Catalog No.	PA007200.m2c
Product Name	Anti-CD4 Antibody (mouse), clone GK1.5 | PA007200.m2c
Supplier Name	Syd Labs, Inc.
Brand Name	Syd Labs
Uniprot ID	CD4 on UniProt.org
Gene ID	12504
Clone	GK1.5.
Isotype	Mouse IgG2c 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 IgG2c 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.m2c: Recombinant Anti-mouse CD4 Monoclonal Antibody(Clone: GK1.5), Mouse IgG2c Kapp, In vivo Grade

The Recombinant Anti-mouse CD4 Monoclonal Antibody (Clone: GK1.5) from Syd Labs is a high-purity, in vivo grade research tool designed for the specific detection and functional modulation of mouse CD4 protein. This mouse IgG2c kappa monoclonal antibody is produced recombinantly in mammalian cells, ensuring exceptional consistency and reliability for advanced immunology research,particularly in studies involving T cell biology and immune regulation.

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

1、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.”

2、Skin autonomous antibody production regulates host–microbiota interactions
Inta Gribonika,et al.Nature. 2024.PMCID: PMC11864984
“The microbiota colonizes each barrier site and broadly controls host physiology1. However, when uncontrolled, microbial colonists can also promote inflammation and induce systemic infection2. The unique strategies used at each barrier tissue to control the coexistence of the host with its microbiota remain largely elusive. Here we uncover that, in the skin, host–microbiota symbiosis depends on the ability of the skin to act as an autonomous lymphoid organ. Notably, an encounter with a new skin commensal promotes two parallel responses, both under the control of Langerhans cells. On one hand, skin commensals induce the formation of classical germinal centres in the lymph node associated with immunoglobulin G1 (IgG1) and IgG3 antibody responses. On the other hand, microbial colonization also leads to the development of tertiary lymphoid organs in the skin that can locally sustain IgG2b and IgG2c responses. These phenomena are supported by the ability of regulatory T cells to convert into T follicular helper cells. Skin autonomous production of antibodies is sufficient to control local microbial biomass, as well as subsequent systemic infection with the same microorganism. Collectively, these results reveal a compartmentalization of humoral responses to the microbiota allowing for control of both microbial symbiosis and potential pathogenesis.”

3、IL‐27 produced during acute malaria infection regulates Plasmodium‐specific memory CD4 + T cells
Maria Lourdes Macalinao,et al.EMBO Mol Med. 2023.PMCID: PMC10701605
“Malaria infection elicits both protective and pathogenic immune responses, and IL‐27 is a critical cytokine that regulate effector responses during infection. Here, we identified a critical window of anti CD4 antibodyresponses that is targeted by IL‐27. Neutralization of IL‐27 during acute infection with Plasmodium chabaudi expanded specific anti-CD4 antibody+ T cells, which were maintained at high levels thereafter. In the chronic phase, Plasmodium‐specific CD4+ T cells in IL‐27‐neutralized mice consisted mainly of CD127+KLRG1− and CD127−KLRG1+ subpopulations that displayed distinct cytokine production, proliferative capacity, and are maintained in a manner independent of active infection. Single‐cell RNA‐seq analysis revealed that these CD4+ T cell subsets formed independent clusters that express unique Th1‐type genes. These IL‐27‐neutralized mice exhibited enhanced cellular and humoral immune responses and protection. These findings demonstrate that IL‐27, which is produced during the acute phase of malaria infection, inhibits the development of unique Th1 memory precursor CD4+ T cells, suggesting potential implications for the development of vaccines and other strategic interventions.”

4、Gm40600 promotes CD4+ T‐cell responses by interacting with Ahnak
Youdi He,et al.Immunology. 2021.PMCID: PMC8358717
“It is important to characterize novel proteins involved in T‐ and B‐cell responses. Our previous study demonstrated that a novel protein, Mus musculus Gm40600, reduced the proliferation of Mus musculus plasmablast (PB)‐like SP 2/0 cells and B‐cell responses induced in vitro by LPS. In the present study, we revealed that Gm40600 directly promoted anti-CD4 antibody+ T‐cell responses to indirectly up‐regulate B‐cell responses. Importantly, we found that CD4+ T‐cell responses, including T‐cell activation and differentiation and cytokine production, were increased in Gm40600 transgenic (Tg) mice and were reduced in Gm40600 knockout (KO) mice. Finally, we demonstrated that Gm40600 promoted the Ahnak‐mediated calcium signalling pathway by interacting with Ahnak to maintain a cytoplasmic lateral location of Ahnak in CD4+ T cells. Collectively, our data suggest that Gm40600 promotes CD4+ T‐cell activation to up‐regulate the B‐cell response via interacting with Ahnak to promote the calcium signalling pathway. The results suggest that targeting Gm40600 may be a means to control CD4+ T‐cell‐related diseases.”

5、DDO-adjuvanted influenza A virus nucleoprotein mRNA vaccine induces robust humoral and cellular type 1 immune responses and protects mice from challenge
Victoria Gnazzo,et al.mBio. 2024.PMCID: PMC11796404
“A challenge in viral vaccine development is to produce vaccines that generate both neutralizing antibodies to prevent infection and cytotoxic CD8+ T-cells that target conserved viral proteins and can eliminate infected cells to control virus spread. mRNA technology offers an opportunity to design vaccines based on conserved CD8-targeting epitopes, but achieving robust antigen-specific CD8+ T-cells remains a challenge. Here, we tested the viral-derived oligonucleotide DDO268 as an adjuvant in the context of a model influenza A virus (IAV) nucleoprotein (NP) mRNA vaccine in C57BL/6 mice. DDO268 when co-packaged with mRNA in lipid nanoparticles is sensed by RIG I-like receptors and safely induces local type I interferon (IFN) production followed by dendritic cells type 1 activation and migration to the draining lymph nodes. This early response triggered by DDO268 improved the generation of IgG2c antibodies and antigen-specific Th1 CD4+ and CD8+ T-cells (IFNγ+TNFα+IL2+) that provided enhanced protection against lethal IAV challenge. In addition, the inclusion of DDO268 reduced the antigen dose required to achieve protection. These results highlight the potential of DDO268 as an effective mRNA vaccine adjuvant and show that an IAV NP mRNA/DDO268 vaccine is a promising approach for generating protective immunity against conserved internal IAV epitopes.”

6、Synergistic effect of non-neutralizing antibodies and interferon-γ for cross-protection against influenza
Meito Shibuya,et al.iScience. 2021.PMCID: PMC8482522
“Current influenza vaccines do not typically confer cross-protection against antigenically mismatched strains. To develop vaccines conferring broader cross-protection, recent evidence indicates the crucial role of both cross-reactive antibodies and viral-specific CD4+ T cells; however, the precise mechanism of cross-protection is unclear. Furthermore, adjuvants that can efficiently induce cross-protective CD4+ T cells have not been identified. Here we show that CpG oligodeoxynucleotides combined with aluminum salts work as adjuvants for influenza vaccine and confer strong cross-protection in mice. Both cross-reactive antibodies and viral-specific anti-CD4 antibody+ T cells contributed to cross-protection synergistically, with each individually ineffective. Furthermore, we found that downregulated expression of Fcγ receptor IIb on alveolar macrophages due to IFN-γ secreted by viral-specific CD4+ T cells improves the activity of cross-reactive antibodies. Our findings inform the development of optimal adjuvants for vaccines and how influenza vaccines confer broader cross-protection.”

7、ATG5-regulated CCL2/MCP-1 production in myeloid cells selectively modulates anti-malarial CD4+ Th1 responses
Yuanli Gao,et al.Autophagy. 2024.PMCID: PMC11210915
“Parasite-specific CD4+ Th1 cell responses are the predominant immune effector for controlling malaria infection; however, the underlying regulatory mechanisms remain largely unknown. This study demonstrated that ATG5 deficiency in myeloid cells can significantly inhibit the growth of rodent blood-stage malarial parasites by selectively enhancing parasite-specific anti-CD4 antibody+ Th1 cell responses. This effect was independent of ATG5-mediated canonical and non-canonical autophagy. Mechanistically, ATG5 deficiency suppressed FAS-mediated apoptosis of LY6G− ITGAM/CD11b+ ADGRE1/F4/80− cells and subsequently increased CCL2/MCP-1 production in parasite-infected mice. LY6G− ITGAM+ ADGRE1− cell-derived CCL2 selectively interacted with CCR2 on CD4+ Th1 cells for their optimized responses through the JAK2-STAT4 pathway. The administration of recombinant CCL2 significantly promoted parasite-specific CD4+ Th1 responses and suppressed malaria infection. Conclusively, our study highlights the previously unrecognized role of ATG5 in modulating myeloid cells apoptosis and sequentially affecting CCL2 production, which selectively promotes CD4+ Th1 cell responses. Our findings provide new insights into the development of immune interventions and effective anti-malarial vaccines.
Abbreviations: ATG5: autophagy related 5; CBA: cytometric bead array; CCL2/MCP-1: C-C motif chemokine ligand 2; IgG: immunoglobulin G; IL6: interleukin 6; IL10: interleukin 10; IL12: interleukin 12; MFI: mean fluorescence intensity; JAK2: Janus kinase 2; LAP: LC3-associated phagocytosis; MAP1LC3/LC3: microtubule-associated protein 1 light chain 3; pRBCs: parasitized red blood cells; RUBCN: RUN domain and cysteine-rich domain containing, Beclin 1-interacting protein; STAT4: signal transducer and activator of transcription 4; Th1: T helper 1 cell; Tfh: follicular helper cell; ULK1: unc-51 like kinase 1.”

8、Hem-1 regulates protective humoral immunity and limits autoantibody production in a B cell–specific manner
Alan Avalos,et al.JCI Insight. 2022.PMCID: PMC9090261
“Hematopoietic protein-1 (Hem-1) is a member of the actin-regulatory WASp family verprolin homolog (WAVE) complex. Loss-of-function variants in the NCKAP1L gene encoding Hem-1 were recently discovered to result in primary immunodeficiency disease (PID) in children, characterized by poor specific Ab responses, increased autoantibodies, and high mortality. However, the mechanisms of how Hem-1 deficiency results in PID are unclear. In this study, we utilized constitutive and B cell–specific Nckap1l-KO mice to dissect the importance of Hem-1 in B cell development and functions. B cell–specific disruption of Hem-1 resulted in reduced numbers of recirculating follicular (FO), marginal zone (MZ), and B1 B cells. B cell migration in response to CXCL12 and -13 were reduced. T-independent Ab responses were nearly abolished, resulting in failed protective immunity to Streptococcus pneumoniae challenge. In contrast, T-dependent IgM and IgG2c, memory B cell, and plasma cell responses were more robust relative to WT control mice. B cell–specific Hem-1–deficient mice had increased autoantibodies against multiple autoantigens, and this correlated with hyperresponsive BCR signaling and increased representation of CD11c+T-bet+ age-associated B cell (ABC cells) — alterations associated with autoimmune diseases. These results suggest that dysfunctional B cells may be part of a mechanism explaining why loss-of-function Hem-1 variants result in recurring infections and autoimmunity.”

9、A CD4+ T Cell-NK Cell Axis of Gammaherpesvirus Control
Clara Lawler,et al.J Virol. 2020.PMCID: PMC7000980
“CD4+ T cells are essential to control herpesviruses. Murid herpesvirus 4 (MuHV-4)-driven lung disease in CD4+ T-cell-deficient mice provides a well-studied example. Protective CD4+ T cells have been hypothesized to kill infected cells directly. However, removing major histocompatibility complex class II (MHCII) from LysM+ or CD11c+ cells increased MuHV-4 replication not in those cells but in type 1 alveolar epithelial cells, which lack MHCII, LysM, or CD11c. Disruption of MHCII in infected cells had no effect. Therefore, anti-CD4 antibody+ T cells engaged uninfected presenting cells and protected indirectly. Mice lacking MHCII in LysM+ or CD11c+ cells maintained systemic antiviral anti-CD4 antibody+ T cell responses, but recruited fewer anti-CD4 antibody+ T cells into infected lungs. NK cell infiltration was also reduced, and NK cell depletion normalized infection between MHCII-deficient and control mice. Therefore, NK cell recruitment seemed to be an important component of CD4+ T-cell-dependent protection. Disruption of viral CD8+ T cell evasion made this defense redundant, suggesting that it is important mainly to control CD8-evasive pathogens.
IMPORTANCE Gammaherpesviruses are widespread and cause cancers. CD4+ T cells are a key defense. We found that they defend indirectly, engaging uninfected presenting cells and recruiting innate immune cells to attack infected targets. This segregation of CD4+ T cells from immediate contact with infection helps the immune system to cope with viral evasion. Priming this defense by vaccination offers a way to protect against gammaherpesvirus-induced cancers.”

10、IL-17 mediates protective immunity against nasal infection with Bordetella pertussis by mobilizing neutrophils, especially Siglec-F+ neutrophils
Lisa Borkner,et al.Mucosal Immunol. 2021.PMCID: PMC8379078
“Understanding the mechanism of protective immunity in the nasal mucosae is central to the design of more effective vaccines that prevent nasal infection and transmission of Bordetella pertussis. We found significant infiltration of IL-17-secreting CD4+ tissue-resident memory T (TRM) cells and Siglec-F+ neutrophils into the nasal tissue during primary infection with B. pertussis. Il17A−/− mice had significantly higher bacterial load in the nasal mucosae, associated with significantly reduced infiltration of Siglec-F+ neutrophils. Re-infected convalescent mice rapidly cleared B. pertussis from the nasal cavity and this was associated with local expansion of IL-17-producing CD4+ TRM cells. Depletion of CD4 T cells from the nasal tissue during primary infection or after re-challenge of convalescent mice significantly delayed clearance of bacteria from the nasal mucosae. Protection was lost in Il17A−/− mice and this was associated with significantly less infiltration of Siglec-F+ neutrophils and antimicrobial peptide (AMP) production. Finally, depletion of neutrophils reduced the clearance of B. pertussis following re-challenge of convalescent mice. Our findings demonstrate that IL-17 plays a critical role in natural and acquired immunity to B. pertussis in the nasal mucosae and this effect is mediated by mobilizing neutrophils, especially Siglec-F+ neutrophils, which have high neutrophil extracellular trap (NET) activity.”

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 IgG2c Kappa (Clone: GK1.5): PA007200.m2c Syd Labs

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