抗小鼠CD11c单克隆抗体(克隆号N418) ，体内实验级重组，小鼠IgG1 kappa | Syd Labs PA007390.m1

描述

PA007390.m1: Syd Labs体内实验级重组抗小鼠CD11c单克隆抗体（克隆号N418），小鼠IgG1 Kappa（In vivo Grade Recombinant Anti-mouse CD11c Monoclonal Antibody, Mouse IgG1 Kappa (Clone: N418)）

抗小鼠CD11c抗体（N418）部分参考文献:

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 CD11c+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 CD11c+ 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. 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 CD11c+ 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.”
3. Anti-Mouse CD83 Monoclonal Antibody Targeting Mature Dendritic Cells Provides Protection Against Collagen Induced Arthritis
Pablo A. Silveira,et al.Front Immunol. 2022.PMCID: PMC8866188
“Antibodies targeting the activation marker CD83 can achieve immune suppression by targeting antigen-presenting mature dendritic cells (DC). This study investigated the immunosuppressive mechanisms of anti-CD83 antibody treatment in mice and tested its efficacy in a model of autoimmune rheumatoid arthritis. A rat anti-mouse CD83 IgG2a monoclonal antibody, DCR-5, was developed and functionally tested in mixed leukocyte reactions, demonstrating depletion of CD83+ conventional (c)DC, induction of regulatory DC (DCreg), and suppression of allogeneic T cell proliferation. DCR-5 injection into mice caused partial splenic cDC depletion for 2–4 days (mostly CD8+ and CD83+ cDC affected) with a concomitant increase in DCreg and regulatory T cells (Treg). Mice with collagen induced arthritis (CIA) treated with 2 or 6 mg/kg DCR-5 at baseline and every three days thereafter until euthanasia at day 36 exhibited significantly reduced arthritic paw scores and joint pathology compared to isotype control or untreated mice. While both doses reduced anti-collagen antibodies, only 6 mg/kg achieved significance. Treatment with 10 mg/kg DCR-5 was ineffective. Immunohistological staining of spleens at the end of CIA model with CD11c, CD83, and FoxP3 showed greater DC depletion and Treg induction in 6 mg/kg compared to 10 mg/kg DCR-5 treated mice. In conclusion, DCR-5 conferred protection from arthritis by targeting CD83, resulting in selective depletion of mature cDC and subsequent increases in DCreg and Treg. This highlights the potential for anti-CD83 antibodies as a targeted therapy for autoimmune diseases.”

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背景知识

The mouse anti-mouse CD11c monoclonal antibody N418（大鼠抗小鼠CD11c单克隆抗体） (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（重组抗小鼠CD11c单克隆抗体） have a part (variable regions) or complete amino acid sequences of the mouse anti-mouse CD11c monoclonal antibody（大鼠抗小鼠CD11c抗体） (hybridoma clone name or number: N418).

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