Catalog No.	PA007390.hs2
Product Name	Anti-mouse CD11c Antibody (Clone: N418) | PA007390.hs2
Supplier Name	Syd Labs, Inc.
Brand Name	Syd Labs
Synonyms	αX integrin, CR4, p150, integrin alpha X
Summary	The in vivo Grade Recombinant Anti-mouse CD11c Monoclonal Antibody, Hamster IgG2 Kappa (Clone: N418) was produced in mammalian cells.
Clone	N418
Isotype	Hamster IgG2 kappa
Specificity/Sensitivity	The in vivo grade recombinant hamster monoclonal antibody (clone: N418) specifically binds to mouse CD11c.
Applications	ELISA, flow cytometry, neutralization, functional assays such as bioanalytical PK and ADA assays, and those assays for studying biological pathways affected by the mouse CD11c protein.
Form Of Antibody	0.2 μM filtered solution of 1x PBS.
Endotoxin	< 1 EU per 1 mg of the protein by the LAL method.
Purity	>95% by SDS-PAGE under reducing conditions.
Shipping	The in vivo grade recombinant anti-mouse CD11c antibodies (clone of N418) 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. 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 hamster IgG2 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

PA007390.hs2: Recombinant Anti-mouse CD11c Monoclonal Antibody (Clone: N418) , Hamster IgG2 Kappa, In vivo Grade

The in vivo grade recombinant anti-mouse CD11c hamster IgG2 monoclonal antibody was produced in mammalian cells.

The hamster anti-mouse CD11c monoclonal antibody N418 (hamster IgG2 kappa) reacts with the mouse CD11c protein, the most widely used defining marker for dendritic cells (DCs). The CD11c protein helps cells stick together and is involved in many processes, including phagocytosis, cell migration, and the activation of T cells. CD11c helps cells stick together by binding to molecules like ICAM-1, fibrinogen, and iC3b, helps cells engulf and digest other cells, helps Langerhans cells activate T cells, regulates neutrophil maturation and function, and helps dendritic cells capture and activate other cells. In addition to dendritic cells and tissue macrophages, CD11c is expressed in different B-cell lymphomas, including chronic lymphocytic leukemia. CD11c-expressing cells are also found in the mouse nervous system.

Our recombinant N418 antibodies have a part (variable regions) or complete amino acid sequences of the hamster anti-mouse CD11c monoclonal antibody (hybridoma clone name or number: N418).

References for Anti-mouse CD11c (N418):

1、Ligation of CD11c during vaccination promotes germinal centre induction and robust humoral responses without adjuvant
Ann L White,et al.Immunology. 2010.PMCID: PMC2966766
“In this study, we investigated the mouse dendritic cell (DC) receptor, complement receptor 4 (CR4; Anti-mouse CD11c/CD18), as an immunotarget for triggering humoral immunity. Comparison of antibody titres generated against a panel of 13 anti-antigen-presenting cell receptor monoclonal antibodies, with or without conjugated ovalbumin (OVA), revealed uniquely rapid and robust responses following CR4 targeting, with antibody titres approaching 1 : 100 000 7 days after a single dose of antigen. Furthermore, using just 100 ng OVA conjugated to anti-CD11c Fab′, we generated anti-OVA titres greater than those produced by a 100-fold higher dose of OVA in complete Freund’s adjuvant at day 28. These anti-OVA antibody titres were sustained and could be boosted further with targeted OVA on day 21. Investigations to explain this vaccine potency showed that, in addition to targeting splenic DC, anti-CDl1c antibodies delivered a powerful adjuvant effect and could boost humoral immunity against OVA even when the OVA was targeted to other molecules on DC, such as major histocompatibility complex class II, CD11a and CD11b. However, interestingly, this adjuvant effect was lost if OVA was targeted to other cells such as B cells via CD21 or CD19. The adjuvant effect was mediated through a marked enhancement of both germinal centre and extrafollicular plasma cell formation in responding spleens. These results demonstrate that anti-CD11c monoclonal antibody can both target antigen and act as a powerful adjuvant for rapid and sustained antibody responses. They also point to an interesting role for CR4 on DC in triggering B cells during humoral immunity.”

2、Functional characterization of CD11c+ age-associated B cells as memory B cells
Samuel W Du,et al.J Immunol. 2020.PMCID: PMC6864310
“Age-associated B cells (ABCs) are a unique subset of B cells defined by surface CD11b and Anti-mouse CD11c expression. Although ABC expansion has been observed in both human and animal studies in the setting of advanced age, during humoral autoimmunity and following viral infection, the functional properties of this cellular subset remain incompletely defined. In the current study, we demonstrate that ABCs fulfill the criteria for memory B cells, based on evidence of antigen-dependent expansion and persistence in a state poised for rapid differentiation into antibody-secreting plasma cells during secondary responses. First, we show that a majority of ABCs are not actively cycling but exhibit an extensive replication history consistent with prior antigen engagement. Second, despite unswitched surface IgM expression, ABCs show evidence of activation-induced cytidine deaminase (AID)-dependent somatic hypermutation. Third, B cells receptors (BCR) cloned from sorted ABCs exhibit broad autoreactivity and polyreactivity. Although the overall level of ABC self-reactivity was not increased relative to naïve B cells, ABCs lacked features of functional anergy characteristic of autoreactive B cells. Fourth, ABCs express memory B cell surface markers consistent with being poised for rapid plasma cell differentiation during recall responses. Finally, in a murine model of viral infection, adoptively transferred Anti-mouse CD11c+ B cells rapidly differentiated into class-switched antibody-secreting cells (ASCs) upon antigen rechallenge. In summary, we phenotypically and functionally characterize ABCs as IgM-expressing memory B cells, findings that together implicate ABCs in the pathogenesis of systemic autoimmunity.”

3、Dynamics of host immune response development during Schistosoma mansoni infection
Alice H Costain,et al.Front Immunol. 2022.PMCID: PMC9362740
“Schistosomiasis is a disease of global significance, with severity and pathology directly related to how the host responds to infection. The immunological narrative of schistosomiasis has been constructed through decades of study, with researchers often focussing on isolated time points, cell types and tissue sites of interest. However, the field currently lacks a comprehensive and up-to-date understanding of the immune trajectory of schistosomiasis over infection and across multiple tissue sites. We have defined schistosome-elicited immune responses at several distinct stages of the parasite lifecycle, in three tissue sites affected by infection: the liver, spleen, and mesenteric lymph nodes. Additionally, by performing RNA-seq on the livers of schistosome infected mice, we have generated novel transcriptomic insight into the development of schistosome-associated liver pathology and fibrosis across the breadth of infection. Through depletion of Anti-mouse CD11c+ cells during peak stages of schistosome-driven inflammation, we have revealed a critical role for Anti-mouse CD11c+ cells in the co-ordination and regulation of Th2 inflammation during infection. Our data provide an updated and high-resolution account of how host immune responses evolve over the course of murine schistosomiasis, underscoring the significance of CD11c+ cells in dictating host immunopathology against this important helminth infection.”

4、Targeting Viral Antigens to CD11c on Dendritic Cells Induces Retrovirus-Specific T Cell Responses
Asim Ejaz,et al.PLoS One. 2012.PMCID: PMC3444473
“Dendritic cells (DC) represent the most potent antigen presenting cells and induce efficient cytotoxic T lymphocyte (CTL) responses against viral infections. Targeting antigens (Ag) to receptors on DCs is a promising strategy to enhance antitumor and antiviral immune responses induced by DCs. Here, we investigated the potential of Anti-mouse CD11c-specific single-chain fragments (scFv) fused to an immunodominant peptide of Friend retrovirus for induction of virus-specific T cell responses by DCs. In Anti-mouse CD11c-specific scFv selectively targeted viral antigens to DCs and thereby significantly improved the activation of virus-specific T cells. In vaccination experiments DCs loaded with viral Ag targeted to CD11c provided improved rejection of FV-derived tumors and efficiently primed virus-specific CTL responses after virus challenge. Since the induction of strong virus-specific T cell responses is critical in viral infections, CD11c targeted protein vaccines might provide means to enhance the cellular immune response to prophylactic or therapeutic levels.”

5、Tumoricidal efficacy coincides with CD11c up-regulation in antigen-specific CD8+ T cells during vaccine immunotherapy
Yohei Takeda,et al.J Exp Clin Cancer Res. 2016.PMCID: PMC5020536
“Background
Dendritic cells (DCs) mount tumor-associated antigens (TAAs), and the double-stranded RNA adjuvant Poly(I:C) stimulates Toll-like receptor 3 (TLR3) signal in DC, which in turn induces type I interferon (IFN) and interleukin-12 (IL-12), then cross-primes cytotoxic T lymphocytes (CTLs). Proliferation of CTLs correlates with tumor regression. How these potent cells expand with high quality is crucial to the outcome of CTL therapy. However, good markers reflecting the efficacy of DC-target immunotherapy have not been addressed.
Methods
Using an EG7 (ovalbumin, OVA-positive) tumor-implant mouse model, we examined what is a good marker for active CTL induction in treatment with Poly(I:C)/OVA.
Results
Simultaneous administration of Poly(I:C) and antigen (Ag) OVA significantly increased a minor population of CD8+ T cells, that express CD11c in lymphoid and tumor sites. The numbers of the Anti-mouse CD11c+ CD8+ T cells correlated with those of induced Ag-specific CD8+ T cells and tumor regression. The CD11c+ CD8+ T cell moiety was characterized by its high killing activity and IFN-γ-producing ability, which represent an active phenotype of the effector CTLs. Not only a TLR3-specific (TICAM-1-dependent) signal but also TLR2 (MyD88) signal in DC triggered the expansion of Anti-mouse CD11c+ CD8+ T cells in tumor-bearing mice. Notably, human CD11c+ CD8+ T cells also proliferated in peripheral blood mononuclear cells (PBMC) stimulated with cytomegalovirus (CMV) Ag.
Conclusions
CD11c expression in CD8+ T cells reflects anti-tumor CTL activity and would be a marker for immunotherapeutic efficacy in mouse models and probably cancer patients as well.”

6、Renal‐infiltrating CD11c+ cells are pathogenic in murine lupus nephritis through promoting CD4+ T cell responses
X Liao,et al.Clin Exp Immunol. 2017.PMCID: PMC5629427
“Lupus nephritis (LN) is a major manifestation of systemic lupus erythematosus (SLE), causing morbidity and mortality in 40–60% of SLE patients. The pathogenic mechanisms of LN are not completely understood. Recent studies have demonstrated the presence of various immune cell populations in lupus nephritic kidneys of both SLE patients and lupus‐prone mice. These cells may play important pathogenic or regulatory roles in situ to promote or sustain LN. Here, using lupus‐prone mouse models, we showed the pathogenic role of a kidney‐infiltrating Anti-mouse CD11c+ myeloid cell population in LN. These Anti-mouse CD11c+ cells accumulated in the kidneys of lupus‐prone mice as LN progressed. Surface markers of this population suggest their dendritic cell identity and differentiation from lymphocyte antigen 6 complex (Ly6C)low mature monocytes. The cytokine/chemokine profile of these renal‐infiltrating CD11c+ cells suggests their roles in promoting LN, which was confirmed further in a loss‐of‐function in‐vivo study by using an antibody‐drug conjugate (ADC) strategy targeting CX3CR1, a chemokine receptor expressed highly on these Anti-mouse CD11c+ cells. However, CX3CR1 was dispensable for the homing of Anti-mouse CD11c+ cells into lupus nephritic kidneys. Finally, we found that these CD11c+ cells co‐localized with infiltrating T cells in the kidney. Using an ex‐ vivo co‐culture system, we showed that renal‐infiltrating CD11c+ cells promoted the survival, proliferation and interferon‐γ production of renal‐infiltrating CD4+ T cells, suggesting a T cell‐dependent mechanism by which these CD11c+ cells promote LN. Together, our results identify a pathogenic kidney‐infiltrating CD11c+ cell population promoting LN progression, which could be a new therapeutic target for the treatment of LN.”

7、CD11c/CD18 signals very late antigen-4 activation to initiate foamy monocyte recruitment during the onset of hypercholesterolemia1
Greg A Foster,et al.J Immunol. 2016.PMCID: PMC4655135
“Recruitment of foamy monocytes to inflamed endothelium expressing vascular cell adhesion molecule-1 (VCAM-1) contributes to the development of plaque during atherogenesis. Foamy Anti-mouse CD11c+ monocytes arise in the circulation during the onset of hypercholesterolemia and recruit to nascent plaque, but the mechanism of CD11c/CD18 and very late antigen-4 (VLA-4) activation and cooperation in shear resistant cell arrest on VCAM-1 is ill defined. Within one week of the onset of a Western high-fat diet (WD) in apoE-/- mice, an inflammatory subset of foamy monocytes emerged comprising ¼ of the circulating population. These cells expressed ∼3-fold more Anti-mouse CD11c/CD18 and 50% higher chemokine receptors than non-foamy monocytes. Recruitment from blood to a VCAM-1 substrate under shear stress was assessed ex-vivo using a unique artery-chip microfluidic assay. It revealed that foamy monocytes from mice on a WD increased their adhesiveness over 5 weeks, rising to twice that of mice on a normal diet (ND) or Anti-mouse CD11c-/- fed a WD. Shear resistant capture of foamy human or mouse monocytes was initiated by high affinity CD11c, which directly activated VLA-4 adhesion via phosphorylated spleen tyrosine kinase and paxillin within focal adhesion complexes. Lipid uptake and activation of CD11c are early and critical events in signaling VLA-4 adhesive function on foamy monocytes competent to recruit to VCAM-1 on inflamed arterial endothelium.”

8、Vaccination with CD47 deficient tumor cells elicits an antitumor immune response in mice
Yang Li,et al.Nat Commun. 2020.PMCID: PMC6989506
“Cancer cells are poorly immunogenic and have a wide range of mutations, which makes them unsuitable for use in vaccination treatment. Here, we show that elimination of CD47, a ligand for the myeloid cell inhibitory receptor SIRPα, from tumor cells by genetic deletion or antibody blocking, significantly improves the effectiveness of the immune response to tumour cells. In both solid and hematopoietic mouse tumor models, vaccination with tumor cells or tumor antigen-expressing cells, that lack CD47 or were pre-coated with anti-CD47 antibodies, achieved an antitumor immune response. The efficacy of this approach was synergistically enhanced when used in combination with anti-PD-1 antibodies. The induction of antitumor responses depends on SIRPα+CD11c+ DCs, which exhibit rapid expansion following introduction of CD47-deficient tumor cells. Our results indicate that CD47-deficient whole tumor cells can induce antitumor responses.”

9、Dendritic Cells Promote Macrophage Infiltration and Comprise a Substantial Proportion of Obesity-Associated Increases in CD11c+ Cells in Adipose Tissue and Liver
Maja Stefanovic-Racic,et al.Diabetes. 2012.PMCID: PMC3425427
“Obesity-associated increases in adipose tissue (AT) Anti-mouse CD11c+ cells suggest that dendritic cells (DC), which are involved in the tissue recruitment and activation of macrophages, may play a role in determining AT and liver immunophenotype in obesity. This study addressed this hypothesis. With the use of flow cytometry, electron microscopy, and loss-and-gain of function approaches, the contribution of DC to the pattern of immune cell alterations and recruitment in obesity was assessed. In AT and liver there was a substantial, high-fat diet (HFD)–induced increase in DC. In AT, these increases were associated with crown-like structures, whereas in liver the increase in DC constituted an early and reversible response to diet. Notably, mice lacking DC had reduced AT and liver macrophages, whereas DC replacement in DC-null mice increased liver and AT macrophage populations. Furthermore, delivery of bone marrow–derived DC to lean wild-type mice increased AT and liver macrophage infiltration. Finally, mice lacking DC were resistant to the weight gain and metabolic abnormalities of an HFD. Together, these data demonstrate that DC are elevated in obesity, promote macrophage infiltration of AT and liver, contribute to the determination of tissue immunophenotype, and play a role in systemic metabolic responses to an HFD.”

10、Cholesterol accumulation in CD11c+ immune cells is a causal and targetable factor in autoimmune disease
Ayaka Ito,et al.Immunity. 2017.PMCID: PMC5181791
“Liver X receptors (LXRs) are regulators of cholesterol metabolism that also modulate immune responses. Inactivation of LXR α and β in mice leads to autoimmunity; however, how the regulation of cholesterol metabolism contributes to autoimmunity is unclear. Here we found that cholesterol loading of Anti-mouse CD11c+ cells triggered the development of autoimmunity, whereas preventing excess lipid accumulation by promoting cholesterol efflux was therapeutic. LXRβ-deficient mice crossed to the hyperlipidemic ApoE-deficient background or challenged with a high-cholesterol diet developed autoantibodies. Cholesterol accumulation in lymphoid organs promoted T cell priming and stimulated the production of the B cell growth factors Baff and April. Conversely, B cell expansion and the development of autoantibodies in ApoE−/−Lxrβ−/− mice was reversed by ApoA-I expression. These findings implicate cholesterol imbalance as a contributor to immune dysfunction and suggest that stimulating HDL-dependent reverse cholesterol transport could be beneficial in the setting of autoimmune disease.”

Related Recombinant IgG Reference Antibodies:

In vivo grade recombinant hamster IgG2 isotype control antibody

Anti-mouse CD11c (N418) from: Recombinant Anti-mouse CD11c Monoclonal Antibody, Hamster IgG2 Kappa (Clone: N418): PA007390.hs2 Syd Labs

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