重组抗小鼠TGFβ单抗(H57-597)流式 | Syd Labs PA007523.h1Fs

文献

重组抗小鼠TGFβ单克隆抗体(克隆号H57-597)，人IgG1 Fc Silent Kappa（Recombinant Anti-mouse TCR beta Monoclonal Antibody (Clone: H57-597), Human IgG1 Fc Silent Kappa，货号：PA007523.h1Fs）

重组抗小鼠TCRβ单抗（克隆号H57-597）能够特异性识别并结合小鼠T细胞受体β链（TCR beta）。TCRβ是小鼠αβ T细胞受体复合物的核心组成部分，广泛表达于胸腺细胞、外周成熟T淋巴细胞以及NKT细胞表面。TCRβ通过与TCRα配对形成异二聚体，在抗原识别、信号转导及T细胞的活化与发育过程中发挥着决定性作用。H57-597抗体作为免疫学研究中的经典克隆，是研究小鼠T细胞免疫应答、受体交联活化及T细胞亚群分析的重要工具。

Syd Labs重组抗小鼠TCRβ单抗（H57-597，Mouse IgG2a Lambda）采用哺乳动物细胞重组表达系统生产，具备极高的纯度与卓越的批间一致性。该H57-597抗体不仅适用于流式细胞术（FACS）和冰冻切片免疫组化（IHC-F），还可广泛用于体内T细胞功能研究、活化诱导或细胞群体的特异性检测。本产品具备优异的体内实验级品质，可配套Syd Labs重组Mouse IgG2a同型对照抗体使用，确保科研人员获得科学严谨、高度可重复的实验数据。

抗小鼠TGFβ单抗(H57-597)流式部分参考文献:

1. Anti-TCRβ mAb induces long-term allograft survival by reducing antigen-reactive T cells and sparing regulatory T cells
Miyahara, Y., et al. Am J Transplant. 2012;12(6):1409-1418. PMID: 22420295
“TCR specific antibodies may modulate the TCR engagement with antigen-MHC complexes, and in turn regulate in vivo T cell responses to alloantigens. Herein, we found that in vivo administration of mAbs specific for mouse TCRβ (H57-597), TCRα or CD3 promptly reduced the number of CD4(+) and CD8(+) T cells in normal mice, but H57-597 mAb most potently increased the frequency of CD4(+) Foxp3(+) Treg cells. When mice were injected with staphylococcal enterotoxin B (SEB) superantigen and H57-597 mAb, the expansion of SEB-reactive Vβ8(+) T cells was completely abrogated while SEB-nonreactive Vβ2(+) T cells remained unaffected.”

2. Transient Anti-TCRβ mAb Treatment Induces CD4 + T Cell Exhaustion and Prolongs Survival in a Mouse Model of Systemic Lupus Erythematosus
Gonzalez, N. M., et al. Immunology. 2025;174(2):239-246. PMID: 39648274
“T cells play a critical role in the pathogenesis of systemic lupus erythematosus (SLE). Chronic T cell receptor (TCR) signalling induces T cell exhaustion, characterised by reduced capacity to induce tissue damage. Here, we investigated the therapeutic potential of the anti-TCRβ (H57-597) monoclonal antibody (mAb) in a mouse model of SLE. Four-month-old MRL/lpr mice exhibiting SLE phenotypes received 5 weekly doses of anti-TCRβ mAb or phosphate-buffered saline (PBS) vehicle control. Subsequently, mouse survival was monitored daily.”

3. Alpha beta T-lymphocyte depleted mice, a model for gamma delta T-lymphocyte functional studies
Carbone, A., et al. Immunol Rev. 1991;120:35-50. PMID: 1830862
“Adult mice can be depleted of essentially all mature alpha beta T lymphocytes by chronic treatment with the framework-recognizing, pan-specific anti-TCR alpha beta mAb, H57-597. Similar findings have been reported in rats, gamma delta cell populations remain essentially unaltered in size and reactivity. Suppression of alpha beta T-cell development results in the loss of alloantigen reactivity and of B-cell help, suggesting that gamma delta and alpha beta populations differ in their functional capabilities.”

4. Anti-TCRβ mAb in Combination With Neurogenin3 Gene Therapy Reverses Established Overt Type 1 Diabetes in Female NOD Mice
Xie, A., et al. Endocrinology. 2017;158(10):3140-3151. PMID: 28977608
“Insulin-producing β cells in patients with type 1 diabetes (T1D) are destroyed by T lymphocytes. We investigated whether targeting the T-cell receptor (TCR) with a monoclonal antibody (mAb) abrogates T-cell response against residual and newly formed islets in overtly diabetic nonobese diabetic (NOD) mice. NOD mice with blood glucose levels of 250 to 350 mg/dL or 350 to 450 mg/dL were considered as new-onset or established overt diabetes, respectively.”

5. Monoclonal antibody against T-cell receptor alphabeta induces self-tolerance in chronic experimental autoimmune encephalomyelitis
Lavasani, S., et al. Scand J Immunol. 2007;65(1):39-47. PMID: 17212765
“The therapeutic effect of monoclonal antibody (H57-597 MoAb) against T-cell receptor (TCR) alphabeta has been investigated on MOG(35-55)-induced experimental autoimmune encephalomyelitis (EAE), as a model system for T-cell-mediated chronic inflammation in the central nervous system (CNS). Short-term administration of the anti-TCR alphabeta immediately after immunization protected the mice from EAE. Furthermore, anti-TCR alphabeta treatment on an established disease restored the self-tolerance which led to a complete remission of EAE and a dramatic reduction of inflammatory cells in the CNS.”