREML2

01 May 2025·Life Sciences

The role of the TREM receptor family in cardiovascular diseases: Functions, mechanisms, and therapeutic target

Review

Author: Xue, Jin-Yi ; Chen, Ming-Tai ; Yang, Xin-Rui ; Liu, Qiu-Yu ; Liang, Ling-Ling ; Jian, Yu-Hong ; Liu, Ping ; Jiang, Yan ; Liu, Meng-Nan ; Sun, Shi-Han

The Triggering Receptor Expressed in the Myeloid Cells (TREM) family represents an emerging subgroup within the immunoglobulin superfamily, which includes key members such as TREM-1, TREM-2, TREM-3, TREM-like transcript-1 (TLT-1), TLT-2, and TLT-4. TREM-1 serves as a potent amplifier of immune responses, exacerbating atherosclerosis and myocardial injury by enhancing inflammatory reactions. In contrast, TREM-2 exerts protective effects by regulating lipid metabolism, mitigating inflammation, and promoting phagocytic activity, thereby attenuating cardiovascular damage. Both soluble TLT-1 and TLT-4 have been identified as potential biomarkers for cardiovascular risk. In recent years, the roles of the TREM family in the pathogenesis of cardiovascular diseases (CVD) have garnered growing interest within the scientific community. This review aims to illuminate the functional roles, underlying mechanisms, and clinical relevance of TREM family members in the regulation of CVD, while exploring their potential applications in early diagnosis, disease monitoring, and the development of novel therapeutic targets for CVD, ultimately laying a foundation for their clinical translation and advancement in precision medicine.

01 Feb 2025·Multiple Sclerosis and Related Disorders

Cerebrospinal fluid biomarkers as predictors of multiple sclerosis severity

Article

Author: Chahin, Salim ; Mikesell, Robert ; Ghezzi, Laura ; Perantie, Dana C ; Huecker, Julia ; Piccio, Laura ; Pace, Francesca ; Tolentino, Miguel ; Cross, Anne H

BACKGROUNDPrognostic biomarkers at multiple sclerosis (MS) onset to predict disease severity may help guide initial therapy selection for people with MS. Over 20 disease-modifying treatments (DMTs) of varying levels of risk and efficacy now exist. The ability to predict MS severity would help to identify those patients at higher risk where a highly effective, but potentially risky, therapy would be optimal. The goal of this project was to determine if cerebrospinal fluid (CSF) soluble markers obtained near time of diagnosis can predict disease severity in people with relapsing remitting MS (RRMS).METHODSWe identified 42 RRMS subjects with 4 or more years of clinical follow-up at our center, 8 subjects with other inflammatory neurological diseases (OIND), and 4 subjects with non-inflammatory neurological diseases (NIND) who had donated CSF samples collected for disease diagnosis. This study evaluated soluble CSF biomarkers chosen to reflect neuroinflammation (chemokine ligand 13 - CXCL13), microglia activity (soluble triggering receptor expressed on myeloid cells 2 - sTREM2), demyelination (myelin basic protein -MBP), axon injury and loss (neurofilament light, heavy, and intermediate chains - NFL, NFH, internexin-alpha - INT-α) and neuronal loss (parvalbumin - PVALB) to determine whether any of these CSF factors might predict future MS disease severity. The main outcome measure was MS Severity Score (MSSS), which takes into account disability accumulation (expanded disability status scale - EDSS) and duration of disease. EDSS at last clinical visit was a secondary outcome measure. Univariate and multivariable regression models were used for analysis. Spearman correlations were performed to evaluate correlation between laboratory and clinical variables.RESULTSForty-two RRMS patients with mean 9.4 years follow-up since lumbar puncture (LP) contributed data. Higher NFH, NFL, and sTREM2 each predicted worse MSSS using both univariate and multivariable regression models. Older age at the time of LP predicted worse MSSS both in the univariate and multivariable models. NFL correlated with NFH, and both were positively correlated with sTREM2 and CXCL13. In the combined OIND and NIND comparator group, NFH correlated with both NFL and CXCL13.CONCLUSIONThese data support that CSF sTREM2, NFH, and NFL are predictors of MSSS, a measure of MS disease aggressiveness. This study adds to a growing literature implicating microglial activity and axonal injury in MS progression, starting from early stages of the disease.

01 Jan 2025·American Journal of Physiology-Renal Physiology

Exosomes derived from TREM-2 knocked-out macrophages alleviated renal fibrosis via HSPa1b/AKT pathway

Article

Author: Cao, Yuhan ; Liu, Can ; Wang, Yajie ; Chen, Yuye ; Xiao, Zihao ; Jin, Ling ; Shi, Yuanhui ; Fu, Cong

Renal fibrosis is a common pathological feature of CKD, resulting in irreversible loss of function and structure. However, effective therapies for CKD are currently limited. We found that the deletion of TREM-2 in macrophages increased the MMP-9/TIMP-1 ratio in exosomes, shifting toward the degradation of the extracellular matrix (ECM) and the alleviation of renal fibrosis. Furthermore, polyclonal antibodies against TREM-2 effectively suppressed renal fibrosis. These findings provide evidence that TREM-2 is a potential therapeutic target for CKD.

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