Catalog No.	PA007200.m2b
Product Name	Anti-mouse CD4 Antibody (GK1.5, mouse IgG2b) | PA007200.m2b
Supplier Name	Syd Labs, Inc.
Brand Name	Syd Labs
Uniprot ID	CD4 on UniProt.org
Gene ID	12504
Clone	GK1.5.
Isotype	Mouse IgG2b 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.m2b: Recombinant Anti-mouse CD4 Monoclonal Antibody(Clone: GK1.5), Mouse IgG2b Kappa，In vivo Grade

The Recombinant Anti-mouse CD4 Monoclonal Antibody (Clone: GK1.5), Mouse IgG2b Kappa, In vivo Grade from Syd Labs is a state-of-the-art research reagent tailored for advanced studies in immunology and T cell biology. This antibody specifically targets the mouse CD4 receptor, a key marker for T helper cells, and is essential for investigating immune responses, autoimmunity, cancer, and transplantation. Produced using cutting-edge recombinant technology in mammalian cells, it ensures exceptional consistency, purity, and performance, setting a new standard for reliability in experimental workflows.

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

1、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 in vivo anti mouse CD4 antibody 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.”

2、Marginal zone B cells mediate a CD4 T-cell–dependent extrafollicular antibody response following RBC transfusion in mice
Patricia E Zerra,et al.Blood. 2021.PMCID: PMC8394907
“Red blood cell (RBC) transfusions can result in alloimmunization toward RBC alloantigens that can increase the probability of complications following subsequent transfusion. An improved understanding of the immune mechanisms that underlie RBC alloimmunization is critical if future strategies capable of preventing or even reducing this process are to be realized. Using the HOD (hen egg lysozyme [HEL] and ovalbumin [OVA] fused with the human RBC antigen Duffy) model system, we aimed to identify initiating immune factors that may govern early anti-HOD alloantibody formation. Our findings demonstrate that HOD RBCs continuously localize to the marginal sinus following transfusion, where they colocalize with marginal zone (MZ) B cells. Depletion of MZ B cells inhibited immunoglobulin M (IgM) and IgG anti-HOD antibody formation, whereas in vivo anti mouse CD4 antibody T-cell depletion only prevented IgG anti-HOD antibody development. HOD-specific CD4 T cells displayed similar proliferation and activation following transfusion of HOD RBCs into wild-type or MZ B-cell–deficient recipients, suggesting that IgG formation is not dependent on MZ B-cell–mediated CD4 T-cell activation. Moreover, depletion of follicular B cells failed to substantially impact the anti-HOD antibody response, and no increase in antigen-specific germinal center B cells was detected following HOD RBC transfusion, suggesting that antibody formation is not dependent on the splenic follicle. Despite this, anti-HOD antibodies persisted for several months following HOD RBC transfusion. Overall, these data suggest that MZ B cells can initiate and then contribute to RBC alloantibody formation, highlighting a unique immune pathway that can be engaged following RBC transfusion.”

3、The constitutive presence of commensal bacteria contributes to the abundance of cecal IgG2b+ B cells and the supply of serum IgG2b reactive to commensal bacteria in adult mice
Hiraku OKADA,et al.Biosci Microbiota Food Health. 2024.PMCID: PMC11957761
“Immunoglobulin (Ig) G isotypes in the sera of healthy mice and humans react to commensal bacteria. We previously reported that BALB/c mice with normal gut microbiota possessed abundant B cells that produced IgG2b reactive to commensal bacteria in cecal patches (CePs), indicating a potential source of a systemic pool of commensal bacteria-reactive IgG2b. Mice housed under germ-free conditions demonstrate the importance of the gut microbiota in driving cecal IgG2b responses. However, it is unclear whether the constitutive presence of the gut microbiota and specific bacterial taxa are important for IgG2b responses in adult mice. In this study, we showed that elimination of the gut microbiota by mixed antibiotic treatment in adult mice decreased the abundance of IgG2b+ B cells, follicular helper T (Tfh) cells in CePs, and the serum levels of commensal bacteria-reactive IgG2b. Reduced IgG2b responses have also been observed in mice with an altered gut microbiota following treatment with ampicillin or vancomycin. Changes in the diversity and composition of the cecal microbiota, particularly a decrease in Lachnospiraceae, Muribaculaceae, Ruminococcaceae, and Bacteroidaceae abundance at the family level, were observed in these mice. In addition, depletion of CD4+ T cells by the injection of neutralizing antibodies in adult mice reduced IgG2b responses. Our results suggest that specific gut bacteria susceptible to ampicillin and vancomycin play roles in providing an abundance of Tfh cells to help the generation of IgG2b+ B cells in CePs in adult mice, which may contribute to the supply of systemic commensal bacteria-reactive IgG2b.”

4、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 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.”

5、Markedly Different Pathogenicity of Four Immunoglobulin G Isotype-Switch Variants of an Antierythrocyte Autoantibody Is Based on Their Capacity to Interact in Vivo with the Low-Affinity Fcγ Receptor III
Liliane Fossati-Jimack,et al.J Exp Med. 2000.PMCID: PMC2193130
“Using three different Fcγ receptor (FcγR)-deficient mouse strains, we examined the induction of autoimmune hemolytic anemia by each of the four immunoglobulin (Ig)G isotype-switch variants of a 4C8 IgM antierythrocyte autoantibody and its relation to the contributions of the two FcγR, FcγRI, and FcγRIII, operative in the phagocytosis of opsonized particles. We found that the four IgG isotypes of this antibody displayed striking differences in pathogenicity, which were related to their respective capacity to interact in vivo with the two phagocytic FcγRs, defined as follows: IgG2a > IgG2b > IgG3/IgG1 for FcγRI, and IgG2a > IgG1 > IgG2b > IgG3 for FcγRIII. Accordingly, the IgG2a autoantibody exhibited the highest pathogenicity, ∼20–100-fold more potent than its IgG1 and IgG2b variants, respectively, while the IgG3 variant, which displays little interaction with these FcγRs, was not pathogenic at all. An unexpected critical role of the low-affinity FcγRIII was revealed by the use of two different IgG2a anti–red blood cell autoantibodies, which displayed a striking preferential utilization of FcγRIII, compared with the high-affinity FcγRI. This demonstration of the respective roles in vivo of four different IgG isotypes, and of two phagocytic FcγRs, in autoimmune hemolytic anemia highlights the major importance of the regulation of IgG isotype responses in autoantibody-mediated pathology and humoral immunity.”

6、Anti-commensal IgG Drives Intestinal Inflammation and Type 17 Immunity in Ulcerative Colitis
Tomas Castro-Dopico,et al.Immunity. 2019.PMCID: PMC6477154
“Inflammatory bowel disease is a chronic, relapsing condition with two subtypes, Crohn’s disease (CD) and ulcerative colitis (UC). Genome-wide association studies (GWASs) in UC implicate a FCGR2A variant that alters the binding affinity of the antibody receptor it encodes, FcγRIIA, for immunoglobulin G (IgG). Here, we aimed to understand the mechanisms whereby changes in FcγRIIA affinity would affect inflammation in an IgA-dominated organ. We found a profound induction of anti-commensal IgG and a concomitant increase in activating FcγR signaling in the colonic mucosa of UC patients. Commensal-IgG immune complexes engaged gut-resident FcγR-expressing macrophages, inducing NLRP3- and reactive-oxygen-species-dependent production of interleukin-1β (IL-1β) and neutrophil-recruiting chemokines. These responses were modulated by the FCGR2A genotype. In vivo manipulation of macrophage FcγR signal strength in a mouse model of UC determined the magnitude of intestinal inflammation and IL-1β-dependent type 17 immunity. The identification of an important contribution of IgG-FcγR-dependent inflammation to UC has therapeutic implications.”

7、Fc-optimized antibodies elicit CD8 immunity to viral respiratory infection
Stylianos Bournazos,et al.Nature. 2020.PMCID: PMC7672690
“Antibodies against viral pathogens represent promising therapeutic agents for the control of infection, and their antiviral efficacy has been shown to require the coordinated function of both the Fab and Fc domains1. The Fc domain engages a wide spectrum of receptors on discrete cells of the immune system to trigger the clearance of viruses and subsequent killing of infected cells1–4. Here we report that Fc engineering of anti-influenza IgG monoclonal antibodies for selective binding to the activating Fcγ receptor FcγRIIa results in enhanced ability to prevent or treat lethal viral respiratory infection in mice, with increased maturation of dendritic cells and the induction of protective CD8+ T cell responses. These findings highlight the capacity for IgG antibodies to induce protective adaptive immunity to viral infection when they selectively activate a dendritic cell and T cell pathway, with important implications for the development of therapeutic antibodies with improved antiviral efficacy against viral respiratory pathogens.”

8、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 CD4+ T cells 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.”

9、Migrant memory B cells secrete luminal antibody in the vagina
Ji Eun Oh,et al.Nature. 2019.PMCID: PMC6609483
“Antibodies secreted into the mucosal barriers serve to protect the host from a variety of pathogens, and are the basis for successful vaccines1. In type I mucosa such as the intestinal tract, dimeric IgA secreted by local plasma cells is transported through polymeric Ig receptors (pIgR)2, and mediates robust protection against viruses in the vaccinees3,4. However, due to the paucity of pIgR and plasma cells, how and whether antibodies are delivered to the type II mucosa represented by the lower female reproductive tract (FRT) lumen remains unclear. Here, using genital herpes infection in mice, we show that primary infection does not establish plasma cells in the lamina propria of FRT. Instead, upon secondary challenge with herpes simplex virus 2 (HSV-2), circulating memory B cells that enter the FRT serve as the source of rapid and robust antibody secretion into the FRT lumen. CD4 tissue-resident memory T cells (TRM) secrete interferon gamma (IFN-γ), which induces expression of chemokines including CXCL9 and CXCL10. Circulating memory B cells are recruited to the vaginal mucosa in CXCR3-dependent manner, and secrete virus-specific IgG2b, IgG2c and IgA into the FRT lumen. These results reveal circulating memory B cells as a rapidly inducible source of mucosal antibodies for the FRT.”

10、Targeting Xcr1 on Dendritic Cells Rapidly Induce Th1-Associated Immune Responses That Contribute to Protection Against Influenza Infection
Demo Yemane Tesfaye,et al.Front Immunol. 2022.PMCID: PMC8918470
“Targeting antigen to conventional dendritic cells (cDCs) can improve antigen-specific immune responses and additionally be used to influence the polarization of the immune responses. However, the mechanisms by which this is achieved are less clear. To improve our understanding, we here evaluate molecular and cellular requirements for in vivo anti mouse CD4 antibody+ T cell and antibody polarization after immunization with Xcl1-fusion vaccines that specifically target cDC1s. Xcl1-fusion vaccines induced an IgG2a/IgG2b-dominated antibody response and rapid polarization of Th1 cells both in vitro and in vivo. For comparison, we included fliC-fusion vaccines that almost exclusively induced IgG1, despite inducing a more mixed polarization of T cells. Th1 polarization and IgG2a induction with Xcl1-fusion vaccines required IL-12 secretion but were nevertheless maintained in BATF3-/- mice which lack IL-12-secreting migratory DCs. Interestingly, induction of IgG2a-dominated responses was highly dependent on the early kinetics of Th1 induction and was important for optimal protection in an influenza infection model. Early Th1 induction was dominant, since a combined Xcl1- and fliC-fusion vaccine induced IgG2a/IgG2b polarized antibody responses similar to Xcl1-fusion vaccines alone. In summary, our results demonstrate that targeting antigen to Xcr1+ cDC1s is an efficient strategy for enhancing IgG2a antibody responses through rapid Th1 induction, which can be utilized for improved vaccine design.”

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 IgG2b Kappa (Clone: GK1.5): PA007200.m2b Syd Labs

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