Anti-mouse CD11c Antibody (Clone: N418) | PA007390.m1

Catalog No.	PA007390.m1
Product Name	Anti-mouse CD11c Antibody (Clone: N418) | PA007390.m1
Supplier Name	Syd Labs, Inc.
Brand Name	Syd Labs
Synonyms	X integrin, CR4, p150, integrin alpha X
Clone	N418.
Isotype	Mouse IgG1 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	Less than 1 EU/mg of protein as determined by LAL method.
Purity	>95% by SDS-PAGE under reducing conditions.
Shipping	The In vivo Grade Recombinant Anti-mouse CD11c Monoclonal Antibody, Mouse IgG1 Kappa (Clone: 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 Mouse IgG1 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.m1: Recombinant Anti-mouse CD11c Monoclonal Antibody(Clone: N418), Mouse IgG1 Kappa, In vivo Grade

The in vivo grade recombinant anti-mouse CD11c mouse IgG1 monoclonal antibody was produced in mammalian cells.

The anti-mouse CD11c monoclonal antibody N418 (Mouse IgG1 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 Antibody(N418)

1、Altered function and differentiation of age-associated B cells contribute to the female bias in lupus mice
Edd Ricker,et al.Nat Commun. 2021.PMCID: PMC8355159
“Differences in immune responses to viruses and autoimmune diseases such as systemic lupus erythematosus (SLE) can show sexual dimorphism. Age-associated B cells (ABC) are a population of anti-mouse CD11c antibody+T-bet+ B cells critical for antiviral responses and autoimmune disorders. Absence of DEF6 and SWAP-70, two homologous guanine exchange factors, in double-knock-out (DKO) mice leads to a lupus-like syndrome in females marked by accumulation of ABCs. Here we demonstrate that DKO ABCs show sex-specific differences in cell number, upregulation of an ISG signature, and further differentiation. DKO ABCs undergo oligoclonal expansion and differentiate into both anti-mouse CD11c antibody+ and CD11c− effector B cell populations with pathogenic and pro-inflammatory function as demonstrated by BCR sequencing and fate-mapping experiments. Tlr7 duplication in DKO males overrides the sex-bias and further augments the dissemination and pathogenicity of ABCs, resulting in severe pulmonary inflammation and early mortality. Thus, sexual dimorphism shapes the expansion, function and differentiation of ABCs that accompanies TLR7-driven immunopathogenesis.”

2、Rab8a restores diverse innate functions in CD11c+CD11b+ dendritic cells from aged mice
Sudhakar Singh,et al.Nat Commun. 2024.PMCID: PMC11603169
“Age-related alterations of the immune system compromise the host’s ability to respond to pathogens, but how immune aging is regulated is still poorly understood. Here, we identify via transcriptomic analysis of splenic DCs and bone marrow derived dendritic cells (BMDC) of young and aged mice, the small GTPase Rab8a as a regulator of dendritic cell (DC) functions in mice. anti-mouse CD11c antibody+CD11b+ DCs of aged in comparison to young host exhibit a diminished type I IFN response upon viral stimulation and inefficiently present exogenous antigens to CD8+ T cells in vitro and in vivo. Rab8a overexpression, which is accompanied by the upregulation of Rab11, restores the functionality of these aged DCs, whereas knockdown of Rab8a reduces functionality of DCs from young mice. Mechanistically, Rab8a and Rab11 cooperate to induce efficient trafficking of peptide loaded class I MHC molecules from the ER to the cell surface. We propose that targeting Rab8a might serve as a strategy to restore DC functionality in the context of immune aging.”

3、Transplantation-Induced Ischemia-Reperfusion Injury Modulates Antigen Presentation by Donor Renal CD11c+F4/80+ Macrophages through IL-1R8 Regulation
Sistiana Aiello,et al.J Am Soc Nephrol. 2020.PMCID: PMC7062225
“Renal macrophages are key cells in controlling processes related to inflammation or repair after ischemia-reperfusion injury. Although macrophages from a donor kidney could also guide adaptive immune responses against renal tissue by virtue of their ability to act as antigen-presenting cells, data are lacking on whether donor-derived renal macrophages can function in this manner after being subjected to transplant-induced ischemia-reperfusion injury. The authors demonstrate in mice that such injury is sufficient to dampen donor renal macrophages’ ability to present antigens, skewing them toward a proreparative phenotype. Donor renal macrophages lacking IL-1R8 failed to orchestrate tissue repair, indicating that IL-1R8 is a key regulator of this shift. IL-1R8 thus represents a pathway that merits exploration in terms of modulating responses against autoantigens and alloantigens after kidney transplant.”

4、Dendritic Cells and Microglia Have Non-redundant Functions in the Inflamed Brain with Protective Effects of Type 1 cDCs
Mattia Gallizioli,et al.Cell Rep. 2020.PMCID: PMC7578563
“Brain CD11c+ cells share features with microglia and dendritic cells (DCs). Sterile inflammation increases brain CD11c+ cells, but their phenotype, origin, and functions remain largely unknown. We report that, after cerebral ischemia, microglia attract DCs to the inflamed brain, and astroglia produce Flt3 ligand, supporting development and expansion of anti-mouse CD11c antibody+ cells. CD11c+ cells in the inflamed brain are a complex population derived from proliferating microglia and infiltrating DCs, including a major subset of OX40L+ conventional cDC2, and also cDC1, plasmacytoid, and monocyte-derived DCs. Despite sharing certain morphological features and markers, CD11c+ microglia and DCs display differential expression of pattern recognition receptors and chemokine receptors. DCs excel CD11c− and CD11c+ microglia in the capacity to present antigen through MHCI and MHCII. Of note, cDC1s protect from brain injury after ischemia. We thus reveal aspects of the dynamics and functions of brain DCs in the regulation of inflammation and immunity.”

5、CD11c regulates hematopoietic stem and progenitor cells under stress
Lifei Hou,et al.Blood Adv. 2020.PMCID: PMC7757003
“β2 integrins are well-known leukocyte adhesion molecules consisting of 4 members: CD11a-d. Their known biological functions range widely from leukocyte recruitment, phagocytosis, to immunological synapse formation, but the studies have been primarily focused on CD11a and CD11b. CD11c is 1 of the 4 members and is extremely homologous to CD11b. It has been well known as a dendritic cell marker, but the characterization of its function has been limited. We found that CD11c was expressed on the short-term hematopoietic stem cells and multipotent progenitor cells. The lack of CD11c did not affect the number of hematopoietic stem and progenitor cells (HSPCs) in healthy CD11c knockout mice. Different from other β2 integrin members, however, CD11c deficiency was associated with increased apoptosis and significant loss of HSPCs in sepsis and bone marrow transplantation. Although integrins are generally known for their overlapping and redundant roles, we showed that CD11c had a distinct role of regulating the expansion of HSPCs under stress. This study shows that CD11c, a well-known dendritic cell marker, is expressed on HSPCs and serves as their functional regulator. CD11c deficiency leads to the loss of HSPCs via apoptosis in sepsis and bone marrow transplantation.”

6、Adenosine receptor 2a agonists target mouse CD11c+T-bet+ B cells in infection and autoimmunity
Russell C Levack,et al.Nat Commun. 2022.PMCID: PMC8782827
“CD11c+T-bet+ B cells are recognized as an important component of humoral immunity and autoimmunity. These cells can be distinguished from other B cells by their higher expression of the adenosine receptor 2a. Here we address whether A2A receptor activation can affect anti-mouse CD11c antibody+T-bet+ B cells. We show that administration of the A2A receptor agonist CGS-21680 depletes established anti-mouse CD11c antibody+T-bet+ B cells in ehrlichial-infected mice, in a B cell-intrinsic manner. Agonist treatment similarly depletes anti-mouse CD11c antibody+T-bet+ B cells and CD138+ B cells and reduces anti-nuclear antibodies in lupus-prone mice. Agonist treatment is also associated with reduced kidney pathology and lymphadenopathy. Moreover, A2A receptor stimulation depletes pathogenic lymphocytes and ameliorates disease even after disease onset, highlighting the therapeutic potential of this treatment. This study suggests that targeting the adenosine signaling pathway may provide a method for the treatment of lupus and other autoimmune diseases mediated by T-bet+ B cells.”

7、CD11c+ dendritic cells PlexinD1 deficiency exacerbates airway hyperresponsiveness, IgE and mucus production in a mouse model of allergic asthma
Lianyu Shan,et al.PLoS One. 2024.PMCID: PMC11364237
“Dendritic cells (DCs) are pivotal in regulating allergic asthma. Our research has shown that the absence of Sema3E worsens asthma symptoms in acute and chronic asthma models. However, the specific role of PlexinD1 in these processes, particularly in DCs, remains unclear. This study investigates the role of PlexinD1 in anti-mouse CD11c antibody+ DCs using a house dust mite (HDM) model of asthma. We generated anti-mouse CD11c antibody+ DC-specific PlexinD1 knockout (CD11cPLXND1 KO) mice and subjected them, alongside wild-type controls (PLXND1fl/fl), to an HDM allergen protocol. Airway hyperresponsiveness (AHR) was measured using FlexiVent, and immune cell populations were analyzed via flow cytometry. Cytokine levels and immunoglobulin concentrations were assessed using mesoscale and ELISA, while collagen deposition and mucus production were examined through Sirius-red and periodic acid Schiff (PAS) staining respectively. Our results indicate that CD11cPLXND1 KO mice exhibit significantly exacerbated AHR, characterized by increased airway resistance and tissue elastance. Enhanced mucus production and collagen gene expression were observed in these mice compared to wild-type counterparts. Flow cytometry revealed higher CD11c+ MHCIIhigh CD11b+ cell recruitment into the lungs, and elevated total and HDM-specific serum IgE levels in CD11cPLXND1 KO mice. Mechanistically, co-cultures of B cells with DCs from CD11cPLXND1 KO mice showed significantly increased IgE production compared to wild-type mice.These findings highlight the critical regulatory role of the plexinD1 signaling pathway in CD11c+ DCs in modulating asthma features.”

8、Stearic acid induces CD11c expression in proinflammatory macrophages via epidermal fatty acid binding protein
Jun Zeng,et al.J Immunol. 2019.PMCID: PMC5940522
“Obesity is associated with elevated levels of free fatty acids (FFAs) and pro-inflammatory CD11c+ macrophages. However, whether and how FFAs contribute to anti-mouse CD11c antibodies+ macrophage differentiation and pro-inflammatory functions remain unclear. Here we report that dietary saturated FAs, but not unsaturated FAs, promoted the differentiation and function of anti-mouse CD11c antibodies+ macrophages. Specifically, we demonstrated that stearic acid (SA) significantly induced anti-mouse CD11c expression in monocytes through activation of the nuclear retinoid acid receptor (RAR). More importantly, cytosolic expression of epidermal fatty acid binding protein (E-FABP) in monocytes/macrophages was shown to be critical to the mediation of the SA-induced effect. Depletion of E-FABP not only inhibited SA-induced CD11c upregulation in macrophages in vitro, but also abrogated high saturated fat diet-induced skin lesions in obese mouse models in vivo. Altogether, our data demonstrate a novel mechanism by which saturated FAs promote obesity-associated inflammation through inducing E-FABP/RAR-mediated differentiation of CD11c+ macrophages.”

9、Increased susceptibility to oral Trichuris muris infection in the specific absence of CXCR5+ CD11c+ cells
Barry M Bradford,et al.Parasite Immunol. 2018.PMCID: PMC6099414
“Trichuris muris is a natural mouse helminth pathogen which establishes infection specifically in the caecum and proximal colon. The rapid expulsion of T. muris in resistant mouse strains is associated with the induction of a protective T helper cell type 2 (Th2)‐polarized immune response. Susceptible mouse strains, in contrast, mount an inappropriate Th1 response to T. muris infection. Expression of the chemokine CXCL13 by stromal follicular dendritic cells attracts CXCR5‐expressing cells towards the B‐cell follicles. Previous studies using a complex in vivo depletion model have suggested that CXCR5‐expressing conventional dendritic cells (cDC) help regulate the induction of Th2‐polarized responses. Here, transgenic mice with CXCR5 deficiency specifically restricted to CD11c+ cells were used to determine whether the specific absence CXCR5 on anti-mouse CD11c antibodies+ cells such as cDC would influence susceptibility to oral T. muris infection by affecting the Th1/Th2 balance. We show that in contrast to control mice, those which lacked CXCR5 expression on CD11c+ cells failed to clear T. muris infection and developed cytokine and antibody responses that suggested a disturbed Th1/Th2 balance with enhanced IFN‐γ expression. These data suggest an important role of CXCR5‐expressing CD11c+ cells such as cDC in immunity to oral T. muris infection.”

10、Modulation of surface CD11c expression tracks plasticity in murine intestinal tissue eosinophils
Leigha D Larsen,et al.J Leukoc Biol. 2023.PMCID: PMC9829035
“Intestinal eosinophils are implicated in the inflammatory pathology of eosinophilic gastrointestinal diseases and inflammatory bowel diseases. Eosinophils also contribute to intestinal immunologic and tissue homeostasis and host defense. Recent studies in allergic airway disease suggest functional subphenotypes of eosinophils may underly their pathogenic versus protective roles. However, subphenotypes of intestinal eosinophils have not been defined and are complicated by their constitutive expression of the putative eosinophil inflammatory marker CD11c. Here, we propose a framework for subphenotype characterization of intestinal eosinophils based on relative intensity of surface anti-mouse CD11c antibodies expression. Using this flow cytometry framework in parallel with histology and BrdU tracing, we characterize intestinal eosinophil subphenotypes and monitor their plasticity at baseline and within the context of acute allergic and chronic systemic inflammation. Data reveal a conserved continuum of anti-mouse CD11c expression amongst intestinal eosinophils in health and acute disease states that overall tracked with other markers of activation. Oral allergen challenge induced recruitment of eosinophils into small intestinal lamina propria surrounding crypts, followed by in situ induction of CD11c expression in parallel with eosinophil redistribution into intestinal villi. Allergen challenge also elicited eosinophil transepithelial migration and the appearance of CD11cloCD11bhi eosinophils in the intestinal lumen. Chronic inflammation driven by overexpression of TNFα led to a qualitative shift in the relative abundance of CD11c-defined eosinophil subphenotypes favoring CD11chi-expressing eosinophils. These findings provide new insights into heterogeneity of intestinal tissue eosinophils and offer a framework for measuring and tracking eosinophil subphenotype versatility in situ in health and disease.”

Related Recombinant IgG Reference Antibodies:

In vivo grade recombinant hamster IgG2 isotype control antibody

Anti-mouse CD11c Monoclonal Antibody(N418) from: In vivo Grade Recombinant Anti-mouse CD11c Monoclonal Antibody, Mouse IgG1 Kappa (Clone: N418): PA007390.m1 Syd Labs

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