ArticleRheumatology (Oxford, England)2026
CD72 downregulation on DN2 B cells is associated with disease activity and resistance to rituximab in systemic lupus erythematosus.
Article in Rheumatology (Oxford, England), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- The Complexity of Soluble Checkpoint Molecules in Modulating Immune-Mediated Diseases and Autoimmunity.International journal of molecular sciences · 2026Review
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Authors and funding
9 authors.
Funding
Abstract
objectivesIn SLE, expanded B cell subtypes like double-negative 2 (DN2) may harbour autoreactivity, which may be linked to impaired checkpoint regulation. We investigated checkpoint molecule CD72 on B cells, its clinical associations, and dynamic changes upon rituximab (RTX) treatment.
methodsThirty SLE patients (26 with active disease) were studied. Seven received RTX treatment with sampling at baseline, 3 months and 6 months. B cell phenotypes were analysed using spectral flow cytometry, and clinical associations were evaluated. B cell receptor (BCR) signalling was studied through downstream phosphorylation in vitro.
resultsPatients with active SLE showed increased frequencies of CD72-negative B cells in switched memory (SWM), activated naïve (aNAV), DN2 and plasmablast (PB) subsets compared with healthy controls (HCs). CD72-negative DN2 cells (CD27-IgD-CD21-CD11c+) were elevated in LN patients. These cells expressed higher CD95 and lower CD20 compared with HCs and canonical SLE DN2. Upon BCR stimulation, lupus CD72-negative SWM and DN2 B cells displayed increased pSYK phosphorylation compared with their CD72-positive counterparts and the overall cell population. CD72-negative DN2 frequencies associated positively with SLEDAI-2K and inversely with C3 levels and were increased in anti-dsDNA-positive patients. After RTX treatment, the remaining DN2 cells were primarily CD72-negative at 3 months.
conclusionThe DN2 B cell subset have been associated with autoimmunity. We showed that DN2 B cells in SLE have reduced CD72 expression, which is associated with anti-dsDNA positivity, complement consumption, and enhanced BCR downstream signalling. The relative resistance of CD72-negative B cells to RTX indicates that an impaired checkpoint programme in lupus B cells may potentially contribute to disease relapse. These findings require validation in larger cohorts.
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