Anti-Mouse TCR-beta Monoclonal Antibodies for Flow Cytometry

PA007523.m2a: Recombinant Anti-mouse TCRβ Monoclonal Antibody (Clone: H57-597), Mouse IgG2a Lambda

Recombinant mouse IgG2a Monoclonal Antibody.
Clone: H57-597.
Isotype: Mouse IgG2a Lambda.
Source: The anti-mouse TCRβ monoclonal antibody (clone: H57-597) was produced in mammalian cells.
Conjugation: non-conjugated.
Specificity/Sensitivity: The recombinant mouse monoclonal antibody (clone: H57-597) specifically binds to the mouse TCRβ.
Applications: Flow cytometry (FC), and Immunohistochemistry - Frozen (IHC-F).
Form of Antibody: 0.2 uM filtered solution, pH 7.4, no stabilizers or preservatives.
Purity: >95% by SDS-PAGE under reducing conditions and HPLC.

PA007523.h1Fs: Recombinant Anti-mouse TCRβ Monoclonal Antibody (Clone: H57-597), Human IgG1 Fc Silent Kappa

Recombinant human IgG1 Monoclonal Antibody with Fc silent mutation.
Clone: H57-597.
Isotype: Human IgG1 Fc Silent Kappa.
Source: The anti-mouse TCRβ monoclonal antibody (clone: H57-597) was produced in mammalian cells.
Conjugation: non-conjugated.
Specificity/Sensitivity: The recombinant H57-597 antibody specifically binds to the mouse TCRβ.
Applications: Flow cytometry (FC), and Immunohistochemistry - Frozen (IHC-F).
Form of Antibody: 0.2 uM filtered solution, pH 7.4, no stabilizers or preservatives.
Purity: >95% by SDS-PAGE under reducing conditions and HPLC.

PA007775.h1Fs-b: Biotinylated Recombinant Anti-mouse TCRβ Monoclonal Antibody (Clone: H57-597), Human IgG1 Fc Silent Kappa

Recombinant human IgG1 Monoclonal Antibody with site-directed biotinylation through the Avi tag at the C-terminus of the antibody heavy chain.
Clone: H57-597.
Isotype: Human IgG1 Fc Silent Kappa.
Source: The site-directed biotinylated anti-mouse TCRβ monoclonal antibody (clone: H57-597) was produced in mammalian cells.
Conjugation: Biotin-conjugated.
Specificity/Sensitivity: The site-directed biotinylated recombinant H57-597 antibody specifically binds to the mouse TCRβ.
Applications: Flow cytometry (FC) with various dye conjugation through streptavidin; conjugation to streptavidin agarose beads or streptavidin magnetic beads.
Form of Antibody: 0.2 uM filtered solution, pH 7.4, no stabilizers or preservatives.
Purity: >95% by SDS-PAGE under reducing conditions and HPLC.

Shipping: The antibody is shipped with ice pack. Upon receipt, store it immediately at the temperature recommended below.
Stability & Storage: Use a manual defrost freezer and avoid repeated freeze-thaw cycles.
12 months from date of receipt, -20 to -70°C as supplied.
1 month from date of receipt, 2 to 8°C as supplied.

References of anti-mouse TCR beta antibody for Flow Cytometry (Clone: H57-597):

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 Jun;12(6):1409-18. doi: 10.1111/j.1600-6143.2012.04006.x. 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. More importantly, transient H57-597 mAb treatment exerted long-lasting effect in preventing T cell responses to alloantigens, and produced long-term cardiac allograft survival (>100 days) in 10 out of 11 recipients. While Treg cells were involved in maintaining donor-specific long-term graft survival, T cell homeostasis recovered over time and immunity was retained against third party allografts. Moreover, transient H57-597 mAb treatment significantly prolonged survival of skin allografts in naïve recipients as well as heart allografts in skin-sensitized recipients. Thus, transient modulation of the TCRβ chain by H57-597 mAb exhibits potent, long-lasting therapeutic effects to control alloimmune responses.
Tags: activity of H57-597 antibody; activity of H57-597 mAb

Transient Anti-TCRβ mAb Treatment Induces CD4 + T Cell Exhaustion and Prolongs Survival in a Mouse Model of Systemic Lupus Erythematosus
Gonzalez NM, et al. Immunology. 2025 Feb;174(2):239-246. doi: 10.1111/imm.13881. 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. On day 1 post the final dose of treatment, SLE pathogenesis was determined using histological staining and spot urine test. T and B cell states in the brain, kidney, and secondary lymphoid organs were determined by flow cytometry. Transient treatment of anti-TCRβ mAb significantly prolonged the survival of MRL/lpr mice. Accordingly, MRL/lpr mice in the anti-TCRβ mAb group exhibited decreased proteinuria scores and minimal renal pathological damage compared to the PBS control group. Flow cytometric analysis revealed that anti-TCRβ mAb treatment resulted in a reduction in the frequencies of CD4+ T cells and CD138+B220lo/- plasma cells, plus an increase in Foxp3+ regulatory T cell frequency. Furthermore, CD4+ T cells from anti-TCRβ mAb treated mice exhibited elevated expression levels of PD-1 and TIM-3, with reduced IFN-γ production, indicative of an exhaustion-like phenotype. Therefore, transient administration of anti-TCRβ mAb treatment induces an exhaustion-like phenotype in CD4+ T cells, resulting in prolonged survival of MRL/lpr mice. Inducing autoreactive T-cell exhaustion holds promise as an attractive therapeutic approach for SLE.
Tags: function of H57-597 mAb; H57-597 antibody

Alpha beta T-lymphocyte depleted mice, a model for gamma delta T-lymphocyte functional studies
Carbone A, et al. Immunol Rev. 1991 Apr;120:35-50. doi: 10.1111/j.1600-065x.1991.tb00586.x. 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. Indirect effects of the antibody treatment include quantitative changes in splenic B cells, as well as reduced sizes and weights of experimental animals. alpha beta-suppressed mice and rats may provide model systems for studies on gamma delta cell function in vivo.
Tags: H57-597 antibody for flow cytometry; H57-597 antibody for mouse tumor model

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 Oct 1;158(10):3140-3151. doi: 10.1210/en.2016-1947. 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. These diabetic NOD mice were transiently treated with an anti-TCR β chain (TCRβ) mAb, H57-597, for 5 days. Two weeks later, some NOD mice with established overt diabetes further received hepatic gene therapy using the islet-lineage determining gene Neurogenin3 (Ngn3), in combination with the islet growth factor gene betacellulin (Btc). We found that anti-TCRβ mAb (50 µg/d) reversed >80% new-onset diabetes in NOD mice for >14 weeks by reducing the number of effector T cells in the pancreas. However, anti-TCRβ mAb therapy alone reversed only ∼20% established overt diabetes in these mice. Among those overtly diabetic NOD mice whose diabetes was resistant to anti-TCRβ mAb treatment, ∼60% no longer had diabetes when they also received Ngn3-Btc hepatic gene transfer 2 weeks after initial anti-TCRβ mAb treatment. This combination of Ngn3-Btc gene therapy and anti-TCRβ mAb treatment induced the sustained formation of periportal insulin-producing cells in the liver of overtly diabetic mice. Therefore, directly targeting TCRβ with a mAb potently reverses new-onset T1D in NOD mice and protects residual and newly formed gene therapy-induced hepatic neo-islets from T-cell?mediated destruction in mice with established overt diabetes.
Tags: H57-597 antibody mouse dose range; H57-597 mAb for animal model

Monoclonal antibody against T-cell receptor alphabeta induces self-tolerance in chronic experimental autoimmune encephalomyelitis
Lavasani S, et al. Scand J Immunol. 2007 Jan;65(1):39-47. doi: 10.1111/j.1365-3083.2006.01866.x. 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, while treatment with control antibody (hamster IgG) was ineffective. The remission was durable and not associated with disappearance of autoreactive T cells as measured by persistence of MOG-reactive T-cell proliferation in vitro. However, MOG-reactive T cells from anti-TCR-treated animals produced significantly lower amounts of inflammatory TNF-alpha and IFN-gamma. In addition, while a transient deletion of CD4(+) and CD8(+) T cells was observed, a population of T cells expressing CD3, NK1.1 and CD69 (NKT cells) were expanding. By transfer of spleen cells from anti-TCR MoAb-treated animals, we could show that the tolerogenic capacity can be transferred to untreated recipients with EAE. The data indicate therapeutic effect of anti-TCR alphabeta MoAb (H57-597), which represents a promising approach in treatment of T-cell-mediated autoimmune diseases.
Tags: H57-597 mAb for mouse tumor model; H57-597 monoclonal antibody

For more references about anti-mouse TCR beta antibody for Flow Cytometry (Clone: H57-597), please contact our scientific support team with message@sydlabs.com.

Syd Labs provides the following in vivo grade recombinant anti-mouse TCRβ monoclonal antibodies:
In Vivo Grade Recombinant Anti-mouse TCRβ Monoclonal Antibody (Clone: H57-597)