Catalog No.	PA007166.m2a
Product Name	Anti-Mouse CD8a Antibody (YTS 169.4) | PA007166.m2a
Supplier Name	Syd Labs, Inc.
Brand Name	Syd Labs
Synonyms	CD8 alpha, T-cell surface glycoprotein CD8 alpha chain, CD_antigen CD8a
Summary	The in vivo grade recombinant anti-mouse CD8a mouse IgG2a monoclonal antibody was produced in mammalian cells.
Clone	YTS 169.4.
Isotype	mouse IgG2a, kappa.
Specificity/Sensitivity	CD8a.
Applications	Western blot, immunohistochemistry (IHC), Flow Cytometry (FC), and in vivo CD8+ T cell depletion.
Form Of Antibody	0.2 μM filtered solution of 1x PBS.
Endotoxin	Less than 1 EU/mg of protein as determined by LAL method.
Purity	>95% by SDS-PAGE under reducing conditions.
Shipping	The in vivo grade recombinant anti-mouse CD8a antibodies (clone of YTS 169.4) are 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. 1 month from date of receipt, 2 to 8°C as supplied. 3 months from date of receipt, -20°C to -70°C as supplied.
Note	Recombinant anti-mouse CD8a monoclonal antibodies from the variable region sequences of the rat anti-mouse CD8a monoclonal antibody (clone number: YTS 169.4) are produced from mammalian cells and good for in vitro and in vivo studies.
Order Offline	Phone: 1-617-401-8149 Fax: 1-617-606-5022 Email: message@sydlabs.com Or leave a message with a formal purchase order (PO) Or credit card.

Description

PA007166.m2a: Recombinant Anti-Mouse CD8a Monoclonal Antibody(Clone YTS 169.4), Mouse IgG2a Kappa, In vivo Grade

The Recombinant Anti-Mouse CD8a Monoclonal Antibody (Clone YTS 169.4) from Syd Labs is a meticulously engineered tool for researchers studying the immune system. CD8a is a crucial marker for cytotoxic T cells, playing a pivotal role in cell-mediated immunity. This antibody, with its Mouse IgG2a Kappa isotype, offers unparalleled specificity and affinity for mouse CD8a.Produced using state-of-the-art recombinant technology, this monoclonal antibody ensures batch-to-batch consistency and exceptional purity. Its in vivo grade designation signifies its suitability for use in live animal studies, making it an invaluable asset for in vivo research applications.

Our recombinant YTS 169.4 antibodies have a part (variable regions) or complete amino acid sequences of the rat anti-mouse CD8a monoclonal antibody (hybridoma clone name or number: YTS 169.4). Whether you’re investigating immune responses, studying T cell populations, or developing new therapies, this anti-mouse CD8a antibody is designed to meet the rigorous demands of modern research.

Syd Labs offers two high-performance variants of the Recombinant Anti-Mouse CD8a Monoclonal Antibody (Clone YTS 169.4) for advanced immunology research: one with Mouse IgG2a Kappa and the other with Rat IgG2b Kappa isotypes, each tailored to meet specific experimental needs. Both antibodies are produced using cutting-edge recombinant technology, ensuring exceptional batch-to-batch consistency and purity, making them ideal for in vivo applications such as T cell depletion studies. They specifically target the mouse CD8a antigen, a key marker for cytotoxic T cells, and are essential for investigating cell-mediated immunity and immune system dynamics. The Mouse IgG2a Kappa variant is particularly suited for experiments requiring effector functions like antibody-dependent cellular cytotoxicity (ADCC) and complement-dependent cytotoxicity (CDC), while the Rat IgG2b Kappa variant excels in minimizing background in mouse models by reducing cross-reactivity. Both antibodies are versatile for use in flow cytometry, immunohistochemistry (IHC), and T cell functional assays, providing researchers with reliable tools to advance their studies in T cell biology and beyond. Choose Syd Labs for precision and excellence in your scientific discoveries.

1、CD39 inhibition and VISTA blockade may overcome radiotherapy resistance by targeting exhausted CD8+ T cells and immunosuppressive myeloid cells
Yuhan Zhang,et al.Cell Rep Med. 2023.PMCID: PMC10439278
“Although radiotherapy (RT) has achieved great success in the treatment of non-small cell lung cancer (NSCLC), local relapses still occur and abscopal effects are rarely seen even when it is combined with immune checkpoint blockers (ICBs). Here, we characterize the dynamic changes of tumor-infiltrating immune cells after RT in a therapy-resistant murine tumor model using single-cell transcriptomes and T cell receptor sequencing. At the early stage, the innate and adaptive immune systems are activated. At the late stage, however, the tumor immune microenvironment (TIME) shifts into immunosuppressive properties. Our study reveals that inhibition of CD39 combined with RT preferentially decreases the percentage of exhausted anti-mouse CD8a antibody+ T cells. Moreover, we find that the combination of V-domain immunoglobulin suppressor of T cell activation (VISTA) blockade and RT synergistically reduces immunosuppressive myeloid cells. Clinically, high VISTA expression is associated with poor prognosis in patients with NSCLC. Altogether, our data provide deep insight into acquired resistance to RT from an immune perspective and present rational combination strategies.”

2、Rationalized inhibition of mixed lineage kinase 3 and CD70 enhances life span and antitumor efficacy of CD8+ T cells
Sandeep Kumar,et al.J Immunother Cancer. 2020.PMCID: PMC7410077
“Background
The mitogen-activated protein kinases (MAPKs) are important for T cell survival and their effector function. Mixed lineage kinase 3 (MLK3) (MAP3K11) is an upstream regulator of MAP kinases and emerging as a potential candidate for targeted cancer therapy; yet, its role in T cell survival and effector function is not known.
Methods
T cell phenotypes, apoptosis and intracellular cytokine expressions were analyzed by flow cytometry. The apoptosis-associated gene expressions in anti-mouse CD8a antibody+CD38+ T cells were measured using RT2 PCR array. In vivo effect of combined blockade of MLK3 and CD70 was analyzed in 4T1 tumor model in immunocompetent mice. The serum level of tumor necrosis factor-α (TNFα) was quantified by enzyme-linked immunosorbent assay.
Results
We report that genetic loss or pharmacological inhibition of MLK3 induces CD70-TNFα-TNFRSF1a axis-mediated apoptosis in CD8+ T cells. The genetic loss of MLK3 decreases CD8+ T cell population, whereas CD4+ T cells are partially increased under basal condition. Moreover, the loss of MLK3 induces CD70-mediated apoptosis in CD8+ T cells but not in CD4+ T cells. Among the activated CD8+ T cell phenotypes, CD8+CD38+ T cell population shows more than five fold increase in apoptosis due to loss of MLK3, and the expression of TNFRSF1a is significantly higher in CD8+CD38+ T cells. In addition, we observed that CD70 is an upstream regulator of TNFα-TNFRSF1a axis and necessary for induction of apoptosis in CD8+ T cells. Importantly, blockade of CD70 attenuates apoptosis and enhances effector function of CD8+ T cells from MLK3−/− mice. In immune-competent breast cancer mouse model, pharmacological inhibition of MLK3 along with CD70 increased tumor infiltration of cytotoxic CD8+ T cells, leading to reduction in tumor burden largely via mitochondrial apoptosis.
Conclusion
Together, these results demonstrate that MLK3 plays an important role in CD8+ T cell survival and effector function and MLK3-CD70 axis could serve as a potential target in cancer.”

3、Treg-selective IL-2 starvation synergizes with CD40 activation to sustain durable responses in lymphoma models
Kristin Stirm,et al.J Immunother Cancer. 2023.PMCID: PMC9950978
“Background
Roughly half of all diffuse large B-cell lymphomas (DLBCLs) are infiltrated by large numbers of regulatory T-cells (Tregs). Although the presence of ‘effector’ Tregs in particular is associated with an inferior prognosis in patients on standard rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) immunochemotherapy, the role of this cell type during lymphoma initiation and progression is poorly understood.
Methods
Here, we use tissue microarrays containing prospectively collected DLBCL patient specimens, as well as data from publicly available cohorts to explore the mutational landscape of Treg-infiltrated DLBCL. We further take advantage of a model of MYC-driven lymphoma to mechanistically dissect the contribution of Tregs to lymphoma pathogenesis and to develop a strategy of Treg-selective interleukin-2 (IL-2) starvation to improve immune control of MYC-driven lymphoma.
Results
We find that all genetic DLBCL subtypes, except for one characterized by co-occurring MYD88/CD79 mutations, are heavily infiltrated by Tregs. Spectral flow cytometry and scRNA-sequencing reveal the robust expression of functional and immunosuppressive markers on Tregs infiltrating MYC-driven lymphomas; notably, we find that intratumoral Tregs arise due to local conversion from naïve CD4+ precursors on tumor contact. Treg ablation in Foxp3iDTR mice, or by antibody-mediated Treg-selective blockade of IL-2 signaling, strongly reduces the lymphoma burden. We identify lymphoma B-cells as a major source of IL-2, and show that the effects of Treg depletion are reversed by the simultaneous depletion of Foxp3-negative CD4+ T-cells, but not CD8+ T-cells or natural killer (NK) cells. The inhibition of ATP hydrolyzation and adenosine production by Tregs at least partly phenocopies the effects of Treg depletion. Treg depletion further synergizes with pro-apoptotic CD40 activation to sustain durable responses.
Conclusion
The combined data implicate Tregs as a potential therapeutic target in DLBCL, especially in combination with other immunotherapies.”

4、Cytotoxic CD8+ T cells promote granzyme B-dependent adverse post-ischemic cardiac remodeling
Icia Santos-Zas,et al.Nat Commun. 2021.PMCID: PMC7935973
“Acute myocardial infarction is a common condition responsible for heart failure and sudden death. Here, we show that following acute myocardial infarction in mice, anti-mouse CD8a antibody+ T lymphocytes are recruited and activated in the ischemic heart tissue and release Granzyme B, leading to cardiomyocyte apoptosis, adverse ventricular remodeling and deterioration of myocardial function. Depletion of CD8+ T lymphocytes decreases apoptosis within the ischemic myocardium, hampers inflammatory response, limits myocardial injury and improves heart function. These effects are recapitulated in mice with Granzyme B-deficient CD8+ T cells. The protective effect of CD8 depletion on heart function is confirmed by using a model of ischemia/reperfusion in pigs. Finally, we reveal that elevated circulating levels of GRANZYME B in patients with acute myocardial infarction predict increased risk of death at 1-year follow-up. Our work unravels a deleterious role of CD8+ T lymphocytes following acute ischemia, and suggests potential therapeutic strategies targeting pathogenic CD8+ T lymphocytes in the setting of acute myocardial infarction.”

5、Targeting TMEM176B Enhances Antitumor Immunity and Augments the Efficacy of Immune Checkpoint Blockers by Unleashing Inflammasome Activation
Mercedes Segovia,et al.Cancer Cell. 2019.PMCID: PMC6521897
“Although immune checkpoint blockers have yielded significant clinical benefits in patients with different malignancies, the efficacy of these therapies is still limited. Here, we show that disruption of transmembrane protein 176B (TMEM176B) contributes to anti-mouse CD8a antibody+ T cell-mediated tumor growth inhibition by unleashing inflammasome activation. Lack of Tmem176b enhances the antitumor activity of anti-CTLA-4 antibodies through mechanisms involving caspase-1/IL-1β activation. Accordingly, patients responding to checkpoint blockade therapies display an activated inflammasome signature. Finally, we identify BayK8644 as a potent TMEM176B inhibitor that promotes CD8+ T cell-mediated tumor control and reinforces the antitumor activity of both anti-CTLA-4 and anti-PD-1 antibodies. Thus, pharmacologic de-repression of the inflammasome by targeting TMEM176B may enhance the therapeutic efficacy of immune checkpoint blockers.”

6、Targeting leucine-rich repeat serine/threonine-protein kinase 2 sensitizes pancreatic ductal adenocarcinoma to anti-PD-L1 immunotherapy
Kang Sun,et al.Mol Ther. 2023.PMCID: PMC10556191
“Pancreatic ductal adenocarcinoma (PDAC) is not sensitive to immune checkpoint blockade therapy, and negative feedback of tumor immune evasion might be partly responsible. We isolated anti-mouse CD8a antibody+ T cells and cultured them in vitro. Proteomics analysis was performed to compare changes in Panc02 cell lines cultured with conditioned medium, and leucine-rich repeat kinase 2 (LRRK2) was identified as a differential gene. LRRK2 expression was related to CD8+ T cell spatial distribution in PDAC clinical samples and upregulated by CD8+ T cells via interferon gamma (IFN-γ) simulation in vitro. Knockdown or pharmacological inhibition of LRRK2 activated an anti-pancreatic cancer immune response in mice, which meant that LRRK2 acted as an immunosuppressive gene. Mechanistically, LRRK2 phosphorylated PD-L1 at T210 to inhibit its ubiquitination-mediated proteasomal degradation. LRRK2 inhibition attenuated PD-1/PD-L1 blockade-mediated, T cell-induced upregulation of LRRK2/PD-L1, thus sensitizing the mice to anti-PD-L1 therapy. In addition, adenosylcobalamin, the activated form of vitamin B12, which was found to be a broad-spectrum inhibitor of LRRK2, could inhibit LRRK2 in vivo and sensitize PDAC to immunotherapy as well, which potentially endows LRRK2 inhibition with clinical translational value. Therefore, PD-L1 blockade combined with LRRK2 inhibition could be a novel therapy strategy for PDAC.”

7、CD39+PD-1+CD8+ T cells mediate metastatic dormancy in breast cancer
Paulino Tallón de Lara,et al.Nat Commun. 2021.PMCID: PMC7859213
“Some breast tumors metastasize aggressively whereas others remain dormant for years. The mechanism governing metastatic dormancy remains largely unknown. Through high-parametric single-cell mapping in mice, we identify a discrete population of CD39+PD-1+CD8+ T cells in primary tumors and in dormant metastasis, which is hardly found in aggressively metastasizing tumors. Using blocking antibodies, we find that dormancy depends on TNFα and IFNγ. Immunotherapy reduces the number of dormant cancer cells in the lungs. Adoptive transfer of purified CD39+PD-1+CD8+ T cells prevents metastatic outgrowth. In human breast cancer, the frequency of CD39+PD-1+CD8+ but not total CD8+ T cells correlates with delayed metastatic relapse after resection (disease-free survival), thus underlining the biological relevance of CD39+PD-1+CD8+ T cells for controlling experimental and human breast cancer. Thus, we suggest that a primary breast tumor could prime a systemic, CD39+PD-1+CD8+ T cell response that favors metastatic dormancy in the lungs.”

8、Combined PARP and WEE1 inhibition triggers anti-tumor immune response in BRCA1/2 wildtype triple-negative breast cancer
Zhi Ling Teo,et al.NPJ Breast Cancer. 2023.PMCID: PMC10427618
“Novel therapeutic strategies that can effectively combine with immunotherapies are needed in the treatment of triple-negative breast cancer (TNBC). We demonstrate that combined PARP and WEE1 inhibition are synergistic in controlling tumour growth in BRCA1/2 wild-type TNBC preclinical models. The PARP inhibitor (PARPi) olaparib combined with the WEE1 inhibitor (WEE1i) adavosertib triggered increases in anti-tumour immune responses, including STING pathway activation. Combinations with a STING agonist resulted in further improved durable tumour regression and significant improvements in survival outcomes in murine tumour models of BRCA1/2 wild-type TNBC. In addition, we have identified baseline tumour-infiltrating lymphocyte (TIL) levels as a potential predictive biomarker of response to PARPi, WEE1i and immunotherapies in BRCA1/2 wild-type TNBC.”

9、Antitumor efficacy of combined CTLA4/PD-1 blockade without intestinal inflammation is achieved by elimination of FcγR interactions
David Bauché,et al.J Immunother Cancer. 2020.PMCID: PMC7604872
“Background
Programmed cell death protein 1 (PD-1) and CTLA4 combination blockade enhances clinical efficacy in melanoma compared with targeting either checkpoint alone; however, clinical response improvement is coupled with increased risk of developing immune-related adverse events (irAE). Delineating the mechanisms of checkpoint blockade-mediated irAE has been hampered by the lack of animal models that replicate these clinical events.
Methods
We have developed a mouse model of checkpoint blockade-mediated enterocolitis via prolonged administration of an Fc-competent anti-CTLA4 antibody.
Results
Sustained treatment with Fc-effector, but not Fc-mutant or Fc-null, anti-CTLA4 antagonist for 7 weeks resulted in enterocolitis. Moreover, combining Fc-null or Fc-mutant CTLA4 antagonists with PD-1 blockade results in potent antitumor combination efficacy indicating that Fc-effector function is not required for combination benefit.
Conclusion
These data suggest that using CTLA4 antagonists with no Fc-effector function can mitigate gut inflammation associated with anti-CTLA4 antibody therapy yet retain potent antitumor activity in combination with PD-1 blockade.”

10、The immunocytokine L19-IL2: An interplay between radiotherapy and long-lasting systemic anti-tumour immune responses
Nicolle H Rekers,et al.Oncoimmunology. 2018.PMCID: PMC5889197
“Recently, we have shown that the administration of the tumour-targeted antibody-based immunocytokine L19-IL2 after radiotherapy (RT) resulted in synergistic anti-tumour effect. Here we show that RT and L19-IL2 can activate a curative abscopal effect, with a long-lasting immunological memory. Ionizing radiation (single dose of 15Gy, 5 × 2Gy or 5 × 5Gy) was delivered to primary C51 colon tumour-bearing immunocompetent mice in combination with L19-IL2 and response of secondary non-irradiated C51 or CT26 colon tumours was evaluated. 15Gy + L19-IL2 triggered a curative (20%) abscopal effect, which was T cell dependent. Moreover, 10Gy + L19-IL2 treated and cured mice were re-injected after 150 days with C51 tumour cells and tumour uptake was assessed. Age-matched controls (matrigel injected mice treated with 10Gy + L19-IL2, mice cured after treatment with surgery + L19-IL2 and mice cured after high dose RT 40Gy + vehicle) were included. Several immunological parameters in blood, tumours, lymph nodes and spleens were investigated. Treatment with 10Gy + L19-IL2 resulted in long-lasting immunological memory, associated with CD44+CD127+ expression on circulating T cells. This combination treatment can induce long-lasting curative abscopal responses, and therefore it has also great potential for treatment of metastatic disease. Preclinical findings have led to the initiation of a phase I clinical trial (NCT02086721) in our institute investigating stereotactic ablative radiotherapy with L19-IL2 in patients with oligometastatic solid tumours.”

We provide the following recombinant anti-human CD8a monoclonal antibodies:
Recombinant anti-human CD8a antibodies (clone OKT8)
Recombinant anti-human CD8a antibodies (clone OKT8) for flow cytometry

We provide the following recombinant anti-mouse CD8a monoclonal antibodies:
Recombinant anti-mouse CD8a antibodies (clone 2.43), In vivo grade
Recombinant anti-mouse CD8a antibodies (clone YTS 169.4), In vivo grade
Recombinant anti-mouse CD8a antibodies (clone YTS 105.18), In vivo grade

Syd Labs provides the following recombinant anti-mouse CD8b monoclonal antibodies:
Recombinant anti-mouse CD8b antibodies (clone YTS 156.7), In vivo grade

Anti-Mouse CD8a Antibody (YTS 169.4) from: In Vivo Grade Recombinant Anti-Mouse CD8a Mouse IgG2a Kappa Monoclonal Antibody (Clone YTS 169.4): PA007166.m2a Syd Labs

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