Are your therapeutic strategies hindered by complex complement-mediated pathologies or inefficient validation of immunomodulatory targets? Creative Biolabs' C3d specific Neutra™ antibody products empower your research with rigorously validated, high-affinity antibodies engineered through advanced recombinant protein platforms. Our solutions enable precise modulation of complement signaling, accelerating drug discovery for inflammatory and autoimmune disorders.
Complement protein C3d, a 35 kDa proteolytic fragment derived from the alpha chain of C3, serves as a critical link between innate and adaptive immunity. It acts as a molecular bridge, enhancing antigen presentation by binding to complement receptor 2 (CR2) on B cells. This interaction amplifies B cell activation and antibody production, positioning C3d as a central regulator in immune complex clearance and pathogen opsonization.
C3d adopts a compact, thioester-containing domain structure stabilized by disulfide bonds. Its surface features a conserved binding interface for CR2, facilitating interaction with B cells. Cryo-EM studies reveal that conformational changes in the thioester domain enable covalent attachment to pathogen surfaces, marking them for immune destruction.
C3d intersects with multiple pathways:
1. Complement Cascade: Integrates signals from classical, alternative, and lectin pathways, driving inflammation and pathogen clearance.
2. B Cell Activation: Binding to CR2-CD21 co-receptor complexes lowers the threshold for B cell receptor (BCR) signaling, enhancing antigen-specific antibody responses.
3. Immune Tolerance: Dysregulation of C3d-CR2 interactions contribute to autoantibody production in systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA).
Fig.1 CR2 activation by interaction with C3d-opsonized antigen.1
Elevated C3d levels correlate with severe inflammatory conditions, including C3 glomerulopathy, age-related macular degeneration, and autoimmune diseases. In cancer, C3d deposition within tumors suppresses anti-tumor immunity by promoting regulatory B cell activity. Therapeutic targeting of C3d offers promise for mitigating complement-driven tissue injury and immune hyperactivation.
Anti-C3d antibodies disrupt CR2-mediated B cell activation, reducing autoantibody production in SLE and RA models. Early-phase trials demonstrate reduced glomerular inflammation in C3 glomerulopathy patients treated with C3d inhibitors.
By neutralizing tumor-associated C3d, these antibodies reverse complement-mediated suppression of cytotoxic T cells. This approach synergizes with checkpoint inhibitors to improve tumor clearance in solid malignancies.
In age-related macular degeneration, anti-C3d therapies reduce subretinal complement deposition, slowing disease progression. Similarly, neuroinflammatory models show attenuated neuronal damage by blocking C3d-driven microglial activation.
C3d-specific antibodies serve as biomarkers for monitoring disease activity in SLE and predicting renal flare risks. Their high sensitivity supports early intervention in complement-driven pathologies.
Creative Biolabs' anti-C3d antibodies exhibit exceptional specificity for epitopes within the CR2-binding domain, effectively blocking pathogenic immune complex formation. Validated in ELISA, flow cytometry, and immunohistochemistry, these antibodies enable:
- Quantitative assessment of C3d deposition in renal or synovial biopsies.
- Functional studies on complement-mediated B cell hyperactivity.
- Preclinical evaluation of C3d-targeted inhibitors.
Creative Biolabs delivers rigorously validated C3d-specific antibodies tailored to your various research needs.
Contact our scientific team today to discuss customized solutions for your complement-focused projects.
REFERENCE
Recombinant Anti-C3d Antibody (V3S-0622-YC54) (CAT#: V3S-0622-YC54)
Target: C3d
Host Species: Mouse
Target Species: Human,
Application: ELISA,
Recombinant Anti-C3d Neutralizing Antibody (V3S-0622-YC55) (CAT#: V3S-0622-YC55)
Target: C3d
Host Species: Human
Target Species: Human,
Application: WB,FuncS,