International journal of infectious diseases : IJID : official publication of the International Society for Infectious Diseases · 2026
Type 2 diabetes reshapes the B-cell compartment in tuberculosis, with reduction of transitional B cells and expansion of plasmablasts.
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Petrone Linda, Najafi-Fard Saeid, Altera Anna Maria Gerarda, Aiello Alessandra, Cuzzi Gilda, Farroni Chiara, Petruccioli Elisa, Vanini Valentina, Salmi Andrea, Barbarossa Giulia, Pajno Maria Chiara, Scolieri Palma, Dockrell Hazel M, Joosten Simone A, Mellini Valeria, Palmieri Fabrizio, Gualano Gina, Goletti Delia, INMI TB-T2D Study Group
Аннотация
OBJECTIVE: Type 2 diabetes (T2D) increases the risk of tuberculosis (TB) and TB severity; however, its effects on B-cells in the TB-T2D syndemic are not fully understood.
METHODS: We evaluated by flow cytometry, the distribution of circulating B-cell subsets in patients with TB disease, TB-T2D, subjects with TB infection (TBI), TBI-T2D, healthy controls (HCs), T2D, patients with pulmonary respiratory diseases other than TB (ORDs), and ORD-T2D. Plasma levels of unspecific or PPD-specific IgG and B-cell-related soluble factors were measured by multiplex assays or ELISA.
RESULTS: Total B-cell frequency was similar across groups. TB-T2D patients showed decreased transitional B cells compared to TB, TBI-T2D, HC, and T2D. Transitional B-cell frequency significantly and negatively correlated with HbA1c levels in the TB-T2D group. Moreover, plasmablast frequency was increased in TB-T2D compared to TB, TBI-T2D, and T2D. Unspecific or PPD-specific IgG levels were not modulated by T2D. BAFF levels increased in TB and TB-T2D compared to the other groups, whereas the levels of SDF-1 were decreased in TB and TBI irrespective of T2D, compared to the controls.
CONCLUSIONS: Overall, T2D reshapes B-cell compartments in TB, reducing potentially anti-inflammatory transitional B-cells and increasing plasmablasts, possibly reinforcing inflammation and impacting B-cell development and humoral immunity in TB-T2D.
METHODS: We evaluated by flow cytometry, the distribution of circulating B-cell subsets in patients with TB disease, TB-T2D, subjects with TB infection (TBI), TBI-T2D, healthy controls (HCs), T2D, patients with pulmonary respiratory diseases other than TB (ORDs), and ORD-T2D. Plasma levels of unspecific or PPD-specific IgG and B-cell-related soluble factors were measured by multiplex assays or ELISA.
RESULTS: Total B-cell frequency was similar across groups. TB-T2D patients showed decreased transitional B cells compared to TB, TBI-T2D, HC, and T2D. Transitional B-cell frequency significantly and negatively correlated with HbA1c levels in the TB-T2D group. Moreover, plasmablast frequency was increased in TB-T2D compared to TB, TBI-T2D, and T2D. Unspecific or PPD-specific IgG levels were not modulated by T2D. BAFF levels increased in TB and TB-T2D compared to the other groups, whereas the levels of SDF-1 were decreased in TB and TBI irrespective of T2D, compared to the controls.
CONCLUSIONS: Overall, T2D reshapes B-cell compartments in TB, reducing potentially anti-inflammatory transitional B-cells and increasing plasmablasts, possibly reinforcing inflammation and impacting B-cell development and humoral immunity in TB-T2D.