Image 9_Single-cell mass cytometry cartography highlights systemic lupus erythematosus and Sjögren’s disease immune differences.jpeg

Both had an activated phenotype with elevated CD38, CD86, and Ki-67. In SLE, the costimulatory molecules CD86 and CD226 were upregulated on memory and DN B cells. By contrast, B cell changes in pSjD were more modest.

We found 12 T cells clusters. Both diseases had increased CD4⁺ PD-1⁺ ICOS⁺ circulating T follicular helper-like cells, and pSjD showed expansion of CD8⁺ effector memory (Tem) and terminally differentiated (Temra) T cell subsets. Relative innate cell frequencies did not differ substantially between groups, however, intermediate CD226^hi monocytes were reduced in SLE but showed higher activation marker expression (CD86, HLA-DR).

Network correlation analysis revealed higher immune‐cell connectivity in SLE compared to pSjD.</p>Conclusion<p>SLE is characterized by B cell activation, plasmablast expansion, and costimulatory upregulation, while pSjD is mainly defined by alterations in the CD8⁺ T cell compartment. These disease‐specific immunologic signatures highlight distinct patterns in SLE and pSjD and generate hypotheses for future studies investigating targeted therapeutic approaches.</p>