Autoantigens, Core Signaling Pathways, and Organ Damage Mechanisms in Systemic Lupus Erythematosus
Autoantigens, Core Signaling Pathways, and Organ Damage Mechanisms in Systemic Lupus Erythematosus
Systemic lupus erythematosus (SLE) is a systemic autoimmune disease characterized by disruption of immune tolerance, persistent exposure of nucleic acid autoantigens, autoantibody production, and immune-complex-mediated tissue injury. Its pathology is not driven by a single immune-cell population or inflammatory factor but by mutually amplifying signaling networks involving nucleic acid sensing, type I interferons, B cells, T-cell help, complement, and Fc receptors, ultimately producing highly heterogeneous multiorgan damage among individual patients.
Keywords: systemic lupus erythematosus; autoantigens; type I interferons; BAFF; B cells; immune complexes; complement; lupus nephritis
1 Disease Characteristics of Systemic Lupus Erythematosus
1.1 Disease Definition and Immunological Basis
The core abnormality in SLE is a persistent immune response against DNA, RNA, nucleosomes, Sm/RNP complexes, ribosomal P proteins, and other nuclear components. Autoantibodies bind their corresponding antigens to form immune complexes, which may persist in the circulation or deposit in glomeruli, skin, blood vessels, and other tissues and cause injury through the classical complement pathway, Fcγ receptors, and inflammatory cells. Autoantibody profiles, type I interferon signatures, immune-cell composition, and organ involvement vary among patients, giving SLE substantial mechanistic heterogeneity.
1.2 Genetic Susceptibility and Environmental Triggers
Susceptibility to SLE involves multiple categories of genes associated with HLA, complement components, nucleic acid metabolism, pattern-recognition receptors, Fc receptors, and lymphocyte signaling regulation. Genetic abnormalities generally lower the threshold for disruption of immune tolerance, allowing ultraviolet radiation, infection, sex hormones, smoking, and certain drugs to more readily induce cell death, autoantigen release, and inflammatory responses. Interactions between environmental-stimulus-induced tissue injury and pre-existing immune abnormalities can establish a persistent cycle of “antigen exposure-autoantibody production-tissue injury-additional antigen release.”
1.3 Multiorgan Involvement
SLE can affect the skin, joints, hematopoietic system, kidneys, nervous system, cardiopulmonary system, and blood vessels. Damage in different organs may be predominantly driven by immune-complex deposition, direct autoantibody effects, complement activation, vascular endothelial injury, or local cytokine networks. Disease-activity assessment therefore cannot rely on a single serum indicator.
Table 1 Major Organ Involvement and Pathological Basis of SLE
Affected System | Common Manifestations | Major Pathological Processes | Evaluation Focus |
Skin and mucosa | Malar rash, photosensitivity, and oral ulcers | Ultraviolet injury, nuclear-antigen exposure, and local IFN responses | Skin-lesion activity, basal-layer injury, and inflammatory infiltration |
Joints | Arthralgia, synovitis, and restricted movement | Immune complexes and inflammatory factors | Joint inflammation and its relationship with systemic disease activity |
Hematopoietic system | Anemia, leukopenia, and thrombocytopenia | Autoantibodies, complement-mediated destruction, and bone-marrow suppression | Blood-cell counts, hemolysis, and immune-cell subsets |
Kidneys | Proteinuria, hematuria, and abnormal renal function | Immune-complex deposition and activation of complement and Fcγ receptors | Urinary protein, urinary sediment, renal function, and histopathology |
Nervous system | Seizures and cognitive or psychiatric abnormalities | Autoantibodies, vascular injury, barrier abnormalities, and inflammation | Neurological function, imaging, and cerebrovascular status |
Cardiopulmonary system and blood vessels | Pericarditis, pleuritis, pulmonary injury, and thrombosis | Serositis, endothelial injury, NETs, and antiphospholipid antibodies | Cardiopulmonary function, coagulation, and endothelial inflammation |
2 Autoantigen Exposure and Disruption of Immune Tolerance
2.1 Impaired Clearance of Cell-Death Products
Under normal conditions, apoptotic cells and their nucleic acid components are rapidly cleared by phagocytes and degraded in a low-inflammatory environment. In SLE, increased apoptosis, reduced efferocytosis efficiency, abnormal nuclease activity, or insufficient lysosomal degradation can result in persistent exposure of nucleosomes, DNA, RNA, Sm/RNP, and ribosomal proteins. These self-components can be internalized by antigen-presenting cells and activate autoreactive T cells or bind the BCR and form immune complexes that enter immune cells through Fcγ receptors, delivering nucleic acids to endosomal TLR7 and TLR9. This establishes a pathological chain in which autoantigen exposure, nucleic acid sensing, and lymphocyte activation mutually amplify one another.
Figure 1. Impaired efferocytosis promotes autoantigen exposure and type I interferon activation in systemic lupus erythematosus
2.2 Nucleosomes and Nucleic Acid Antigens
Nucleosomes consist of DNA and histones and are important composite autoantigens released after cell death. Nucleosomes can induce anti-DNA and anti-histone responses and can simultaneously promote BCR crosslinking and nucleic acid receptor activation through their multivalent structure, giving them greater immunostimulatory capacity than individual protein antigens. Complexes formed by dsDNA, nucleosomes, and their corresponding antibodies can also deposit in glomeruli, linking autoantibody production to lupus nephritis.
2.3 Sm/RNP and Other Nuclear Protein Antigens
Sm proteins are important components of small nuclear ribonucleoprotein complexes, and subunits such as SmD1, SmD2, and SmD3 can contain multiple epitopes recognized by autoantibodies. RNP/Sm, ribosomal P0/P1/P2, PCNA, Ku, and nucleolar proteins further expand the SLE autoantigen spectrum. Different antigens can be used to investigate autoantibody specificity, cross-reactivity, and epitope spreading, but positivity for a single antibody generally cannot independently represent the degree of disease activity.
2.4 Epitope Spreading
Persistent tissue injury can release additional self-components located near the initial antigen or within the same protein complex, allowing the immune response to gradually spread from a localized epitope to multiple epitopes within the same molecule or other molecules. This process can increase the diversity of autoantibodies, allowing initially restricted immune abnormalities to develop into systemic autoimmunity and increasing the compositional complexity and tissue-deposition capacity of immune complexes.
3 Core Signaling Pathways in SLE
3.1 TLR7/9-MyD88-IRF7 Signaling
After self-RNA, RNPs, and corresponding immune complexes enter endosomes, they can activate TLR7, whereas DNA, nucleosomes, and DNA-containing immune complexes can activate TLR9. Receptor activation recruits MyD88 and activates IRF7 and NF-κB through IRAK4, IRAK1, TRAF6, and related kinase complexes. In plasmacytoid dendritic cells, this pathway mainly produces IFN-α, whereas in B cells it enhances proliferation, antigen presentation, costimulatory-molecule expression, and antibody secretion. After BCR-mediated internalization of self-antigens, nucleic acids within the complexes can further stimulate TLR7/9, producing coordinated activation of the BCR and endosomal nucleic acid receptors.
3.2 cGAS-STING-TBK1-IRF3 Signaling
Mitochondrial injury, nuclear-envelope instability, impaired DNA degradation, or insufficient NET clearance can cause DNA to enter the cytoplasm, where it is recognized by cGAS, promoting cyclic GMP-AMP production. After cGAMP binds STING, STING translocates and recruits TBK1, which phosphorylates IRF3 and induces type I interferon expression. The NF-κB branch can simultaneously enhance transcription of inflammatory genes. Because cGAS-STING and TLR9 recognize cytoplasmic and endosomal DNA, respectively, experiments should separately examine STING, p-TBK1, p-IRF3, and TLR9-associated nodes.
3.3 IFNAR-JAK1/TYK2-STAT1/2 Signaling
After IFN-α or IFN-β binds IFNAR1/IFNAR2, JAK1 and TYK2 are activated, promoting phosphorylation of STAT1 and STAT2 and formation of the ISGF3 complex with IRF9. ISGF3 enters the nucleus and induces expression of interferon-stimulated genes such as MX1, ISG15, OAS1, and the IFIT family, thereby enhancing antigen presentation, B-cell survival, monocyte activation, and neutrophil responses. Evaluation of this pathway should cover IFN proteins, p-STAT1/2, and ISG expression and should not rely solely on serum IFN-α levels.
3.4 BCR-SYK-BTK-PLCγ2 Signaling
Binding of self-antigens to the BCR induces phosphorylation of ITAM motifs on CD79A and CD79B and recruitment of SYK, followed by activation of BLNK, BTK, and PLCγ2. PLCγ2 catalyzes the conversion of PIP2 into IP3 and DAG, causing an increase in intracellular Ca²⁺ and activation of PKCβ and subsequently initiating NF-κB, NFAT, and MAPK signaling. These events promote B-cell proliferation, antigen presentation, and plasma-cell differentiation. Composite self-antigens containing DNA or RNA can also enter endosomes through the BCR, allowing BCR signaling to cooperate with TLR7/9 signaling.
3.5 BAFF-BAFF-R/TACI/BCMA Signaling
BAFF can bind BAFF-R, TACI, and BCMA. BAFF-R mainly maintains the survival of transitional and mature B cells, and its activation promotes NIK stabilization, IKKα activation, and p100 processing, ultimately producing p52/RelB-mediated noncanonical NF-κB signaling. Elevated BAFF reduces the probability that autoreactive B cells will be eliminated in the periphery, allowing cells that would normally become anergic or undergo apoptosis to survive. TACI and BCMA are more involved in regulation of plasmablasts, plasma cells, and antibody secretion. Different B-cell subsets therefore have different sensitivities to intervention in the BAFF axis.
3.6 CD40-CD40L and IL-21-STAT3 Signaling
After B cells present antigens to follicular helper T cells, CD40 on B cells binds CD40L on T cells and activates TRAF, NF-κB, and MAPK pathways, promoting germinal-center formation, immunoglobulin class switching, and affinity maturation. IL-21 secreted by Tfh cells binds IL-21R and promotes plasmablast differentiation and antibody production through JAK1/JAK3 and STAT3, whereas ICOS-ICOSL and BCL6 maintain Tfh and germinal-center responses. This pathway provides sustained T-cell help to autoreactive B cells and is an important basis for production of high-affinity autoantibodies.
3.7 PI3K-AKT-mTOR Signaling
The PI3K-AKT-mTOR pathway integrates antigen-receptor, cytokine, and nutrient signals and regulates immune-cell growth, metabolism, and differentiation. Abnormalities in this pathway in SLE can affect the balance among Treg, Th17, Tfh, and plasma cells and alter immune-cell effector states through changes in glycolysis, mitochondrial function, and protein synthesis. Experimental research should combine p-AKT, p-S6, metabolic flux, and cell-subset analysis and should avoid directly interpreting a single phosphorylation indicator as evidence of increased overall disease activity.
3.8 Classical Complement Pathway
After IgG or IgM in immune complexes binds C1q, C1r and C1s are activated, followed by cleavage of C4 and C2 and formation of the C3 convertase C4b2a. C3 cleavage produces C3a and C3b. C3b participates in immune-complex opsonization and formation of C5 convertase. C5 cleavage produces C5a and C5b, and C5b subsequently participates in assembly of the C5b-9 terminal complement complex. C3a and C5a increase vascular permeability and recruit inflammatory cells, while persistent pathway activation consumes C3 and C4. Low complement levels can therefore serve as auxiliary indicators of immune-complex-associated activity but should be interpreted together with anti-dsDNA antibodies, organ involvement, and urinary findings.
3.9 FcγR-SYK Inflammatory Signaling
IgG immune complexes can bind Fcγ receptors on neutrophils, monocytes, macrophages, and dendritic cells. Activating FcγRs recruit SYK through ITAM motifs and activate PI3K, PLCγ, MAPK, and NF-κB, promoting phagocytosis, ROS production, lysosomal release, and inflammatory-factor expression. The inhibitory receptor FcγRIIB restricts BCR and FcγR signaling through ITIM and SHIP. The balance between activating and inhibitory Fc receptors determines whether immune complexes are cleared under low-inflammatory conditions or induce persistent tissue injury.
3.10 NETs-ROS-PAD4 Signaling
After stimulation by immune complexes, C5a, and inflammatory factors, neutrophils can produce ROS and activate PAD4, resulting in histone citrullination, chromatin decondensation, and NET release. DNA, histones, and granule proteins within NETs can serve as new autoantigens and further activate pDCs, complement, and vascular endothelium, forming a positive-feedback cycle of “nucleic acid exposure-IFN production-neutrophil activation-additional NET release.” Experiments should jointly evaluate MPO-DNA complexes, CitH3, extracellular DNA, the form of cell death, and DNA-degradation capacity.
Table 2 Major SLE Signaling Pathways and Experimental Readouts
Signaling Pathway | Major Stimulus | Key Nodes | Major Output | Common Experimental Readouts |
TLR7/9-MyD88 | RNA, DNA, and nucleic acid immune complexes | MyD88, IRAK4, TRAF6, and IRF7 | IFN-α and NF-κB inflammatory outputs | p-IRAK4, IRF7, IFN-α, and ISGs |
cGAS-STING | Cytoplasmic DNA and mitochondrial DNA | cGAS, STING, TBK1, and IRF3 | Type I IFNs and inflammatory genes | cGAMP, p-STING, p-TBK1, and p-IRF3 |
IFNAR-JAK-STAT | IFN-α and IFN-β | JAK1, TYK2, STAT1/2, and IRF9 | ISG expression and immune amplification | p-STAT1/2, MX1, ISG15, and OAS1 |
BCR-BTK | Self-antigens | SYK, BTK, PLCγ2, and NF-κB | B-cell activation and antibody production | p-SYK, p-BTK, Ca²⁺, and CD69 |
BAFF-BAFF-R | BAFF | NIK, IKKα, p100/p52, and RelB | B-cell survival and maturation | BAFF, BAFF-R, p52, and B-cell subsets |
CD40-IL-21 | T-cell help signals | CD40, STAT3, and BCL6 | Germinal-center and plasma-cell differentiation | Tfh cells, plasmablasts, IgG, and antibody affinity |
Classical complement | Immune complexes | C1q, C4, C3, and C5 | Opsonization, inflammatory recruitment, and terminal-complex formation | C3, C4, C3a, C5a, and SC5b-9 |
FcγR-SYK | IgG immune complexes | FcγR, SYK, PI3K, and NF-κB | Phagocytosis, ROS, and inflammatory factors | FcγR, p-SYK, ROS, and TNF-α |
NETs-PAD4 | Immune complexes, C5a, and inflammatory factors | ROS, PAD4, and CitH3 | Nucleic acid exposure and vascular injury | MPO-DNA, CitH3, and extracellular DNA |
4 Abnormalities in Key Immune-Cell Populations
4.1 B Cells and Plasma Cells
Autoreactive B cells can escape tolerance checkpoints and expand under the combined effects of the BCR, TLR7/9, BAFF, CD40, and IL-21 and subsequently differentiate into autoantibody-producing plasmablasts and plasma cells. Total peripheral B-cell counts do not fully reflect the pathological state. Studies should distinguish naïve B cells, memory B cells, age-associated B cells, plasmablasts, and long-lived plasma cells and simultaneously evaluate autoantibody specificity, antibody levels, and immune-complex-forming capacity.
4.2 Plasmacytoid Dendritic Cells
pDCs highly express TLR7, TLR9, and IRF7 and are an important source of type I interferons after nucleic acid stimulation. Autoantibodies can promote entry of nucleic acid immune complexes into pDC endosomes through FcγRIIa, causing persistent activation of TLR7/9-IRF7 signaling. The type I interferons produced subsequently enhance B-cell, monocyte, and conventional dendritic-cell responses, making pDCs an important upstream node in the SLE immune-amplification network.
4.3 T-Cell Subsets
Tfh and peripheral helper T cells can promote B-cell differentiation and antibody production through CD40L, IL-21, and other helper signals. Th17 cells and related inflammatory factors participate in tissue injury, whereas reduced Treg numbers or suppressive function weaken immune tolerance. T-cell abnormalities also involve changes in TCR signaling, costimulation, mTOR metabolism, and cytokine receptors. T-cell function therefore cannot be evaluated solely using the CD4⁺/CD8⁺ ratio.
4.4 Neutrophils and Monocytes
Increased low-density granulocytes, enhanced NET formation, and elevated ROS can promote autoantigen exposure, complement activation, and endothelial injury. Monocytes and macrophages participate in immune-complex uptake, Fc-receptor signaling, inflammatory-factor production, and dying-cell clearance. Reduced efferocytosis and inflammatory activation can coexist in SLE, allowing insufficient clearance and tissue injury to mutually reinforce one another.
5 Mechanisms of Organ Damage
5.1 Lupus Nephritis
Immune complexes formed by DNA, nucleosomes, and corresponding autoantibodies can deposit in glomeruli and activate mesangial cells, monocytes, and neutrophils through C1q, C3, C5, and Fcγ receptors. C3a, C5a, type I interferons, NF-κB, and chemokines collectively promote glomerular inflammation, whereas injury to podocytes, endothelial cells, and renal tubular epithelial cells leads to proteinuria and declining renal function. Urinary protein alone cannot distinguish active inflammation from chronic scarring and should be interpreted together with urinary sediment, complement, autoantibodies, renal function, and histopathology.
5.2 Skin Injury
Ultraviolet radiation can induce keratinocyte apoptosis, oxidative stress, and nucleic acid release and can promote chemokine and adhesion-molecule expression through cGAS-STING, TLR, and type I interferon signaling. After immune cells enter the skin, they further damage basal-layer cells, establishing a cycle involving photosensitivity, antigen exposure, and local inflammation. The level of cutaneous activity may not be synchronized with renal or hematological activity.
5.3 Hematological and Vascular Injury
Anemia, leukopenia, and thrombocytopenia can result from multiple factors, including autoantibodies, complement-mediated destruction, chronic inflammation, impaired renal function, and drug effects. Antiphospholipid antibodies, NETs, C5a, platelet activation, and endothelial injury can collectively promote coagulation, causing arterial or venous thrombosis and pregnancy-related complications in patients with SLE. Cytopenia and thrombotic risk therefore need to be analyzed separately.
5.4 Nervous-System Injury
Neuropsychiatric SLE may involve neuroreactive autoantibodies, blood-brain barrier disruption, cerebrovascular abnormalities, complement activation, and local cytokine responses. Anti-ribosomal P antibodies and other neural-associated autoantibodies can be used in mechanistic research, but antibody positivity alone cannot demonstrate that a particular neurological symptom is directly caused by the antibody. Neurological imaging, cerebrovascular status, infection, and drug-related factors should also be considered.
6 Experimental Detection and Model Design
6.1 Autoantibody and Complement Detection
ANA is suitable for screening nuclear-antigen-associated autoimmunity but cannot independently establish SLE. Anti-dsDNA antibodies are closely associated with DNA immune complexes and renal involvement, anti-Sm antibodies have strong disease association, and anti-ribosomal P, anti-PCNA, anti-Ku, and anti-nucleolar protein antibodies can be used for autoantibody-profile stratification. C3 and C4 mainly reflect complement-component abundance and consumption, C3a and C5a reflect complement cleavage and inflammatory activation, and SC5b-9 represents the terminal complement pathway. Indicators representing different pathway levels cannot substitute for one another.
6.2 In Vitro Cellular Models
B-cell models can use individual or combined stimulation with the BCR, TLR7/9, CD40, BAFF, and IL-21 and measure p-SYK, p-BTK, NF-κB, plasmablast differentiation, and immunoglobulin production. pDC models are suitable for analyzing IFN-α induction by nucleic acid immune complexes. Neutrophil, monocyte, and endothelial-cell models can be used to investigate NETs, Fcγ receptors, complement, and vascular inflammation, respectively. Experiments should include individual stimulation, combined stimulation, receptor-blocking, and downstream-inhibition groups to establish causal relationships among upstream stimuli, signal transduction, and functional outputs.
6.3 Animal Models
NZB/W F1 mice develop anti-dsDNA antibodies, complement consumption, and immune-complex nephritis and are suitable for investigating B cells and lupus nephritis. MRL/lpr mice develop lymphocyte accumulation and multiorgan autoimmunity because of abnormal Fas signaling and are suitable for studying cell death and lymphocyte homeostasis. Inducible models can be used to analyze nucleic acid sensing and type I interferons. Different models have distinct genetic backgrounds and predominant pathological mechanisms. Drug efficacy in a single model only demonstrates activity against the major pathological processes of that model.
7 Therapeutic Targets and Mechanistic Research Directions
7.1 B Cells and the BAFF Axis
B-cell targeting can involve CD20, BAFF, BAFF-R, TACI, BCMA, and the plasma-cell survival environment. CD20 targeting mainly affects mature B cells, whereas BAFF blockade mainly reduces survival support for certain transitional and mature B cells. Long-lived plasma cells may depend more strongly on APRIL, BCMA, and the bone-marrow microenvironment. Evaluation of intervention effects should therefore simultaneously examine B-cell subsets, plasmablasts, autoantibodies, and organ activity.
7.2 Type I Interferons and the JAK-STAT Axis
IFN or IFNAR blockade can reduce JAK-STAT activation and ISG expression and is suitable for mechanistic research in models with prominent type I interferon signatures. JAK or TYK2 inhibition may simultaneously affect multiple cytokine pathways. Experiments should measure IFN proteins, p-STAT1/2, representative ISGs, and other cytokine pathways to distinguish direct IFN inhibition from broad immunomodulatory effects.
7.3 BTK, TLR, and Nucleic Acid-Sensing Axes
BTK connects BCR signaling with certain myeloid receptor pathways, whereas TLR7/9 and cGAS-STING connect self-nucleic acids with type I interferon responses. Intervention in these upstream nodes may simultaneously affect B-cell activation and innate immune amplification. However, these pathways also participate in normal anti-infective immunity, so experimental evaluation should cover disease-pathway outputs, cell survival, and immune-defense-associated functions.
7.4 Complement and Fc-Receptor Axes
Complement blockade can reduce tissue injury associated with C3a, C5a, and C5b-9, whereas Fc-receptor intervention affects immune-complex uptake, inflammatory-cell activation, and ROS release. These strategies mainly act during the effector stage after immune-complex formation and have limited effects on upstream autoantibody production. They should therefore be evaluated together with B-cell and autoantibody indicators.
8 Products for Systemic Lupus Erythematosus Research
8.1 SLE-Related Autoantigen Products
Cat. No. | Product Name | Grade & Purity | Application Positioning |
RNP/Sm (non recombinant; bovine) | Carrier Free, ≥95% (SDS-PAGE), See COA | Used for RNP/Sm-associated autoantibody binding, immunoblotting, and antigen-profile research | |
SmD | ≥80% (SDS-PAGE) | Used for SmD-associated autoantibody recognition and epitope-response research | |
SmD1 | ≥80% (SDS-PAGE) | Used for SmD1 antibody-detection systems and analysis of Sm-complex antigen specificity | |
SmD2 | ≥80% (SDS-PAGE) | Used for SmD2-associated antibody binding and antigen-epitope comparison | |
SmD3 | ≥80% (SDS-PAGE) | Used for SmD3 autoantibody responses and cross-recognition studies of the Sm protein family | |
dsDNA (plasmid) |
| Used for anti-dsDNA antibody binding, immune-complex formation, and nucleic acid-stimulation research | |
Ribosomal Phosphoprotein P0 | ≥80% (SDS-PAGE) | Used for anti-ribosomal P0 antibody recognition and autoantibody-profile research | |
Ribosomal Phosphoprotein P1 | ≥80% (SDS-PAGE) | Used for anti-ribosomal P1 antibody binding and epitope-specificity analysis | |
Ribosomal Phosphoprotein P2 | ≥80% (SDS-PAGE) | Used for anti-ribosomal P2 antibody detection and combined P-protein antigen research | |
Proliferating Cell Nuclear Antigen (PCNA) | ≥90% (SDS-PAGE) | Used for anti-PCNA autoantibody research, antigen binding, and methodological controls | |
Ku (p70/p80) | ≥85% (SDS-PAGE) | Used for anti-Ku70/Ku80 autoantibody recognition and nuclear-protein antigen-profile research | |
Sm (non recombinant; bovine) | ≥70% (SDS-PAGE) | Used to compare antibody recognition of native Sm antigen and recombinant Sm components | |
Recombinant Human Nucleolin Protein | Animal Free, Carrier Free, Fc Tag, ≥92% (SDS-PAGE) | Used for nucleolar-protein-associated autoantibodies, protein interactions, and antigen-recognition research | |
Nucleosome (non-recombinant;bovine) | ≥80% (SDS-PAGE) | Used for anti-nucleosome antibodies, DNA-histone composite antigens, and immune-complex research |
8.2 Products for Type I Interferon, BAFF, and B-Cell Axis Research
Cat. No. | Product Name | Grade & Purity | Application Positioning |
Belimumab (anti-TNFSF13B) | Animal Free, Carrier Free, Recombinant, ExactAb™, Low Endotoxin, Azide Free, Validated, ≥95% (SDS-PAGE & SEC-HPLC), See COA | Used for BAFF neutralization, blockade of B-cell survival signaling, and autoimmune-mechanism research | |
Ianalumab (anti-TNFRSF13C) | Animal Free, Carrier Free, Recombinant, ExactAb™, Low Endotoxin, Azide Free, Validated, ≥95% (SDS-PAGE & SEC-HPLC), See COA | Used for BAFF-R blockade and research on B-cell survival-receptor function | |
Rituximab (anti-CD20) | Animal Free, ≥97%, See COA | Used for targeting CD20-positive B cells and investigating B-cell-depletion mechanisms | |
BAFF Antibody | ExactAb™, Validated, 1.0 mg/mL | Used to detect BAFF protein expression and localization | |
Recombinant Human BAFF Protein | ≥95% (SDS-PAGE) | Used for BAFF-receptor binding, B-cell stimulation, and antibody screening | |
Recombinant Human BAFF/BLyS/TNFSF13B Protein | Carrier Free, Bioactive, ActiBioPure™, High Performance, PBS Only, ≥90% (SDS-PAGE), See COA | Used for BAFF-pathway activation and blockade validation | |
Recombinant Human BAFFR/TNFRSF13C Protein | Animal Free, Carrier Free, Bioactive, ActiBioPure™, Azide Free, PBS Only, ≥95% (SDS-PAGE) | Used for BAFF-BAFF-R binding and receptor-blockade research | |
Human BAFF/BLyS/TNFSF13B ELISA Kit | Bioactive, for Enzyme immunoassay(ELISA), For ELISA | Used to detect BAFF in human serum, plasma, or cell-culture supernatants | |
Human B-Cell Activating Factor (BAFF) ELISA Kit | BioReagent | Used for BAFF quantification in human samples | |
Mouse B-Cell Activating Factor (BAFF/CD257) ELISA Kit | BioReagent | Used to detect BAFF in mouse autoimmune models | |
Human B-Cell Activation Factor Receptor (BAFFR) ELISA Kit | BioReagent | Used to detect BAFFR levels in human samples | |
TNFSF13B Human Pre-designed siRNA Set A |
| Used for BAFF gene knockdown and validation of pathway dependence | |
TNFRSF13C Human Pre-designed siRNA Set A |
| Used for BAFF-R gene knockdown and receptor-function research | |
Sifalimumab (anti-IFNa1) | Animal Free, Carrier Free, Recombinant, ExactAb™, Low Endotoxin, Azide Free, Validated, ≥95% (SDS-PAGE & SEC-HPLC), See COA | Used for neutralization of multiple IFN-α subtypes and type I interferon-pathway research | |
Human Interferon Alpha (IFN-α) ELISA Kit | BioReagent | Used to detect IFN-α in human samples | |
Mouse Interferon Alpha (IFN-α) ELISA Kit | BioReagent | Used to evaluate type I interferon responses in mouse SLE models |
8.3 Products for Complement, Inflammasome, and Tissue-Inflammation Research
Cat. No. | Product Name | Grade & Purity | Application Positioning |
C1q Protein from Normal human serum | Bioactive, ActiBioPure™, Native, High Performance, ≥98% (SDS-PAGE), See COA | Used for research on immune-complex-mediated initiation of the classical complement pathway | |
ANX005 (anti-C1q) | Animal Free, Carrier Free, Recombinant, ExactAb™, Low Endotoxin, Azide Free, Validated, ≥95% (SDS-PAGE & SEC-HPLC), See COA | Used for C1q blockade and validation of the classical complement pathway | |
SC5b-9 Complex | Moligand™, PBS Only, 1.0 mg/mL, 0.22 µm Filtered | Used for functional research and detection-system development involving the terminal complement complex | |
Rabbit Anti-Human SC5b-9 Neoantigen | High Performance, PBS Only, 5 mg/mL Purified IgG Concentration, 0.09% Sodium Azide, Filtered Through a 0.22 µm Filter | Used to detect SC5b-9 deposition and terminal complement activation | |
Human Complement Component 5a (C5a) ELISA Kit | BioReagent | Used for C5a quantification in human samples and evaluation of inflammatory-recruitment signaling | |
Human Terminal Complement Complex C5b-9 (Sc5b-9) ELISA Kit | BioReagent | Used to detect activation of the terminal complement pathway | |
Mouse Complement Fragment 5a (C5a) ELISA Kit | BioReagent | Used to detect C5a in mouse SLE and lupus-nephritis models | |
Human NLR Family, Pyrin Domain Containing Protein 3 (NALP3/NLRP3) ELISA Kit | BioReagent | Used for NLRP3-associated inflammasome research | |
Caspase-1 Mouse mAb | Carrier Free, ExactAb™, Azide Free, Validated, High Performance, PBS Only, ≥95% (SDS-PAGE), 1.0 mg/mL | Used to detect Caspase-1 expression and inflammasome effector activity | |
GSDMD Antibody | Carrier Free, ExactAb™, Azide Free, Validated, High Performance, See COA | Used for research on GSDMD-associated pyroptotic signaling | |
Adenosine triphosphate（ATP） | Moligand™, ≥95% | Used as a second signal for NLRP3 inflammasome stimulation | |
MCC950 | Moligand™, ≥97% | Used for NLRP3 inhibition and validation of pathway dependence | |
Recombinant NF-kB p65 Antibody | Recombinant, ExactAb™, Validated, 0.6 mg/mL | Used to detect NF-κB-mediated pro-inflammatory signaling | |
Human Cyclooxygenase-2 (COX-2) ELISA Kit | BioReagent | Used to evaluate COX-2 and tissue-inflammatory pathways |
The pathological core of SLE is a continuously amplifying network formed among autoantigen exposure, nucleic acid sensing, type I interferons, B-cell activation, T-cell help, and complement effector mechanisms. Experimental research needs to cover upstream antigens, signaling nodes, immune-cell subsets, and organ-damage readouts simultaneously to accurately interpret disease mechanisms and intervention effects.
For more related articles, please see below:
[1] Complement System: Key Effector and Regulatory Mechanisms of the Immune System
危险品化学品经营许可证（带存储）