Systemic sclerosis & Raynaud's

Teclistamab induces rapid clinical response and deep tissue depletion in refractory systemic sclerosis—a case series

Ann Rheum DisPublished Case series

Authors' conclusion

Teclistamab induced deep tissue depletion of B-cells and plasma cells and rapid clinical and serological responses, with evidence for resolution of inflammation and potential modification of fibrotic processes.

Study context

Population
Patients with severe and treatment-refractory systemic sclerosis (SSc)completed 1 cycle
Participants
10 patients
Outcome
Revised ACR-CRISS 25 and 50 responses
Follow-up
Median 3.75 months (IQR: 2.5 months)
Methodological detailsoff-label therapy
  • Off-label therapy

Main finding

As reported in the abstract

median follow-up 3.75 months (IQR: 2.5 months)

Revised American College of Rheumatology Composite Response Index in Systemic Sclerosis (ACR-CRISS) 25 response

71%

Revised ACR-CRISS 50 response

43%

Observational data: associations, not effects.

Further findings

Antitopoisomerase antibody titres, median reduction

Median reduction in antitopoisomerase antibody titres (IQR: 39%)
70.6%
  • Accompanied by decreases in serum IgG and vaccination titres

FVC in patients with ILD, median increase · week 12

Median increase in FVC (IQR: 15%)
7%
  • Radiographic and functional improvement observed by week 12

Modified Rodnan skin score, median decrease

Median decrease in modified Rodnan skin score (IQR: 17.9%)
35.9%
  • Accompanied by reductions in fibroblast activation protein (FAP)-alpha-positive fibroblasts in skin biopsy specimens

Original publication

Teclistamab induces rapid clinical response and deep tissue depletion in refractory systemic sclerosis—a case series. Ann Rheum Dis. Published 19 June 2026. doi:10.1016/j.ard.2026.05.023

Composed by AI from the published abstract and checked against it. How Briefs are made →

Get them every week

New studies on this topic in My Week and in your Monday e-mail.

We e-mail you a sign-in link and a code. No password, no spam.