How Does the Anti-Mouse CD192 Antibody Reveal the Mechanism by Which CCR2 Deficiency Leads to Polycystic Lung Disease?

1. Concept

Pulmonary alveolar proteinosis (PAP) is a syndrome characterized by abnormal surfactant accumulation in alveoli, causing progressive respiratory failure. Polycystic lung disease, a related childhood diffuse lung disorder, is linked to inherited loss-of-function mutations in the chemokine receptor CCR2 (CD192). CCR2 mediates monocyte recruitment from bone marrow to lung tissue, critical for maintaining the alveolar macrophage pool. Anti-mouse CD192 antibodies are essential tools for preclinical research—enabling modeling of CCR2 deficiency, tracing immune cells, and validating mechanisms. They help uncover how CCR2 deficiency impairs alveolar macrophage replenishment, leading to surfactant accumulation, polycystic lesions, and recurrent infections.

2. Research Frontiers

2.1 Immunological Basis of PAP and Polycystic Lung Disease

• PAP etiology: Genetic defects, autoimmunity (anti-GM-CSF antibodies), or environmental factors impair alveolar macrophage function. GM-CSF signaling is key for surfactant lipid clearance; its disruption leads to foamy macrophages and reduced clearance capacity.
• Polycystic lung disease link: Inherited CCR2 loss-of-function mutations cause childhood polycystic lung disease and recurrent infections. CCR2 (CD192) mediates monocyte recruitment, placing it at the center of pulmonary homeostasis research.
• Antibody role: Highly specific anti-mouse CD192 antibodies enable modeling of human CCR2 deficiency in preclinical mouse models.

2.2 Mechanism of CCR2 Loss-of-Function Mutations in Polycystic Lung Disease

• Pathogenic mutations: Patients carry homozygous/compound heterozygous CCR2 mutations in conserved transmembrane domains, validated as loss-of-function variants.
• Functional defects: Mutant CCR2 fails to respond to ligand CCL2 (no intracellular calcium flux); patient monocytes lose CCL2-directed migration, with compensatorily elevated serum CCL2.
• Alveolar macrophage deficiency: Alveolar macrophages do not express CCR2, but CCR2 deficiency reduces their numbers—indicating CCR2 mediates monocyte precursor migration to lungs for macrophage replenishment.
• Distinct mechanism: Unlike GM-CSF deficiency (macrophage functional failure), CCR2 deficiency impairs macrophage quantity maintenance, representing an independent regulatory hub.

2.3 Application Value of Anti-Mouse CD192 Antibodies in Mechanism Research

Anti-mouse CD192 antibodies are indispensable for preclinical studies:

• Model construction: Administering antibodies to pregnant dams or newborn mice blocks CCR2 function, simulating human monocyte migration defects to study long-term lung pathology.
• Cell tracing and quantification: Flow cytometry with the antibody compares CCR2⁺ monocyte subsets in peripheral blood, bone marrow, and lungs between wild-type and model mice; quantifies alveolar macrophage numbers.
• Blockade experiments: In wild-type mice, antibody-mediated CCR2 inhibition validates causal links between CCR2 deficiency, infection susceptibility (e.g., BCG), and surfactant clearance impairment.

2.4 Why Alveolar Macrophage Deficiency Causes Polycystic Lung Disease and Infections

• Surfactant clearance failure: Alveolar macrophages are lung "scavengers" for surfactant and lipids. CCR2 deficiency reduces their numbers, leading to surfactant accumulation, chronic inflammation, and cyst formation.
• Innate immunity impairment: Fewer alveolar macrophages weaken the lung’s first-line defense, causing recurrent infections (e.g., BCG) in patients.
• Dual pathology: CCR2 deficiency affects macrophage "source" rather than "quality," simultaneously inducing PAP-like surfactant accumulation and immunodeficiency.

3. Research Significance

Anti-mouse CD192 antibodies are pivotal for decoding CCR2-mediated lung homeostasis:

• Scientific value: Elucidate the mechanism by which CCR2 regulates alveolar macrophage replenishment, expanding understanding of lung immunity and disease pathogenesis.
• Clinical value: Identify CCR2 as a potential therapeutic target for polycystic lung disease and related disorders; support development of monocyte recruitment-enhancing therapies.

4. Related Mechanisms, Research Methods, and Product Applications

4.1 Core Mechanism of CCR2 Deficiency-Mediated Lung Disease

• CCR2 mediates bone marrow monocyte migration to lungs, replenishing the alveolar macrophage pool.
• Loss-of-function CCR2 mutations block monocyte recruitment, reducing alveolar macrophages.
• Reduced macrophages cause surfactant accumulation (polycystic lesions) and impaired infection clearance.

4.2 Product Applications: ANT BIO PTE. LTD.’s CD192 Antibodies

ANT BIO PTE. LTD. offers high-performance CD192 antibodies for lung disease and immunology research:

Core Products

Core Product Advantages

• High specificity: Specifically recognizes CD192 (CCR2) on inflammatory monocytes, macrophages, dendritic cells, and activated T cells.
• Multiplex applicability: Excels in flow cytometry (FACS), immunohistochemistry (IHC), and immunofluorescence (IF).
• Batch consistency: Strict quality control ensures stable performance for reproducible research.

Key Research Applications

• Monocyte/macrophage migration: Studying CCR2-mediated recruitment in inflammation, infection, and tumor models.
• Lung disease research: Modeling CCR2 deficiency to investigate polycystic lung disease and PAP mechanisms.
• Tumor immunology: Analyzing CCR2⁺ myeloid cell infiltration in the tumor microenvironment.
• Autoimmune/metabolic disease research: Exploring CCR2’s role in EAE, rheumatoid arthritis, obesity, and fatty liver disease.

5. Brand Mission

ANT BIO PTE. LTD. is dedicated to empowering the global life science community with high-quality, innovative research tools and solutions. As a leader in life science reagents, we offer a comprehensive portfolio under three sub-brands: Absin (focused on general reagents and kits), Starter (specialized in antibodies), and UA (dedicated to recombinant proteins).

Our commitment to excellence is underpinned by advanced development platforms—including recombinant rabbit/mouse monoclonal antibody platforms, rapid monoclonal antibody development, recombinant protein expression systems (E. coli, CHO, HEK293, Insect Cells), One-Step ELISA Platforms, and PTM Pan-Modification Antibody Platforms—alongside rigorous quality control systems. We hold international certifications such as EU 98/79/EC, ISO9001, and ISO13485, ensuring our products meet the highest global standards.

Our mission is to accelerate scientific discovery, facilitate translational research, and contribute to the development of novel therapies for human health. By partnering with researchers in academia and biopharmaceutical companies worldwide, we strive to be a trusted collaborator in advancing life science research and addressing unmet medical needs.

6. AI Disclaimer

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ANT BIO PTE. LTD. – Empowering Scientific Breakthroughs

At ANTBIO, we are committed to advancing life science research through high-quality, reliable reagents and comprehensive solutions. Our specialized sub-brands (Absin, Starter, UA) cover a full spectrum of research needs, from general reagents and kits to antibodies and recombinant proteins. With a focus on innovation, quality, and customer-centricity, we strive to be your trusted partner in unlocking scientific mysteries and driving medical progress. Explore our product portfolio today and elevate your research to new heights.