| Biomarker | HLA-DRB1 alleles (e.g., HLA-DRB1*04/*01) | Full name | Human Leukocyte Antigen DRB1 alleles | Molecular Type | nucleic acid (genetic marker) |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Genetic risk prediction | ||
| Disease(or Constitution) | Rheumatoid Arthritis (RA) | Disease Subtypes | / | ||
| Organ | Immune system | Test Sample / Technology Platform | Blood (PCR-seq, gene chip) | ||
| Pathobiological Mechanisms | The RA core genetic susceptibility locus activates T cells by presenting self-antigens, with a familial contribution rate of approximately 60%. | ||||
| Clinical Availability Status | Research phase | ||||
| Notes and Dynamics | Individuals carrying the HLA-DRB1*04/*04 homozygote have a 5.8-fold higher risk of developing rheumatoid arthritis (RA) compared to the general population; this risk is further increased when combined with environmental factors. | ||||
| Biomarker | Tfh cells | Full name | T follicle helper cells | Molecular Type | immunocyte,immunological cell |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Response Prediction to Treatment (Abazap) | ||
| Disease(or Constitution) | Rheumatoid Arthritis (RA) | Disease Subtypes | / | ||
| Organ | Immune system | Test Sample / Technology Platform | Peripheral blood (flow cytometry, HIPC standardized protocol) | ||
| Pathobiological Mechanisms | Regulates germinal center formation and autoantibody production, mediates B cell activation, and its peripheral blood proportion is closely associated with the therapeutic response to abacizumab. | ||||
| Clinical Availability Status | Scientific research verification | ||||
| Notes and Dynamics | Independent predictive factors provide a basis for clinical individualized selection of biologics; they should be combined with other immune cell phenotype analyses. | ||||
| Biomarker | pDCs | Full name | plasmacytoid dendritic cells | Molecular Type | immunocyte,immunological cell |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Response Prediction to Treatment (TNF-α Inhibitors) | ||
| Disease(or Constitution) | Rheumatoid Arthritis (RA) | Disease Subtypes | / | ||
| Organ | Immune system | Test Sample / Technology Platform | Peripheral blood (flow cytometry, HIPC standardized protocol) | ||
| Pathobiological Mechanisms | Participates in the type I interferon response, regulates autoantibody production and immune cell activation, with its peripheral blood proportion positively correlated with the efficacy of TNF-α inhibitors. | ||||
| Clinical Availability Status | Scientific research verification | ||||
| Notes and Dynamics | It is an independent predictor of TNF-α inhibitor efficacy, with a high proportion of patients showing an improvement in treatment response rate by more than 30%; standardized flow panel testing is required to ensure comparability of results. | ||||
| Biomarker | IL-6 | Full name | Interleukin-6 | Molecular Type | cell factor |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Systemic inflammation assessment and treatment monitoring | ||
| Disease(or Constitution) | Rheumatoid Arthritis (RA) | Disease Subtypes | / | ||
| Organ | Joint (Synovium, Systemic) | Test Sample / Technology Platform | Serum, synovial fluid (ELISA, electrochemiluminescence assay) | ||
| Pathobiological Mechanisms | Mediates acute-phase reactions (e.g., CRP, SAA synthesis), promotes B-cell differentiation into plasma cells and autoantibody production, and participates in extra-articular manifestations. | ||||
| Clinical Availability Status | Widespread availability (assisted evaluation + target monitoring) | ||||
| Notes and Dynamics | IL-6 inhibitors (e.g., tocilizumab) rapidly reduce systemic inflammatory markers and demonstrate significant advantages in patients with rheumatoid arthritis (RA) who also have anemia or hypercoagulability. | ||||
| Biomarker | TNF-α | Full name | Tumor Necrosis Factor-α | Molecular Type | cell factor |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Inflammatory regulation, targeted therapy monitoring | ||
| Disease(or Constitution) | Rheumatoid Arthritis (RA) | Disease Subtypes | / | ||
| Organ | Joint (Synovium) | Test Sample / Technology Platform | Serum, synovial fluid (ELISA, flow cytometry) | ||
| Pathobiological Mechanisms | The core pro-inflammatory factors secreted by synovial macrophages and T cells activate the NF-κB pathway, promoting the release of inflammatory factors and inducing synovial hyperplasia and bone erosion; this is a key target of TNF-α inhibitors. | ||||
| Clinical Availability Status | Widespread availability (assisted evaluation + target monitoring) | ||||
| Notes and Dynamics | Patients who achieved a serum level of TNF-α inhibitor <8 pg/mL after treatment showed a significant increase in ACR20 attainment rate, which can serve as an immediate monitoring indicator of therapeutic response. | ||||
| Biomarker | SAA | Full name | Serum Amyloid A | Molecular Type | protein |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Assessment of early inflammatory activity | ||
| Disease(or Constitution) | Rheumatoid Arthritis (RA) | Disease Subtypes | Rheumatoid arthritis (early stage, disease duration ≤24 months) | ||
| Organ | Joint (Synovium) | Test Sample / Technology Platform | Serum (immunoturbidimetry, latex-enhanced immunoturbidimetry) | ||
| Pathobiological Mechanisms | Regulated by IL-6 and TNF-α, it participates in neutrophil chemotaxis and synovial inflammation amplification, with its level changes occurring earlier than those of CRP. | ||||
| Clinical Availability Status | Clinical Promotion | ||||
| Notes and Dynamics | It demonstrates higher sensitivity than CRP for early inflammatory activity in rheumatoid arthritis (RA); shows good response to conventional disease-modifying anti-rheumatic drugs (DMARDs). | ||||
| Biomarker | AKA | Full name | Antikeratin antibodies | Molecular Type | protein ( autoantibody ) |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Early diagnosis and bone erosion risk assessment | ||
| Disease(or Constitution) | Rheumatoid Arthritis (RA) | Disease Subtypes | Rheumatoid arthritis (early stage, disease duration ≤24 months) | ||
| Organ | Joint (Synovium, Bone) | Test Sample / Technology Platform | Serum (Indirect Immunofluorescence) | ||
| Pathobiological Mechanisms | Identification of keratin protein antigens, associated with synovial fibroblast activation and osteoclast differentiation, can become positive 1-2 years prior to disease onset. | ||||
| Clinical Availability Status | Clinical auxiliary use | ||||
| Notes and Dynamics | Early bone erosion can be predicted; the detection method relies on subjective interpretation and is not used as a standalone first-line diagnostic indicator. | ||||
| Biomarker | APF | Full name | Antipolyadenylate factor | Molecular Type | protein ( autoantibody ) |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Early seronegative RA diagnosis | ||
| Disease(or Constitution) | Rheumatoid Arthritis (RA) | Disease Subtypes | seronegative type | ||
| Organ | Joint (Synovium) | Test Sample / Technology Platform | Serum (Indirect Immunofluorescence) | ||
| Pathobiological Mechanisms | Targeting the perinuclear antigen of buccal mucosal epithelial cells to activate T cell-mediated cellular immune responses can be detected in patients with RF and anti-CCP antibody negativity. | ||||
| Clinical Availability Status | Clinical auxiliary use | ||||
| Notes and Dynamics | The diagnostic specificity is approximately 90%, but the sensitivity is only40%-50%；Concomitant anti-keratin antibodies are required to enhance diagnostic accuracy | ||||
| Biomarker | anti-CSP | Full name | Anticardiacine scavenger receptor A polypeptide antibody | Molecular Type | protein ( autoantibody ) |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Seronegative RA diagnosis and disease management | ||
| Disease(or Constitution) | Rheumatoid Arthritis (RA) | Disease Subtypes | seronegative type | ||
| Organ | Joint (Synovium) | Test Sample / Technology Platform | Serum (ELISA) | ||
| Pathobiological Mechanisms | The carboxylylated SR-A peptide exhibits aberrant glycosylation modifications, which can promote the secretion of inflammatory factors by chondrocyte-like organs, exacerbating synovial inflammation and bone destruction. | ||||
| Clinical Availability Status | Clinical trials | ||||
| Notes and Dynamics | Diagnostic sensitivity of 58.98% and specificity of 93.96%, indicating a potential therapeutic target. | ||||
| Biomarker | anti-PAD4 | Full name | Antipolyarginyldeimidease 4 antibody | Molecular Type | protein ( autoantibody ) |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Seronegative RA diagnosis and bone injury prediction | ||
| Disease(or Constitution) | Rheumatoid Arthritis (RA) | Disease Subtypes | seronegative type | ||
| Organ | Joint (Synovium, Bone) | Test Sample / Technology Platform | Serum (ELISA, electrochemical immunoassay platform) | ||
| Pathobiological Mechanisms | |||||
| Clinical Availability Status | |||||
| Notes and Dynamics | |||||
| Biomarker | anti-PAD4 | Full name | Antipolyarginyldeimidease 4 antibody | Molecular Type | protein ( autoantibody ) |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Supplementary diagnosis and treatment response prediction for seropositive type | ||
| Disease(or Constitution) | Rheumatoid Arthritis (RA) | Disease Subtypes | Serum positive type | ||
| Organ | Joint (Synovium) | Test Sample / Technology Platform | Serum (ELISA, electrochemical immunoassay platform) | ||
| Pathobiological Mechanisms | PAD4 catalyzes the conversion of arginine to citrulline, inducing autoantibody production and participating in the amplification of synovial inflammation; it is associated with disease severity and has predictive value for resistance to TNF inhibitors. | ||||
| Clinical Availability Status | Clinical trials in progress | ||||
| Notes and Dynamics | The electrochemical platform has a detection range of 10-500 IU/mL, superior to ELISA; approximately 60% of early RA patients are RF/anti-CCP negative but anti-PAD4 positive. | ||||
| Biomarker | anti-MCV | Full name | Antimutant carnosine waveform protein antibody | Molecular Type | protein (autoantibody ) |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Early diagnosis and disease monitoring | ||
| Disease(or Constitution) | Rheumatoid Arthritis (RA) | Disease Subtypes | Serum positive type | ||
| Organ | Joint (Synovium) | Test Sample / Technology Platform | Serum, synovial fluid (ELISA, electrochemical immunoassay platform) | ||
| Pathobiological Mechanisms | Regarding carboxylic acid modified proteoglycan, it is involved in synovial hyperplasia and pannus formation | ||||
| Clinical Availability Status | Clinical | ||||
| Notes and Dynamics | The level is positively correlated with disease activity, and predicts joint erosion better than anti-CCP. | ||||
| Biomarker | anti-CCP | Full name | Anticyclopeptidin antibodies | Molecular Type | protein (autoantibody) |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Early diagnosis, prognosis prediction | ||
| Disease(or Constitution) | Rheumatoid Arthritis (RA) | Disease Subtypes | Serum positive type | ||
| Organ | Joint (Synovium, Cartilage, Bone) | Test Sample / Technology Platform | Serum, synovial fluid (ELISA, chemiluminescence, electrochemical immunoassay) | ||
| Pathobiological Mechanisms | Identification of citrullinated protein antigens epitopes in synovial tissue, induction of immune cell activation and release of inflammatory factors, and promotion of osteoclast-mediated bone erosion; high titers indicate increased risk of joint destruction. | ||||
| Clinical Availability Status | Widely available | ||||
| Notes and Dynamics | The diagnostic specificity is 95%-98%, and it can be detected 3-5 years before the onset of the disease. | ||||
| Biomarker | RF | Full name | Rheumatoid Factor | Molecular Type | protein (IgM-class autoantibodies) |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | diagnosis | ||
| Disease(or Constitution) | Rheumatoid Arthritis (RA) | Disease Subtypes | Serum positive type | ||
| Organ | Joint (Synovium, Cartilage, Bone) | Test Sample / Technology Platform | Serum (immunoturbidimetry, enzyme-linked immunosorbent assay (ELISA), electrochemical immunoassay platform) | ||
| Pathobiological Mechanisms | Targeting the Fc segment of IgG antibodies forms immune complexes, activates the complement system, and mediates synovial inflammation and joint tissue damage; it is positively correlated with disease activity indicators such as joint swelling and tenderness. | ||||
| Clinical Availability Status | Widely available | ||||
| Notes and Dynamics | 70%-80% of patients test positive, with a specificity of approximately 70%; the electrochemical platform enables simultaneous detection with other markers, reducing the assay time to within 2 hours. | ||||
| Biomarker | miR-21 | Full name | serum microRNA association (miR-21+miR-23a+miR-125b) | Molecular Type | microRNA (multimarker panel) |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Comprehensive regulation of bone metabolism | ||
| Disease(or Constitution) | Osteoporosis (OP) | Disease Subtypes | / | ||
| Organ | Bone | Test Sample / Technology Platform | Serum (qRT-PCR, miRNA microarray) | ||
| Pathobiological Mechanisms | Collaboratively inhibits osteogenesis-related genes (e.g., RUNX2, BMP2) and promotes osteoclast-related genes (e.g., RANKL) expression, reflecting bone metabolic imbalance. | ||||
| Clinical Availability Status | Scientific research verification | ||||
| Notes and Dynamics | Combinatorial diagnosis of osteoporosis is significantly superior to single biomarkers; it enables dynamic monitoring of therapeutic efficacy. | ||||
| Biomarker | PDFF | Full name | Proton Density Fat Fraction | Molecular Type | Imaging indicators (quantification of fat content) |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Bone marrow adiposity assessment | ||
| Disease(or Constitution) | Osteoporosis (OP) | Disease Subtypes | General (imaging-related markers) | ||
| Organ | Bone (Vertebrae) | Test Sample / Technology Platform | Lumbar MRI (Multi-echo Chemical Shift Encoding MRI, mDixon technique) | ||
| Pathobiological Mechanisms | Osteoporosis patients exhibit increased bone marrow adipocytes, which compress hematopoietic and osteogenic spaces, with elevated PDFF indicating deterioration of the bone formation microenvironment. | ||||
| Clinical Availability Status | Clinical gradual promotion | ||||
| Notes and Dynamics | The PDFF in the osteoporosis/bone loss group was higher than that in the normal group; it was negatively correlated with lumbar BMD and could serve as a supplementary evaluation indicator for DXA. | ||||