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Rheumatoid Arthritis

Pathophysiology description

2025-12-15
Falcon MONDO:0008383 Model: Edison Scientific Literature 16 citations

Pathophysiology description Rheumatoid arthritis is a systemic autoimmune disease characterized by a breakdown of tolerance to post-translationally modified self-antigens (notably citrullinated proteins) and by chronic synovitis with stromal remodeling. Contemporary models converge on mucosal origins in subsets of patients: aberrant immune activation in lung, oral, and gut mucosa (linked to dysbiosis, epithelial barrier dysfunction, and local citrullination) precedes and drives systemic autoimmunity with IgA-class autoantibodies (ACPA, RF) and eventually joint-localized synovitis (Holers et al., 2024) (holers2024distinctmucosalendotypes pages 21-23). Synovial tissue single-cell and spatial studies define heterogeneous inflammatory states marked by pathogenic macrophage and fibroblast programs, T peripheral helper (Tph) cells that sustain B-cell responses, and ectopic lymphoid activation, underpinned by genetic risk centered on HLA-DRB1 shared-epitope alleles presenting citrullinated epitopes to CD4+ T cells (Jonsson, 2024) (jonsson2024synovialtissueinsights pages 9-11).

Core mechanisms - Adaptive autoimmunity and HLA–peptide presentation: HLA-DRB1 shared epitope (SE) alleles preferentially present citrullinated peptides to CD4+ T cells, providing a genetic scaffold for ACPA-positive disease; mucosal priming and epitope spreading are hallmarks in pre-RA (Jonsson, 2024; Holers et al., 2024) (jonsson2024synovialtissueinsights pages 9-11, holers2024distinctmucosalendotypes pages 21-23). - Mucosal origins and microbiome: RA-related autoantibodies and mucosal immune activation are detected in lung/oral/gut mucosa before arthritis; mechanistic links include bacterial PAD (Porphyromonas gingivalis) and LtxA (Aggregatibacter actinomycetemcomitans)–induced neutrophil hypercitrullination; Prevotella copri and metabolite pathways (e.g., indoles) modulate Th17 responses and disease penetrance (Seymour et al., 2024) (seymour2024microbialmechanismsof pages 1-3, seymour2024microbialmechanismsof pages 12-13). Notably, a large 2024 quantitative profiling study in at-risk first-degree relatives found no stage-specific gut microbiome signature overall, underscoring cohort heterogeneity (RMD Open 2024, Gilbert et al., summarized in Holers 2024) (holers2024distinctmucosalendotypes pages 21-23). - Innate immunity and citrullination sources: Neutrophil extracellular traps (NETs) release citrullinated histones and autoantigens; platelets and monocytes add to the antigenic pool via PAD expression and surface PAD4 activity; citrullination of complement C1 inhibitor (C1-INH) impairs complement regulation (Seymour et al., 2024) (seymour2024microbialmechanismsof pages 1-3, seymour2024microbialmechanismsof pages 12-13). These processes interface with stromal and adaptive responses in synovium (Jonsson, 2024) (jonsson2024synovialtissueinsights pages 9-11). - Synovial stromal and myeloid circuits: Perivascular Notch/TGF-β–patterned fibroblast niches (including COMPhi fibrogenic states) and SPP1+ macrophages sustain inflammation and remodeling; Tph cells drive B-cell/plasma cell responses and ectopic lymphoid structures (Jonsson, 2024) (jonsson2024synovialtissueinsights pages 9-11).

Dysregulated pathways - JAK/STAT: Central conduit for IL-6 and interferon signaling; clinical targeting (JAK inhibitors) validates pathogenic relevance in both immune and stromal compartments (Ghang et al., 2025 overview citing 2023–2024 primary work) (ghang2025currentstateand pages 1-3). - TNF/IL-6/IL-17 and NF-κB: Canonical inflammatory axes sustaining synovitis and systemic features (Ghang et al., 2025; Jonsson, 2024) (ghang2025currentstateand pages 1-3, jonsson2024synovialtissueinsights pages 9-11). - PI3K/AKT/mTOR and MAPK/ERK: Drive fibroblast-like synoviocyte (FLS) proliferation, invasiveness, and cytokine production; integrate TNF/IL-1 signals (Jonsson, 2024; Ghang et al., 2025) (jonsson2024synovialtissueinsights pages 9-11, ghang2025currentstateand pages 1-3). - cGAS–STING: DNA-sensing innate pathway implicated in synovial IFN programs and chronic inflammation (Ghang et al., 2025) (ghang2025currentstateand pages 1-3).

Disease progression (sequence of events) 1) Mucosal priming: Dysbiosis, PAD/LtxA-triggered hypercitrullination, barrier dysfunction; emergence of IgA ACPA/RF; mucosal Th17/Tph polarization (Holers et al., 2024; Seymour et al., 2024) (holers2024distinctmucosalendotypes pages 21-23, seymour2024microbialmechanismsof pages 1-3). 2) Systemic autoimmunity: Affinity maturation and epitope spreading of ACPA; HLA-DRB1 SE–restricted CD4+ T-cell responses to citrullinated epitopes; circulating immune complexes (Holers et al., 2024) (holers2024distinctmucosalendotypes pages 21-23). 3) Articular localization: Recruitment of myeloid cells; NETosis and monocyte/macrophage activation; FLS activation via TNF/IL‑1/IL‑6/NF‑κB and PI3K/AKT/MAPK cascades; ectopic lymphoid structures and plasma cell accrual (Jonsson, 2024) (jonsson2024synovialtissueinsights pages 9-11). 4) Chronicity/remodeling: SPP1+ macrophage–fibroblast–T cell circuits, perivascular TGF‑β/Notch niches (COMPhi) drive persistent inflammation and fibrosis; osteoclastogenesis causes erosions (Jonsson, 2024) (jonsson2024synovialtissueinsights pages 9-11).

Key Molecular Players - Genes/Proteins (HGNC): HLA‑DRB1 (shared epitope); PADI4/PADI2 (citrullination enzymes); IL6R (IL‑6 signaling); TNF (master cytokine); JAKs/TYK2 (JAK/STAT conduit) (Jonsson, 2024; Holers, 2024; Ghang, 2025) (jonsson2024synovialtissueinsights pages 9-11, holers2024distinctmucosalendotypes pages 21-23, ghang2025currentstateand pages 1-3). - Chemical Entities (CHEBI/Concepts): Citrullinated peptides; platelet microparticles carrying citrullinated proteins; complement C1‑INH (citrullinated) (Seymour, 2024) (seymour2024microbialmechanismsof pages 1-3, seymour2024microbialmechanismsof pages 12-13). - Cell Types (CL): Fibroblast-like synoviocytes (perivascular, COMPhi); SPP1+ macrophages; Tph CD4+ cells; B cells/plasma cells; neutrophils (NETs); monocytes/osteoclast precursors (Jonsson, 2024) (jonsson2024synovialtissueinsights pages 9-11). - Anatomical Locations (UBERON): Lung, gut, oral mucosa (mucosal endotypes); synovium (Holers, 2024; Jonsson, 2024) (holers2024distinctmucosalendotypes pages 21-23, jonsson2024synovialtissueinsights pages 9-11).

Biological Processes (GO) disrupted - Antigen processing/presentation via MHC class II; cytokine-mediated signaling (JAK/STAT); NF‑κB activation; cell proliferation/migration (PI3K/AKT/mTOR; MAPK/ERK); DNA sensing (cGAS–STING); neutrophil degranulation/NET formation; complement regulation (citrullinated C1‑INH) (Ghang 2025; Jonsson 2024; Seymour 2024; Holers 2024) (ghang2025currentstateand pages 1-3, jonsson2024synovialtissueinsights pages 9-11, seymour2024microbialmechanismsof pages 1-3, holers2024distinctmucosalendotypes pages 21-23, seymour2024microbialmechanismsof pages 12-13).

Cellular Components - Cell surface HLA‑DR peptide-binding groove (shared epitope); nuclear/cytosolic PAD localization and extracellular exposure on monocyte surfaces; extracellular traps (NETs); perivascular synovial niches with endothelial–fibroblast Notch crosstalk; platelet-derived microparticles in synovial/extracellular space; complement components in plasma/synovial fluid (Jonsson, 2024; Seymour, 2024) (jonsson2024synovialtissueinsights pages 9-11, seymour2024microbialmechanismsof pages 1-3, seymour2024microbialmechanismsof pages 12-13).

Phenotype associations (HP) - Chronic symmetric polyarthritis with morning stiffness, synovial hypertrophy, joint erosions; extra-articular mucosal and pulmonary involvement in subsets (Holers, 2024; Jonsson, 2024) (holers2024distinctmucosalendotypes pages 21-23, jonsson2024synovialtissueinsights pages 9-11).

Expert opinions and 2023–2024 developments - Mucosal endotypes: Holers et al. (2024) propose distinct mucosal trajectories (lung, gut, oral) that initiate/drive RA and emphasize that IgA autoimmunity, airway abnormalities, and mucosa-derived immune responses can precede joint disease; dietary fiber/SCFA and indole pathways modulate systemic inflammation (with mechanistic preclinical support) (holers2024distinctmucosalendotypes pages 21-23). - Synovial heterogeneity: Jonsson (2024) summarizes single-cell/spatial insights—B cell–rich synovitis and macrophage/fibroblast niches predict therapeutic responses and highlight Notch/TGF‑β patterning, SPP1+ macrophages, and Tph cells as actionable axes (jonsson2024synovialtissueinsights pages 9-11). - Microbiome mechanisms: Seymour et al. (2024) synthesize bacterial PAD/LtxA-driven hypercitrullination, molecular mimicry (e.g., P. copri antigens), microbial translocation (e.g., Fusobacterium OMVs), and metabolite-immune interactions; importantly, not all cohorts show consistent dysbiosis signals (seymour2024microbialmechanismsof pages 1-3, seymour2024microbialmechanismsof pages 12-13).

Relevant statistics and data - Progression risk: In ACPA-positive individuals, ~40–60% progress to RA over 2–5 years, often with mucosal IgA autoantibodies preceding disease (Seymour 2024; citing cohort data within review) (seymour2024microbialmechanismsof pages 1-3). - Microbiome null findings: A 2024 study of 371 first-degree relatives at preclinical stages found no significant quantitative microbiome profile differences across disease stages (PERMANOVA R2≈0.008, p=0.56), tempering generalizations about universal dysbiosis signatures (as summarized in Holers 2024) (holers2024distinctmucosalendotypes pages 21-23). - Synovial stratification and therapy: B cell–rich synovitis associates with better rituximab response, whereas B cell–poor/inflammatory pathotypes may favor IL‑6 receptor blockade (tocilizumab) (Jonsson 2024) (jonsson2024synovialtissueinsights pages 9-11).

Evidence items with PMIDs/URLs (selection; 2023–2024 priority) - Holers VM et al. Distinct mucosal endotypes as initiators and drivers of rheumatoid arthritis. Nat Rev Rheumatol. 2024 Sep;20(10):601–613. doi:10.1038/s41584-024-01154-0. https://doi.org/10.1038/s41584-024-01154-0 (holers2024distinctmucosalendotypes pages 21-23). - Jonsson AH. Synovial Tissue Insights into Heterogeneity of Rheumatoid Arthritis. Curr Rheumatol Rep. 2024 Dec;26:81–88. doi:10.1007/s11926-023-01129-2. https://doi.org/10.1007/s11926-023-01129-2 (jonsson2024synovialtissueinsights pages 9-11). - Seymour BJ, Allen BE, Kuhn KA. Microbial Mechanisms of Rheumatoid Arthritis Pathogenesis. Curr Rheumatol Rep. 2024 Feb;26:124–132. doi:10.1007/s11926-024-01135-y. https://doi.org/10.1007/s11926-024-01135-y (seymour2024microbialmechanismsof pages 1-3). - Seymour BJ et al. (mechanistic details on PAD/LtxA, mimicry, metabolites) (seymour2024microbialmechanismsof pages 12-13). - Ghang B et al. Current state and future directions of basic research in rheumatoid arthritis. J Rheum Dis. 2025;32:166–181. doi:10.4078/jrd.2024.0151 (overview integrating 2023–2024 insights). https://doi.org/10.4078/jrd.2024.0151 (ghang2025currentstateand pages 1-3).

Ontology-linked annotations - Gene/protein (HGNC): HLA‑DRB1; PADI4; PADI2; IL6R; TNF; JAK1/JAK2/TYK2 (jonsson2024synovialtissueinsights pages 9-11, holers2024distinctmucosalendotypes pages 21-23, ghang2025currentstateand pages 1-3). - Biological process (GO): “cytokine-mediated signaling pathway”; “positive regulation of NF‑κB transcription factor activity”; “phosphatidylinositol 3-kinase signaling”; “MAPK cascade”; “DNA sensing via cGAS–STING”; “neutrophil extracellular trap formation”; “antigen processing and presentation of peptide antigen via MHC class II”; “complement activation, classical pathway” (jonsson2024synovialtissueinsights pages 9-11, ghang2025currentstateand pages 1-3, seymour2024microbialmechanismsof pages 1-3, seymour2024microbialmechanismsof pages 12-13, holers2024distinctmucosalendotypes pages 21-23). - Cell types (CL): fibroblast-like synoviocytes; macrophage SPP1+ subset; neutrophil; monocyte; osteoclast; T peripheral helper (Tph); B cell; plasma cell (jonsson2024synovialtissueinsights pages 9-11, seymour2024microbialmechanismsof pages 1-3). - Anatomical locations (UBERON): synovial membrane; lung; oral mucosa; intestinal mucosa (holers2024distinctmucosalendotypes pages 21-23, jonsson2024synovialtissueinsights pages 9-11). - Chemical entities (CHEBI/concepts): citrullinated peptides; platelet microparticles; complement C1 inhibitor (citrullinated) (seymour2024microbialmechanismsof pages 1-3, seymour2024microbialmechanismsof pages 12-13). - Phenotypes (HP): HP:0001371 (Arthritis); HP:0000988 (Morning stiffness); HP:0011800 (Erosive arthritis); HP:0002093 (Interstitial lung disease) (contextualized in mucosal endotype subsets) (holers2024distinctmucosalendotypes pages 21-23, jonsson2024synovialtissueinsights pages 9-11).

Applications and real-world implementations - Precision stratification: Synovial biopsy and scRNA/spatial signatures (B cell–rich pathotype, SPP1+ macrophages, COMPhi fibroblasts) may inform biologic choice (rituximab vs. tocilizumab) and identify fibrosis-prone, treatment-resistant niches (Jonsson, 2024) (jonsson2024synovialtissueinsights pages 9-11). - Mucosal risk interception: Monitoring IgA ACPA/RF and mucosal imaging/biomarkers in at-risk individuals; dietary fiber/SCFA modulation and periodontal care are being explored to mitigate mucosal drivers (Holers, 2024) (holers2024distinctmucosalendotypes pages 21-23). - Targeted signaling blockade: JAK inhibitors and IL‑6/TNF blockade remain effective across phenotypes, underlining pathway centrality (Ghang, 2025 integrating recent trials and mechanistic data) (ghang2025currentstateand pages 1-3).

Included artifact | Category | Item | Ontology namespace tag | Role/Mechanism | 2023–2024 Evidence | |---|---|---|---|---| | Genetic risk | HLA-DRB1 shared epitope | HGNC | Presents citrullinated peptides to CD4+ T cells; major seropositive RA risk allele driving ACPA-associated immunity. | (jonsson2024synovialtissueinsights pages 9-11, ghang2025currentstateand pages 1-3) | | Enzyme (citrullination) | PADI4 | HGNC | Catalyzes protein citrullination in NETs/METs and immune cells → generates ACPA-target neoepitopes. | (seymour2024microbialmechanismsof pages 1-3, seymour2024microbialmechanismsof pages 12-13, barbera2025theroleof pages 7-11) | | Enzyme (citrullination) | PADI2 | HGNC | Contributes to citrullination at mucosal sites and in inflammatory cells; complements PAD4 in antigen generation. | (seymour2024microbialmechanismsof pages 12-13, barbera2025theroleof pages 7-11) | | Cytokine receptor | IL6R | HGNC | Mediates IL-6 signaling (JAK/STAT) driving systemic and synovial inflammation; therapeutic target (tocilizumab). | (ghang2025currentstateand pages 1-3, jonsson2024synovialtissueinsights pages 9-11) | | Cytokine | TNF | HGNC | Central proinflammatory driver of synovitis, FLS activation and leukocyte recruitment; target of TNF inhibitors. | (ghang2025currentstateand pages 1-3, jonsson2024synovialtissueinsights pages 9-11) | | Signaling pathway | TYK2 / JAK-STAT | GO | Intracellular route for cytokine signals (IL-6, IFNs); dysregulated in RA and targeted by JAK inhibitors. | (ghang2025currentstateand pages 1-3, barbera2025theroleof pages 7-11) | | Signaling pathway | NF-κB signaling | GO | Transcriptional hub for proinflammatory cytokines and survival signals in immune/fibroblast cells. | (ghang2025currentstateand pages 1-3, barbera2025theroleof pages 7-11) | | Signaling pathway | PI3K/AKT/mTOR | GO | Promotes FLS proliferation, survival and invasive phenotype; implicated in synovial hyperplasia. | (jonsson2024synovialtissueinsights pages 9-11, ghang2025currentstateand pages 1-3) | | Signaling pathway | MAPK/ERK | GO | Regulates cytokine production and FLS responses contributing to synovitis and tissue damage. | (ghang2025currentstateand pages 1-3, barbera2025theroleof pages 7-11) | | Innate sensing | cGAS–STING pathway | Pathway | DNA-sensing innate pathway implicated in synovial type-I IFN and inflammatory responses in arthritis. | (barbera2025theroleof pages 7-11, ghang2025currentstateand pages 1-3) | | Stromal niche | Fibroblast-like synoviocytes — perivascular COMPhi / TGF-β–Notch niche | CL / UBERON | Perivascular COMPhi fibroblasts form TGF-β gradients (Notch-regulated) driving fibrogenic remodeling and treatment resistance. | (jonsson2024synovialtissueinsights pages 9-11) | | Myeloid subset | Macrophage SPP1+ subset | CL | Pathogenic synovial macrophage subset that communicates with T cells and fibroblasts to sustain inflammation. | (jonsson2024synovialtissueinsights pages 9-11, seymour2024microbialmechanismsof pages 12-13) | | T cell subset | T peripheral helper (Tph) cells | CL | Provide B-cell help in synovium (CXCL13/IL-21) promoting local ACPA-producing plasma cells and ectopic responses. | (jonsson2024synovialtissueinsights pages 9-11, ghang2025currentstateand pages 1-3) | | Lymphoid structures | B cells / plasma cells & ectopic lymphoid structures | CL | Local antibody generation (ACPA, RF) within synovium/mucosa; predicts response to B-cell targeted therapy. | (jonsson2024synovialtissueinsights pages 9-11, perera2024clinicalphenotypesserological pages 20-21) | | Innate effector | Neutrophils & NETs | CL / GO | NETosis (PAD4-driven) releases citrullinated antigens and DAMPs that amplify autoimmunity and synovial inflammation. | (seymour2024microbialmechanismsof pages 1-3, seymour2024microbialmechanismsof pages 12-13) | | Monocyte lineage | Monocytes → Osteoclastogenesis | CL / GO | Monocyte-derived osteoclast differentiation (RANKL-driven) mediates bone erosion; monocyte activation linked to HLA-SE. | (ghang2025currentstateand pages 1-3, jonsson2024synovialtissueinsights pages 9-11) | | Complement regulation | Complement C1 inhibitor — citrullination | CHEBI / GO | Citrullination of C1-INH impairs complement/contact system regulation, increasing inflammatory complement activity. | (seymour2024microbialmechanismsof pages 12-13, ghang2025currentstateand pages 1-3) | | Extracellular vesicles | Platelet microparticles with citrullinated autoantigens | CHEBI | Platelet-derived microparticles contain PAD4 and citrullinated proteins that can be ACPA targets and activate immunity. | (seymour2024microbialmechanismsof pages 1-3, seymour2024microbialmechanismsof pages 12-13) | | Cell-surface enzyme | Monocyte surface PAD4 | HGNC / Cell surface | Active PAD4 displayed on monocyte surfaces citrullinates extracellular proteins, creating neoantigens at cell interface. | (jonsson2024synovialtissueinsights pages 9-11, seymour2024microbialmechanismsof pages 1-3) | | Mucosal sites | Mucosal endotypes: lung, gut, oral | UBERON | Sites of early citrullination, mucosal inflammation and immune priming; mucosal dysbiosis can precede clinical RA. | (holers2024distinctmucosalendotypes pages 21-23, seymour2024microbialmechanismsof pages 1-3, ghang2025currentstateand pages 1-3) | | Microbiome signals | Prevotella copri; Porphyromonas gingivalis; Aggregatibacter actinomycetemcomitans | Taxon / Concept | Microbial taxa implicated in dysbiosis, citrullination (PPAD/LtxA), molecular mimicry and metabolite-driven immune modulation. | (seymour2024microbialmechanismsof pages 1-3, seymour2024microbialmechanismsof pages 12-13) | | Cytokine circuit | OSM–OSMR macrophage–fibroblast circuit | Pathway / cytokine | Oncostatin M from macrophages activates OSMR+ fibroblasts generating inflammatory and tissue-destructive programs targeted by JAKi. | (jonsson2024synovialtissueinsights pages 9-11, barbera2025theroleof pages 7-11) |

Table: Compact reference table mapping core molecular/cellular entities, ontologies, brief mechanisms, and 2023–2024 supporting evidence (context IDs) to aid rapid curation and knowledgebase annotation.

Direct quotes (supporting statements) - “Evidence suggests that self-tolerance is breached at mucosal sites… Primary sites studied include the lung, gut and oral mucosa” (Holers 2024) (holers2024distinctmucosalendotypes pages 21-23). - “Synovial tissue single-cell studies revealed T peripheral helper cells, macrophage subsets, and Notch-shaped fibroblast niches that underpin RA heterogeneity and may predict therapeutic response” (Jonsson 2024) (jonsson2024synovialtissueinsights pages 9-11). - “Periodontal and enteric pathobionts… produce PAD or leukotoxins that induce hypercitrullination and molecular mimicry, linking dysbiosis to ACPA generation” (Seymour 2024) (seymour2024microbialmechanismsof pages 1-3, seymour2024microbialmechanismsof pages 12-13).

Limitations and open questions - Not all cohorts demonstrate consistent gut dysbiosis signatures in pre-RA; host genetics, geography, and exposures likely stratify mucosal endotypes (Holers 2024) (holers2024distinctmucosalendotypes pages 21-23). - Mechanistic dissection of cGAS–STING in human RA synovia remains an area of active investigation (Ghang 2025) (ghang2025currentstateand pages 1-3).

URLs and dates are provided above alongside each citation. All claims are supported by recent primary/review sources, prioritizing 2023–2024 publications, with integrative context drawn from 2025 overviews where necessary to frame 2023–2024 findings (holers2024distinctmucosalendotypes pages 21-23, jonsson2024synovialtissueinsights pages 9-11, seymour2024microbialmechanismsof pages 1-3, seymour2024microbialmechanismsof pages 12-13, ghang2025currentstateand pages 1-3).

References

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  2. (jonsson2024synovialtissueinsights pages 9-11): Anna Helena Jonsson. Synovial tissue insights into heterogeneity of rheumatoid arthritis. Current rheumatology reports, 26:81-88, Dec 2024. URL: https://doi.org/10.1007/s11926-023-01129-2, doi:10.1007/s11926-023-01129-2. This article has 18 citations and is from a peer-reviewed journal.

  3. (seymour2024microbialmechanismsof pages 1-3): Brenda J. Seymour, Brendan E. Allen, and Kristine A. Kuhn. Microbial mechanisms of rheumatoid arthritis pathogenesis. Current rheumatology reports, 26:124-132, Feb 2024. URL: https://doi.org/10.1007/s11926-024-01135-y, doi:10.1007/s11926-024-01135-y. This article has 14 citations and is from a peer-reviewed journal.

  4. (seymour2024microbialmechanismsof pages 12-13): Brenda J. Seymour, Brendan E. Allen, and Kristine A. Kuhn. Microbial mechanisms of rheumatoid arthritis pathogenesis. Current rheumatology reports, 26:124-132, Feb 2024. URL: https://doi.org/10.1007/s11926-024-01135-y, doi:10.1007/s11926-024-01135-y. This article has 14 citations and is from a peer-reviewed journal.

  5. (ghang2025currentstateand pages 1-3): Byeongzu Ghang, Jin Kyun Park, Ji Hyeon Ju, and Seungwoo Han. Current state and future directions of basic research in rheumatoid arthritis. Journal of Rheumatic Diseases, 32:166-181, Feb 2025. URL: https://doi.org/10.4078/jrd.2024.0151, doi:10.4078/jrd.2024.0151. This article has 1 citations.

  6. (barbera2025theroleof pages 7-11): L LA BARBERA. The role of jak/stat inhibition in modulating the innate immune response in patients with rheumatoid arthritis. Unknown journal, 2025.

  7. (perera2024clinicalphenotypesserological pages 20-21): James Perera, Chiara Aurora Delrosso, Alessandra Nerviani, and Costantino Pitzalis. Clinical phenotypes, serological biomarkers, and synovial features defining seropositive and seronegative rheumatoid arthritis: a literature review. Cells, 13:743, Apr 2024. URL: https://doi.org/10.3390/cells13090743, doi:10.3390/cells13090743. This article has 33 citations and is from a poor quality or predatory journal.