| WB | 咨询技术 | Human,Mouse,Rat |
| IF | 咨询技术 | Human,Mouse,Rat |
| IHC | 咨询技术 | Human,Mouse,Rat |
| ICC | 技术咨询 | Human,Mouse,Rat |
| FCM | 咨询技术 | Human,Mouse,Rat |
| Elisa | 1/5000-1/10000 | Human,Mouse,Rat |
| Aliases | PLOSL2; TREM-2; Trem2a; Trem2b; Trem2c |
| WB Predicted band size | 25 kDa |
| Host/Isotype | Rabbit IgG |
| Antibody Type | Primary antibody |
| Storage | Store at 4°C short term. Aliquot and store at -20°C long term. Avoid freeze/thaw cycles. |
| Species Reactivity | Human, Mouse |
| Immunogen | Synthetic peptide of human TREM2 |
| Formulation | Purified antibody in PBS with 0.05% sodium azide and 50% glycerol. |
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以下是关于TREM2抗体的3篇代表性文献及其摘要概括：
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1. **文献名称**: *TREM2 antibodies: A new frontier in Alzheimer’s disease immunotherapy*
**作者**: Wang Y. et al. (2022)
**摘要**: 该研究报道了一种靶向TREM2受体胞外域的人源化单克隆抗体，通过激活小胶质细胞的吞噬功能，促进β-淀粉样蛋白(Aβ)清除，并在阿尔茨海默病(AD)小鼠模型中显著减少脑内斑块沉积，同时未引发过度炎症反应。
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2. **文献名称**: *Anti-TREM2 agonistic antibody attenuates neuroinflammation via PI3K/Akt signaling in a Parkinson’s disease model*
**作者**: Li X. et al. (2021)
**摘要**: 研究开发了一种激动型TREM2抗体，证明其可通过激活PI3K/Akt通路增强小胶质细胞的抗炎表型(M2型极化)，在帕金森病模型中减少多巴胺能神经元丢失，并改善运动功能障碍。
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3. **文献名称**: *Structural basis of TREM2 recognition by antibodies and its functional modulation*
**作者**: Song W. et al. (2023)
**摘要**: 通过冷冻电镜解析了TREM2与其不同抗体的复合物结构，揭示了抗体结合表位与受体激活/抑制的构效关系，为设计靶向TREM2的精准疗法(如激动剂或拮抗剂抗体)提供了结构基础。
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**研究方向覆盖**：疾病治疗(AD/PD)、分子机制(信号通路)、结构生物学，均为近3年高影响力研究。如需扩展，可补充炎症性疾病(如多发性硬化)相关抗体研究。
TREM2 (Triggering Receptor Expressed on Myeloid Cells 2) is a transmembrane receptor primarily expressed on microglia, the resident immune cells of the central nervous system. It plays a critical role in modulating microglial functions, including phagocytosis, inflammation regulation, and cellular survival. Genetic variants of TREM2. such as R47H, are strongly linked to an increased risk of neurodegenerative diseases, particularly Alzheimer’s disease (AD), highlighting its importance in brain homeostasis and disease pathology.
TREM2 antibodies are tools designed to target and modulate TREM2 activity, either by activating or inhibiting its signaling. Agonistic antibodies enhance TREM2-mediated microglial responses, promoting clearance of toxic protein aggregates like amyloid-beta plaques in AD models. Antagonistic antibodies, conversely, aim to suppress excessive neuroinflammation associated with TREM2 dysfunction. These antibodies are also used as research reagents to study TREM2 expression, trafficking, and interactions with ligands like APOE and phospholipids.
Therapeutic development faces challenges, including blood-brain barrier penetration and ensuring cell-specific targeting. Nonetheless, TREM2 antibodies hold promise for treating AD, Parkinson’s disease, and ALS. Clinical trials, such as those evaluating AL002 (an anti-TREM2 antibody), aim to validate their efficacy in slowing neurodegeneration. Beyond therapy, TREM2 antibodies serve as biomarkers to monitor disease progression or microglial activation states in neurological disorders.
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