Catalog No.	PA007200.r2b
Product Name	Anti-Mouse CD4 Antibody (GK1.5) | PA007200.r2b
Supplier Name	Syd Labs, Inc.
Brand Name	Syd Labs
Synonyms	cluster of differentiation 4, CD4
Summary	The anti-mouse CD4 monoclonal antibody (GK1.5) was produced in mammalian cells.
Uniprot ID	CD4 on UniProt.org
Gene ID	12504
Clone	GK1.5
Isotype	Rat IgG2b kappa
Specificity/Sensitivity	The recombinant rat monoclonal antibody (clone: GK1.5), in vivo grade 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 GK1.5 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.
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.r2b: Recombinant Anti-mouse CD4 Monoclonal Antibody (Clone: GK1.5), Rat IgG2b Kappa, In vivo Grade

The ‌anti mouse CD4 antibody (Clone GK1.5)‌ specifically recognizes the ‌55 kDa CD4 glycoprotein‌, a crucial cell surface marker belonging to the immunoglobulin superfamily that serves as a coreceptor for MHC class II molecules. This ‌rat IgG2b κ monoclonal antibody‌ demonstrates high affinity for mouse CD4 expressed on thymocytes, helper T cells (including Th1, Th2, Th17 subsets), regulatory T cells (Treg), NK-T cells, and weakly on dendritic cells and macrophages. As a ‌well-characterized CD4 antibody‌, GK1.5 plays essential roles in T cell development and function by stabilizing TCR-MHC II interactions through binding to conserved epitopes on the CD4 molecule.

This ‌anti CD4 monoclonal antibody‌ is particularly valuable for flow cytometry (recommended 0.5-1.0 µg per million cells), immunohistochemistry, and functional studies involving T cell activation or depletion in autoimmune disease models like experimental autoimmune encephalomyelitis (EAE). The GK1.5 clone competes with YTS 177 and YTS 191 antibodies for CD4 binding, making it an excellent tool for studying CD4-mediated signaling pathways, immune checkpoint regulation, and viral entry mechanisms (including HIV-1 and HHV-7). Available in multiple conjugates (FITC, PE, APC) or unconjugated formats, this ‌mouse CD4-specific antibody‌ remains a gold standard reagent for immunology research, enabling precise identification of CD4+ T cell subsets and evaluation of therapeutic interventions targeting CD4+ T cell function.

Syd Labs offers anti-mouse CD4 antibodies in various isotypes including Rat IgG2b, Mouse IgG2b, and Mouse IgG2a. The in vivo grade recombinant anti-mouse CD4 rat IgG2b kappa monoclonal antibody (Clone: GK1.5) of Syd Labs was produced in mammalian cells.

References for Recombinant Anti-mouse CD4 Antibodies (GK1.5):
1、In-depth cross-validation of human and mouse CD4-specific minibodies for noninvasive PET imaging of CD4+ cells and response prediction to cancer immunotherapy
Stefania Pezzana,et al.Theranostics. 2024.PMCID: PMC11373626
“Increasing evidence emphasizes the pivotal role of anti mouse CD4 antibody in orchestrating cancer immunity. Noninvasive in vivo imaging of the temporal dynamics of CD4+ T cells and their distribution patterns might provide novel insights into their effector and regulator cell functions during cancer immunotherapy (CIT).

Methods: We conducted a comparative analysis of 89Zr-labeled anti-mouse (m) and anti-human (h) CD4-targeting minibodies (Mbs) for in vivo positron emission tomography (PET)/magnetic resonance imaging (MRI) of CD4+ T cells in human xenografts, syngeneic tumor-bearing wild-type (WT), and human CD4+ knock-in (hCD4-KI) mouse models.”

2、Memory Phenotype Tfh Cells Develop Without Overt Infection and Support Germinal Center Formation and B Cell Responses to Viral Infection
Alistair L J Symonds,et al.Eur J Immunol. 2024.PMCID: PMC11739680
“Pathogen‐induced memory Tfh cells are important to maintain high‐affinity antibodies against pathogens. We have now discovered Tfh cells with a similar memory phenotype (MP) that develop in pathogen‐free conditions. These MP Tfh cells are similar to pathogen‐induced memory Tfh in both phenotype and function. They express FR4 and Egr2, which are both found in pathogen‐induced memory Tfh cells. FR4+Egr2+ anti CD4 antibody MP cells express genes involved in the development of Tfh cells and homeostatic proliferation, as well as key metabolic pathways discovered in pathogen‐induced memory Tfh cells. MP Tfh cells can support B cell–mediated IgG production in vitro and induce germinal center formation and anti‐viral antibodies in response to virus infection. These mouse MP Tfh cells share a similar phenotype to human circulating Tfh cells that are increased in Sjögren’s syndrome patients. Although Foxp3‐positive circulating T follicular regulatory (Tfr) cells are normal, a proportion of circulating Tfh cells from patients express increased levels of T‐bet, which is associated with high levels of inflammatory pathology. Thus, although they do not require overt infection for their development, MP Tfh cells are important for protective immune responses, and dysregulated MP Tfh responses may play a role in autoimmunity.”

3、Fam49b dampens TCR signal strength to regulate survival of positively selected thymocytes and peripheral T cells
Chan-Su Park,et al.eLife. 2024.PMCID: PMC11333044
“The fate of developing T cells is determined by the strength of T cell receptor (TCR) signal they receive in the thymus. This process is finely regulated through the tuning of positive and negative regulators in thymocytes. The Family with sequence similarity 49 member B (Fam49b) protein is a newly discovered negative regulator of TCR signaling that has been shown to suppress Rac-1 activity in vitro in cultured T cell lines. However, the contribution of Fam49b to the thymic development of T cells is unknown. To investigate this important issue, we generated a novel mouse line deficient in Fam49b (Fam49b-KO). We observed that Fam49b-KO double positive (DP) thymocytes underwent excessive negative selection, whereas the positive selection stage was unaffected. Fam49b deficiency impaired the survival of single positive thymocytes and peripheral T cells. This altered development process resulted in significant reductions in anti mouse CD4 antibody and CD8 single-positive thymocytes as well as peripheral T cells. Interestingly, a large proportion of the TCRγδ+ and CD8αα+TCRαβ+ gut intraepithelial T lymphocytes were absent in Fam49b-KO mice. Our results demonstrate that Fam49b dampens thymocytes TCR signaling in order to escape negative selection during development, uncovering the function of Fam49b as a critical regulator of the selection process to ensure normal thymocyte development and peripheral T cells survival.”

4、One CD4+TCR and one CD8+TCR targeting autochthonous neoantigens are essential and sufficient for tumor eradication
Steven P Wolf,et al.Clin Cancer Res. 2024.PMCID: PMC11018470
“To achieve eradication of solid tumors, we examined how many neoantigens need to be targeted with how many TCRs by which type of T cells.

Experimental Design:
Unmanipulated, naturally expressed (autochthonous) neoantigens were targeted with adoptively transferred TCR-engineered autologous T cells (TCR-therapy). TCR-therapy used CD8+ T cell subsets engineered with TCRs isolated from CD8+ T cells (CD8+TCR-therapy), anti mouse CD4 antibody subsets engineered with TCRs isolated from CD4+ T cells (CD4+TCR-therapy) or combinations of both. The targeted tumors were established for at least 3 weeks and derived from primary autochthonous cancer cell cultures, resembling natural solid tumors and their heterogeneity as found in humans.”

5、B cells in the pneumococcus-infected lung are heterogeneous and require CD4+ T cell help including CD40L to become resident memory B cells
Neelou S Etesami,et al.Front Immunol. 2024.PMCID: PMC11074383
“Recovery from respiratory pneumococcal infections generates lung-localized protection against heterotypic bacteria, mediated by resident memory lymphocytes. Optimal protection in mice requires re-exposure to pneumococcus within days of initial infection. Serial surface marker phenotyping of B cell populations in a model of pneumococcal heterotypic immunity revealed that bacterial re-exposure stimulates the immediate accumulation of dynamic and heterogeneous populations of B cells in the lung, and is essential for the establishment of lung resident memory B (BRM) cells. The B cells in the early wave were activated, proliferating locally, and associated with both anti CD4 antibody and CXCL13. Antagonist- and antibody-mediated interventions were implemented during this early timeframe to demonstrate that lymphocyte recirculation, CD4+ cells, and CD40 ligand (CD40L) signaling were all needed for lung BRM cell establishment, whereas CXCL13 signaling was not. While most prominent as aggregates in the loose connective tissue of bronchovascular bundles, morphometry and live lung imaging analyses showed that lung BRM cells were equally numerous as single cells dispersed throughout the alveolar septae. We propose that CD40L signaling from antigen-stimulated CD4+ T cells in the infected lung is critical to establishment of local BRM cells, which subsequently protect the airways and parenchyma against future potential infections.”

6、Oncolytic viruses expressing MATEs facilitate target-independent T-cell activation in tumors
Malin Peter,et al.EMBO Mol Med. 2025.PMCID: PMC11821991
“Oncolytic viruses (OV) expressing bispecific T-cell engagers (BiTEs) are promising tools for tumor immunotherapy but the range of target tumors is limited. To facilitate effective T-cell stimulation with broad-range applicability, we established membrane-associated T-cell engagers (MATEs) harboring the protein transduction domain of the HIV-Tat protein to achieve non-selective binding to target cells. In vitro, MATEs effectively activated murine T cells and improved killing of MC38 colon carcinoma cells. Similarly, humanized MATEs activated T cells in PBMCs from human donors. In MC38-tumors in mice, MATE-expression by the oncolytic adenovirus Ad5/11 facilitated intratumoral T-cell activation, reduced tumor growth and prolonged survival accompanied by infiltration of tumor-directed CD8+ T cells and improved anti mouse CD8/CD4 antibodies ratio. Absence of early T-cell activation in tumor draining lymph nodes suggests the safe applicability of this strategy. Furthermore, MATE-expression by Ad5/11 was capable of breaking resistance to αPD-1 checkpoint therapy thereby promoting T-cell/tumor cell proximity and clustering of CD8+ and CD4+ T cells. In summary, we demonstrated that MATE expressing OVs are powerful T-cell activating tools suitable for local immunotherapy of a broad range of tumors.”

7、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 antibody 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.”

8、CD4+ and CD8+ T cells are required to prevent SARS-CoV-2 persistence in the nasal compartment
Meenakshi Kar,et al.Sci Adv. 2024.PMCID: PMC11343035
“SARS-CoV-2 infection induces the generation of virus-specific CD4+ and CD8+ effector and memory T cells. However, the contribution of T cells in controlling SARS-CoV-2 during infection is not well understood. Following infection of C57BL/6 mice, SARS-CoV-2–specific CD4+ and CD8+ T cells are recruited to the respiratory tract, and a vast proportion secrete the cytotoxic molecule granzyme B. Using depleting antibodies, we found that T cells within the lungs play a minimal role in viral control, and viral clearance occurs in the absence of both CD4+ and CD8+ T cells through 28 days postinfection. In the nasal compartment, depletion of both CD4+ and CD8+ T cells, but not individually, results in persistent, culturable virus replicating in the nasal epithelial layer through 28 days postinfection. Viral sequencing analysis revealed adapted mutations across the SARS-CoV-2 genome, including a large deletion in ORF6. Overall, our findings highlight the importance of T cells in controlling virus replication within the respiratory tract during SARS-CoV-2 infection.”

9、Distinct Requirements for CD4+ T Cell Help for Immune Responses Induced by mRNA and Adenovirus‐Vector SARS‐CoV‐2 Vaccines
Lyn Yong,et al.Eur J Immunol. 2024.PMCID: PMC11739681
“CD4 antibody have been established as central orchestrators of cellular and humoral immune responses to infection or vaccination. However, the need for CD4+ T cell help to generate primary CD8+ T cell responses is variable depending on the infectious agent or vaccine and yet consistently required for the recall of CD8+ T cell memory responses or antibody responses. Given the deployment of new vaccine platforms such as nucleoside‐modified mRNA vaccines, we sought to elucidate the requirement for anti mouse cd4 antibody help in the induction of cellular and antibody responses to mRNA and adenovirus (Ad)‐vectored vaccines against SARS‐CoV‐2. Using antibody‐mediated depletion of CD4+ T cells in a mouse immunization model, we observed that CD4+ T cell help was dispensable for both primary and secondary CD8+ T cell responses to the BNT162b2 and mRNA‐1273 mRNA vaccines but required for the AZD1222 Ad‐vectored vaccine. Nonetheless, CD4+ T cell help was needed by both mRNA and Ad‐vectored vaccine platforms for the generation of antibodies, demonstrating the centrality of CD4+ T cells in vaccine‐induced protective immunity against SARS‐CoV‐2. Ultimately, this highlights the shared and distinct regulation of humoral and cellular responses induced by these vaccine platforms.”

10、Neuronal-enriched small extracellular vesicles trigger a PD-L1-mediated broad suppression of T cells in Parkinson’s disease
Zhichun Chen,et al.iScience. 2024.PMCID: PMC11246066
“Many clinical studies indicate a significant decrease of peripheral T cells in Parkinson’s disease (PD). There is currently no mechanistic explanation for this important observation. Here, we found that small extracellular vesicles (sEVs) derived from in vitro and in vivo PD models suppressed IL-4 and INF-γ production from both purified CD4+ and CD8+ T cells and inhibited their activation and proliferation. Furthermore, neuronal-enriched sEVs (NEEVs) isolated from plasma of A53T-syn mice and culture media of human dopaminergic neurons carrying A53T-syn mutation also suppressed Th1 and Th2 differentiation of naive CD4+ T cells. Mechanistically, the suppressed phenotype induced by NEEVs was associated with altered programmed death ligand 1 (PD-L1) level in T cells. Blocking PD-L1 with an anti-PD-L1 antibody or a small molecule inhibitor BMS-1166 reversed T cell suppression. Our study provides the basis for exploring peripheral T cells in PD pathogenesis and as biomarkers or therapeutic targets for the disease.”

11、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 anti CD4 antibody 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 CD4 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.”

12、Complement C3 and marginal zone B cells promote IgG-mediated enhancement of RBC alloimmunization in mice
Arijita Jash,et al.J Clin Invest. 2024.PMCID: PMC11014669
“Administration of anti-RhD immunoglobulin (Ig) to decrease maternal alloimmunization (antibody-mediated immune suppression [AMIS]) was a landmark clinical development. However, IgG has potent immune-stimulatory effects in other settings (antibody-mediated immune enhancement [AMIE]). The dominant thinking has been that IgG causes AMIS for antigens on RBCs but AMIE for soluble antigens. However, we have recently reported that IgG against RBC antigens can cause either AMIS or AMIE as a function of an IgG subclass. Recent advances in mechanistic understanding have demonstrated that RBC alloimmunization requires the IFN-α/-β receptor (IFNAR) and is inhibited by the complement C3 protein. Here, we demonstrate the opposite for AMIE of an RBC alloantigen (IFNAR is not required and C3 enhances). RBC clearance, C3 deposition, and antigen modulation all preceded AMIE, and both anti mouse CD4 antibody and marginal zone B cells were required. We detected no significant increase in antigen-specific germinal center B cells, consistent with other studies of RBC alloimmunization that show extrafollicular-like responses. To the best of our knowledge, these findings provide the first evidence of an RBC alloimmunization pathway which is IFNAR independent and C3 dependent, thus further advancing our understanding of RBCs as an immunogen and AMIE as a phenomenon.”

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: In vivo Grade Recombinant Anti-mouse CD4 Rat IgG2b Kappa Monoclonal Antibody (Clone: GK1.5): PA007200.r2b Syd Labs

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