Anti-MDA5 antibody testing takes two to eight weeks and fails to detect 17% of cases — so in rapidly progressive ILD, the skin exam is the faster test. This review covers the pathognomonic and characteristic DM rashes, the specific findings that flag anti-MDA5, TIF1γ and NXP2, why DM-specific rashes appear in antisynthetase and overlap myositis, presentations in skin of colour, and the treatments for refractory cutaneous disease.
Antimicrobial peptides are innate defence molecules — but in RA they become autoantigens, immune adjuvants and drivers of bone erosion. This review tracks LL-37, the defensins and the S100 proteins across five stages, from mucosal predisposition through to chronic synovitis, and makes the case that they amplify rather than initiate disease. Calprotectin already outperforms CRP and ESR for reflecting joint inflammation, yet no AMP-based agent has entered an RA trial since a phase II failure in 2019.
A 2026 Personal View arguing that ‘seronegative’ usually describes the assay rather than the patient — and that separating genuinely seronegative disease (myeloid/CD8-driven, MHC class I-associated, rituximab-unresponsive) from merely undetected seropositivity is the field’s necessary next step. Includes a disease-by-disease audit of seronegativity rates and why classification criteria naming the antibody but not the method matters.
RHO is a phase 2 proof-of-concept RCT of the FcRn antagonist efgartigimod in Sjögren’s disease, testing whether removing pathogenic IgG autoantibodies improves disease. It met its exploratory objective (CRESS response 45.5% vs 11.1% at week 24) with deep, selective IgG reduction — but systemic activity improved while patient-reported symptoms did not, and the tiny sample means this justifies phase 3, not practice change.
A contemporary NEJM review of idiopathic inflammatory myopathies — the five-subtype framework (IBM, IMNM, antisynthetase syndrome, overlap, dermatomyositis), the autoantibody revolution that now anchors classification, and the shift toward subtype-specific therapy with biologics, JAK/TYK2 inhibitors, and CAR-T.