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. 2024 Apr 10;27(6):109707. doi: 10.1016/j.isci.2024.109707

Table 2.

Histology characteristics and 10x Genomics chemistries for 25 synovial tissue samples from patients with inflammatory arthritis, included in the generation of the single-cell reference map of the fresh human synovium

Number of biopsies
Protocol
 1: Original, Donlin L. et al.22 10
 2: Optimized, Edalat SG. et al. 15
Sex∗
 Female 18
 Male 5
Age
 Median (range) 55.5 (20–81)

Therapy at biopsy∗∗

No therapy 3
Corticosteroid 1
Corticosteroid + cDMARD 1
cDMARDs 2
bDMARDs 3
cDMARD + bDMARD 2
cDMARD + JAKi 3
Corticosteroid + cDMARD + JAKi 1
Antibiotics 2
Refractory arthritis∗∗∗ 6
Krenn synovitis score∗∗∗∗
 Median (range) 4 (2–9)
Pathotype
 Diffuse myeloid 10
 Lympho-myeloid 9
 Fibroid 5
 Unclassified 1
10x Genomics Chemistry
 3′ v3.0 5
 3′ v3.1 20

See also Figure S1. Numbers denote the biopsies processed. F: female, M: male, DM: diffuse myeloid, LM: lymphoid myeloid, F: fibroid, pauci-immune, U: unclassified. ∗Gender data not reported for 2 patients in protocol 2 cohort, ∗∗The values indicate the number of patients receiving different disease-modifying antirheumatic drugs (DMARDs) at the time of biopsy with data missing for 5 patients. Conventional DMARDs (cDMARDs) included methotrexate, leflunomide, salazopyrin, sulfasalazine and plaquenil. Biological DMARDs (bDMARDs) included anti-TNF, anti-IL-6, anti-IL-17A, anti -IL-12/IL-23 and anti-IL-23 therapies, and therapeutic fusion proteins (soluble TNFa receptor, CTLA4). Janus kinase inhibitors (JAKi) included baricitinib and tofacitinib. Antibiotics included vibramycin and doxycycline. ∗∗∗Indicated is the number of patients failing multiple cDMARDs and bDMARD/JAKi in the period before biopsy data about treatment history are missing for 6 patients. ∗∗∗∗Krenn scoring, based on 21 out of 25 synovial tissues.