Catalog No.	PA007200.m2a
Product Name	Anti-mouse CD4 Antibody – GK1.5(Mouse IgG2a) | PA007200.m2a
Supplier Name	Syd Labs, Inc.
Brand Name	Syd Labs
Uniprot ID	CD4 on UniProt.org
Gene ID	12504
Clone	GK1.5.
Isotype	Mouse IgG2a Kappa (Clone: GK1.5)
Source/Host	The anti-mouse CD4 monoclonal antibody (clone: GK1.5) was produced in mammalian cells.
Specificity/Sensitivity	The in vivo grade recombinant rat monoclonal antibody (clone: GK1.5) specifically binds to the mouse T cell receptor CD4.
Applications	ELISA, neutralization, functional assays such as bioanalytical PK and ADA assays, and those assays for studying biological pathways affected by the mouse CD4 protein.
Form Of Antibody	0.2 uM filtered solution, pH 7.4, no stabilizers or preservatives.
Endotoxin	< 1 EU per 1 mg of the protein by the LAL method.
Purity	>95% by SDS-PAGE under reducing conditions and HPLC.
Shipping	The In vivo Grade Recombinant Anti-mouse CD4 Monoclonal Antibody, Mouse IgG2a Kappa (Clone: GK1.5) 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.
Note	Recombinant rat IgG2b isotype controls are available. Condition of sample preparation and optimal sample dilution should be determined experimentally by the investigator.
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

PA007200.m2a: Recombinant Anti-mouse CD4 Monoclonal Antibody(Clone: GK1.5), Mouse IgG2a Kappa，In vivo Grade

Elevate your immunology research with the Recombinant Anti-mouse CD4 Monoclonal Antibody (Clone: GK1.5), Mouse IgG2a Kappa, In vivo Grade from Syd Labs. This cutting-edge monoclonal antibody is engineered using advanced recombinant technology in mammalian cells, delivering exceptional purity (>95%) and ultra-low endotoxin levels (<1 EU/mg). Designed for precision and reliability, it targets mouse CD4 with the renowned GK1.5 clone, making it an indispensable tool for T cell studies, flow cytometry, ELISA, and in vivo depletion.

References for Anti-mouse CD4 Antibody – GK1.5:

1、Guidelines for the use of flow cytometry and cell sorting in immunological studies (third edition)
Andrea Cossarizza,et al.Eur J Immunol. 2024.PMCID: PMC11115438
“The third edition of anti-mouse CD4 antibody Flow Cytometry Guidelines provides the key aspects to consider when performing flow cytometry experiments and includes comprehensive sections describing phenotypes and functional assays of all major human and murine immune cell subsets. Notably, the Guidelines contain helpful tables highlighting phenotypes and key differences between human and murine cells. Another useful feature of this edition is the flow cytometry analysis of clinical samples with examples of flow cytometry applications in the context of autoimmune diseases, cancers as well as acute and chronic infectious diseases. Furthermore, there are sections detailing tips, tricks and pitfalls to avoid. All sections are written and peer-reviewed by leading flow cytometry experts and immunologists, making this edition an essential and state-of-the-art handbook for basic and clinical researchers.”

2、Guidelines for the use of flow cytometry and cell sorting in immunological studies (second edition)
Andrea Cossarizza,et al.Eur J Immunol. 2020.PMCID: PMC7350392
“These guidelines are a consensus work of a considerable number of members of the immunology and flow cytometry community. They provide the theory and key practical aspects of anti-mouse CD4 antibody flow cytometry enabling immunologists to avoid the common errors that often undermine immunological data. Notably, there are comprehensive sections of all major immune cell types with helpful Tables detailing phenotypes in murine and human cells. The latest flow cytometry techniques and applications are also described, featuring examples of the data that can be generated and, importantly, how the data can be analysed. Furthermore, there are sections detailing tips, tricks and pitfalls to avoid, all written and peer-reviewed by leading experts in the field, making this an essential research companion.”

3、Microglia Require CD4 T Cells to Complete the Fetal-to-Adult Transition
Emanuela Pasciuto,et al.Cell. 2020.PMCID: PMC7427333
“The brain is a site of relative immune privilege. Although anti-mouse CD4 antibody T cells have been reported in the central nervous system, their presence in the healthy brain remains controversial, and their function remains largely unknown. We used a combination of imaging, single cell, and surgical approaches to identify a CD69+ CD4 T cell population in both the mouse and human brain, distinct from circulating CD4 T cells. The brain-resident population was derived through in situ differentiation from activated circulatory cells and was shaped by self-antigen and the peripheral microbiome. Single-cell sequencing revealed that in the absence of murine CD4 T cells, resident microglia remained suspended between the fetal and adult states. This maturation defect resulted in excess immature neuronal synapses and behavioral abnormalities. These results illuminate a role for CD4 T cells in brain development and a potential interconnected dynamic between the evolution of the immunological and neurological systems.”

4、Th1-poised naive CD4 T cell subpopulation reflects anti-tumor immunity and autoimmune disease
Jae-Won Yoon,et al.Nat Commun. 2025.PMCID: PMC11861895
“Naïve CD4 T cells are traditionally viewed as a quiescent, homogeneous, resting population, but emerging evidence reveals their heterogeneity, which can be crucial for understanding disease contexts and therapeutic outcomes. In this study, we identify distinct subpopulations within both murine and human naïve CD4 T cells by single cell-RNA-sequencing (scRNA-seq), particularly focusing on a subpopulation that expresses super-high levels of interleukin-7 receptor (IL-7Rsup-hi), along with CD97, IL-18R, and Ly6C. This subpopulation, absent in the thymus and peripherally induced, exhibits type 1 helper T cell (Th1)-poised characteristics and contributes to the inhibition of cancer progression in B16F10 tumor-bearing mice. In humans, this IL-7Rsup-hi subpopulation expressing CD97 correlates with the responsiveness to anti-PD-1 therapy in cancer patients and the disease state of multiple sclerosis. By elucidating the heterogeneity of naive anti-mouse CD4 antibody T cells and identifying a Th1-poised subpopulation capable of robust type 1 responses, we highlight the importance of this heterogeneity in inflammatory conditions for defining the disease states and predicting drug responsiveness.”

5、Nanoparticle-based modulation of CD4+ T cell effector and helper functions enhances adoptive immunotherapy
Ariel Isser,et al.Nat Commun. 2022.PMCID: PMC9568616
“Helper (CD4+) T cells perform direct therapeutic functions and augment responses of cells such as cytotoxic (CD8+) T cells against a wide variety of diseases and pathogens. Nevertheless, inefficient synthetic technologies for expansion of antigen-specific CD4+ T cells hinders consistency and scalability of CD4+ T cell-based therapies, and complicates mechanistic studies. Here we describe a nanoparticle platform for ex vivo CD4+ T cell culture that mimics antigen presenting cells (APC) through display of major histocompatibility class II (MHC II) molecules. When combined with soluble co-stimulation signals, MHC II artificial APCs (aAPCs) expand cognate murine CD4+ T cells, including rare endogenous subsets, to induce potent effector functions in vitro and in vivo. Moreover, MHC II aAPCs provide help signals that enhance antitumor function of aAPC-activated CD8+ T cells in a mouse tumor model. Lastly, human leukocyte antigen class II-based aAPCs expand rare subsets of functional, antigen-specific human CD4+ T cells. Overall, MHC II aAPCs provide a promising approach for harnessing targeted CD4+ T cell responses.”

6、Crosstalk between CD64+MHCII+ macrophages and CD4+ T cells drives joint pathology during chikungunya
Fok-Moon Lum,et al.EMBO Mol Med. 2024.PMCID: PMC10940729
“Communications between immune cells are essential to ensure appropriate coordination of their activities. Here, we observed the infiltration of activated macrophages into the joint-footpads of chikungunya virus (CHIKV)-infected animals. Large numbers of CD64+MHCII+ and CD64+MHCII- macrophages were present in the joint-footpad, preceded by the recruitment of their CD11b+Ly6C+ inflammatory monocyte precursors. Recruitment and differentiation of these myeloid subsets were dependent on anti-mouse CD4 antibody+ T cells and GM-CSF. Transcriptomic and gene ontology analyses of CD64+MHCII+ and CD64+MHCII- macrophages revealed 89 differentially expressed genes, including genes involved in T cell proliferation and differentiation pathways. Depletion of phagocytes, including CD64+MHCII+ macrophages, from CHIKV-infected mice reduced disease pathology, demonstrating that these cells play a pro-inflammatory role in CHIKV infection. Together, these results highlight the synergistic dynamics of immune cell crosstalk in driving CHIKV immunopathogenesis. This study provides new insights in the disease mechanism and offers opportunities for development of novel anti-CHIKV therapeutics.”

7、Enhancing and inhibitory motifs regulate CD4 activity
Mark S Lee,et al.eLife. 2022.PMCID: PMC9333989
“CD4+ T cells use T cell receptor (TCR)–CD3 complexes, and CD4, to respond to peptide antigens within MHCII molecules (pMHCII). We report here that, through ~435 million years of evolution in jawed vertebrates, purifying selection has shaped motifs in the extracellular, transmembrane, and intracellular domains of eutherian CD4 that enhance pMHCII responses, and covary with residues in an intracellular motif that inhibits responses. Importantly, while CD4 interactions with the Src kinase, Lck, are viewed as key to pMHCII responses, our data indicate that CD4–Lck interactions derive their importance from the counterbalancing activity of the inhibitory motif, as well as motifs that direct CD4–Lck pairs to specific membrane compartments. These results have implications for the evolution and function of complex transmembrane receptors and for biomimetic engineering.”

8、MHC-II presentation by oral Langerhans cells impacts intraepithelial Tc17 abundance and Candida albicans oral infection via CD4 T cells
Peter D Bittner-Eddy,et al.Front Oral Health. 2024.PMCID: PMC11169704
“In a murine model (LCΔMHC-II) designed to abolish MHC-II expression in Langerhans cells (LCs), ∼18% of oral LCs retain MHC-II, yet oral mucosal anti-mouse CD4 antibody T cells numbers are unaffected. In LCΔMHC-II mice, we now show that oral intraepithelial conventional CD8αβ T cell numbers expand 30-fold. Antibody-mediated ablation of CD4 T cells in wild-type mice also resulted in CD8αβ T cell expansion in the oral mucosa. Therefore, we hypothesize that MHC class II molecules uniquely expressed on Langerhans cells mediate the suppression of intraepithelial resident-memory CD8 T cell numbers via a CD4 T cell-dependent mechanism. The expanded oral CD8 T cells co-expressed CD69 and CD103 and the majority produced IL-17A [CD8 T cytotoxic (Tc)17 cells] with a minority expressing IFN-γ (Tc1 cells). These oral CD8 T cells showed broad T cell receptor Vβ gene usage indicating responsiveness to diverse oral antigens. Generally supporting Tc17 cells, transforming growth factor-β1 (TGF-β1) increased 4-fold in the oral mucosa. Surprisingly, blocking TGF-β1 signaling with the TGF-R1 kinase inhibitor, LY364947, did not reduce Tc17 or Tc1 numbers. Nonetheless, LY364947 increased γδ T cell numbers and decreased CD49a expression on Tc1 cells. Although IL-17A-expressing γδ T cells were reduced by 30%, LCΔMHC-II mice displayed greater resistance to Candida albicans in early stages of oral infection. These findings suggest that modulating MHC-II expression in oral LC may be an effective strategy against fungal infections at mucosal surfaces counteracted by IL-17A-dependent mechanisms.”

9、The CD4 transmembrane GGXXG and juxtamembrane (C/F)CV+C motifs mediate pMHCII-specific signaling independently of CD4-LCK interactions
Mark S Lee,et al.eLife. 2024.PMCID: PMC11031086
“CD4+ T cell activation is driven by five-module receptor complexes. The T cell receptor (TCR) is the receptor module that binds composite surfaces of peptide antigens embedded within MHCII molecules (pMHCII). It associates with three signaling modules (CD3γε, CD3δε, and CD3ζζ) to form TCR-CD3 complexes. CD4 is the coreceptor module. It reciprocally associates with TCR-CD3-pMHCII assemblies on the outside of a CD4+ T cells and with the Src kinase, LCK, on the inside. Previously, we reported that the CD4 transmembrane GGXXG and cytoplasmic juxtamembrane (C/F)CV+C motifs found in eutherian (placental mammal) CD4 have constituent residues that evolved under purifying selection (Lee et al., 2022). Expressing mutants of these motifs together in T cell hybridomas increased CD4-LCK association but reduced CD3ζ, ZAP70, and PLCγ1 phosphorylation levels, as well as IL-2 production, in response to agonist pMHCII. Because these mutants preferentially localized CD4-LCK pairs to non-raft membrane fractions, one explanation for our results was that they impaired proximal signaling by sequestering LCK away from TCR-CD3. An alternative hypothesis is that the mutations directly impacted signaling because the motifs normally play an LCK-independent role in signaling. The goal of this study was to discriminate between these possibilities. Using T cell hybridomas, our results indicate that: intracellular CD4-LCK interactions are not necessary for pMHCII-specific signal initiation; the GGXXG and (C/F)CV+C motifs are key determinants of CD4-mediated pMHCII-specific signal amplification; the GGXXG and (C/F)CV+C motifs exert their functions independently of direct CD4-LCK association. These data provide a mechanistic explanation for why residues within these motifs are under purifying selection in jawed vertebrates. The results are also important to consider for biomimetic engineering of synthetic receptors.”

10、Tumor-specific cholinergic CD4+ T lymphocytes guide immunosurveillance of hepatocellular carcinoma
Chunxing Zheng,et al.Nat Cancer. 2023.PMCID: PMC10597839
“Cholinergic nerves are involved in tumor progression and dissemination. In contrast to other visceral tissues, cholinergic innervation in the hepatic parenchyma is poorly detected. It remains unclear whether there is any form of cholinergic regulation of liver cancer. Here, we show that cholinergic T cells curtail the development of liver cancer by supporting antitumor immune responses. In a mouse multihit model of hepatocellular carcinoma (HCC), we observed activation of the adaptive immune response and induction of two populations of CD4+ T cells expressing choline acetyltransferase (ChAT), including regulatory T cells and dysfunctional PD-1+ T cells. Tumor antigens drove the clonal expansion of these cholinergic T cells in HCC. Genetic ablation of Chat in T cells led to an increased prevalence of preneoplastic cells and exacerbated liver cancer due to compromised antitumor immunity. Mechanistically, the cholinergic activity intrinsic in T cells constrained Ca2+–NFAT signaling induced by T cell antigen receptor engagement. Without this cholinergic modulation, hyperactivated CD25+ T regulatory cells and dysregulated PD-1+ T cells impaired HCC immunosurveillance. Our results unveil a previously unappreciated role for cholinergic T cells in liver cancer immunobiology.”

We also provide other related Anti-Mouse CD4 antibody:
Anti-CD4 Antibody (mouse), clone GK1.5 | PA007200.m2c
Anti-mouse CD4 Antibody (Clone: GK1.5) | PA007200.m2b
Anti-mouse CD4 Antibody – GK1.5 | PA007200.m2a
Anti-mouse CD4 Monoclonal Antibody for Flow Cytometry (Clone: GK1.5) | PA007494.h1Fs
Anti-mouse CD4 Monoclonal Antibody for Flow Cytometry (Clone: GK1.5) | PA007494.r2b

We provide the following recombinant anti-human CD4 monoclonal antibodies:
Clenoliximab biosimilar, research grade, anti-human CD4 monoclonal antibody
Ibalizumab biosimilar, research grade, anti-human CD4 monoclonal antibody
Recombinant Anti-human CD4 monoclonal antibody (Clone: OKT4)
Recombinant Anti-human CD4 monoclonal antibody (Clone: OKT4A)
Recombinant Anti-human CD4 monoclonal antibody (Clone: 13B8.2)
Recombinant Anti-human CD4 monoclonal antibody (Clone: SK3 / Anti-LEU 3a)

We provide the following recombinant anti-mouse CD4 monoclonal antibodies:
Recombinant Anti-mouse CD4 monoclonal antibody (Clone: GK1.5)

We provide the following recombinant anti-human CD4 monoclonal antibodies for flow cytometry:
Recombinant Anti-human CD4 monoclonal antibody (Clone: OKT4) for flow cytometry
Recombinant Anti-human CD4 monoclonal antibody (Clone: OKT4A) for flow cytometry
Recombinant Anti-human CD4 monoclonal antibody (Clone: 13B8.2) for flow cytometry
Recombinant Anti-human CD4 monoclonal antibody (Clone: SK3 / Anti-LEU 3a) for flow cytometry

Anti-mouse CD4 Antibody(GK1.5) from: Anti-mouse CD4 Monoclonal Antibody, Mouse IgG2a Kappa (Clone: GK1.5): PA007200.m2a Syd Labs

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