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Objective.Blood microbiome has been analyzed in cancer patients using machine learning. We aimed to study whether the plasma microbiome represents the microbial community in the gut among patients with systemic lupus erythematosus (SLE) and healthy controls (HCs).Methods.Paired plasma and stool samples from female patients with SLE and female HCs were assessed for microbiome composition by microbial 16S ribosomal RNA sequencing.Results.Decreased microbial alpha diversity in stool compared to plasma and distinct plasma and gut beta diversity were found in both HCs and patients with SLE. No difference in gut microbial diversity was found; however, plasma alpha diversity was decreased in patients with SLE compared to HCs. The predominant bacteria differed between plasma and stool in both groups. Although the predominant plasma and stool genus bacteria were similar in patients with SLE and HCs, some were clearly different.Conclusion.Compared to the gut, the plasma microbiome contained distinct community and greater heterogeneity, indicating that the predominant circulating microbiome may originate from sites (eg, oral or skin) other than the gastrointestinal tract. The decreased plasma but not gut alpha diversity in patients with SLE compared to HCs implies an altered plasma microbiome in SLE, which may be important for systemic immune perturbations and SLE disease pathogenesis.

Autoantibodies binding on CD4+T cells may mediate CD4+T cell death, and prevent CD4+T cell recovery in aviremic HIV‐infected patients under ART. Although effective antiretroviral therapy (ART) suppresses HIV viral replication, prevents AIDS‐related complications, and prolongs life, a proportion of patients fails to restore the patients’ CD4+T cell number to the level of healthy individuals. Increased mortality and morbidity have been observed in these patients. In the current study, we have investigated the role of auto‐IgGs in CD4+T cell apoptosis and recovery in a cross‐sectional study. All HIV+subjects were on viral‐suppressive ART treatment with a different degree of CD4+T cell reconstitution. Total auto‐IgG binding on CD4+T cell surfaces and its associated apoptosis and CD4+T cell recovery were analyzed by flow cytometry ex vivo. Total IgGs from plasma were tested for their binding capacities to CD4+T cell surfaces and their mediation to CD4+T cell death through NK cell cytotoxicity in vitro. HIV+subjects had increased surface binding of auto‐IgGs on CD4+T cells compared with healthy controls, and IgG binding was associated with elevated CD4+T cell apoptosis in HIV+subjects but not in healthy controls. Plasma IgGs from HIV+subjects bound to CD4+T cells and induced cell apoptosis through NK cytotoxicity in vitro. Soluble CD4 (sCD4) preincubation prevented NK cell‐mediated CD4+T cell death. Our results suggest that plasma autoantibodies may play a role in some HIV+patients with poor CD4+T cell recovery under viral‐suppressive ART.