Observational studyFrontiers in immunology2026
Cytotoxic T-cell deficiency and sustained B-cell activation in serofast syphilis: a prospective observational study.
Observational study in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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4 authors.
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Abstract
Introduction: The serofast state, defined by persistent non-treponemal reactivity after adequate therapy for syphilis, remains a clinically relevant yet poorly understood condition. Whether serofast reflects residual infection or persistent immune activation remains uncertain. We aimed to characterize peripheral blood lymphocyte subpopulations and anticardiolipin antibodies in patients with serofast syphilis and compare them with individuals achieving a serological cure. Methods: We conducted a prospective observational study including adults with early syphilis treated with benzathine penicillin G. Peripheral blood samples were collected at baseline and six months post-treatment for immunophenotyping and antiphospholipid antibody assessment. Serological outcome was defined by Venereal Disease Research Laboratory (VDRL) response (serofast vs. serologically cured). Twelve healthy volunteers served as controls for anticardiolipin antibody testing. Results: Among 41 included patients, 9 (22%) developed a serofast state. Serofast patients demonstrated significantly lower baseline numbers of cytotoxic T lymphocytes (CD8 Discussion: Serofast syphilis was associated with reduced cytotoxic T-cell counts and persistent B-cell activation, supporting a model in which impaired cytotoxic clearance of antigen-presenting cells may prolong antibody production despite microbiological cure. The transient nature of infection-induced anticardiolipin antibodies further argues against persistent autoimmunity. These findings provide mechanistic insight into serofast responses and suggest potential immunological determinants of post-treatment serological persistence.
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