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Introduction: Low albumin levels, high levels of high-sensitivity C-reactive protein (hs-CRP), and high white blood cell count were risk factors for changes in arterial intima-media thickness (IMT). Femoral artery IMT damages were one of the common peripheral artery type 2 diabetes. This study was conducted to determine the association between femoral artery IMT and plasma albumin, hs-CRP levels, and white blood cell count in newly diagnosed patients with type 2 diabetes mellitus (nT2D). Materials and Methods: From January 2015 to May 2020, 306 patients with nT2D were recruited for this cross-sectional descriptive study at Vietnam's National Endocrinology Hospital. We measured IMT by Doppler ultrasound. Results: There was a statistically significant difference in albumin, hs-CRP levels, hs-CRP-to-albumin ratio, and white blood cell counts between three different IMT groups namely normal IMT, thick IMT, and atherosclerosis (p = 0.003, p = 0.001, p = 0.001 and p = 0.049, respectively). In the multivariate linear regression analysis, white blood cell count, and hs-CRP levels showed a significantly positive correlation to IMT (standardized B and p of 0.17, 0.015 and 0.163, 0.024, respectively), but albumin levels were a significantly negative correlation to IMT (standardized B = – 0.151, p = 0.029). The multivariate logistic regression analysis showed that albumin (OR = 0.79, 95% CI 0.65– 0.90, p = 0.018), hs-CRP (OR = 1.09, 95% CI 1.01– 1.18, p = 0.026), and white blood cell count (OR = 1.36, 95% CI 1.03– 1.81, p = 0.033) had correlation to atherosclerosis of femoral artery. Conclusion: Reduced plasma albumin, elevated hs-CRP, and white blood cell count associated with IMT increased the odds for atherosclerosis of femoral artery among nT2D. [ABSTRACT FROM AUTHOR]

The immune system is tightly controlled by regulatory processes that allow for the elimination of invading pathogens, while limiting immunopathological damage to the host. In the present study, we found that conditional deletion of the cell surface receptor Toso on B cells unexpectedly resulted in impaired proinflammatory T cell responses, which led to impaired immune protection in an acute viral infection model and was associated with reduced immunopathological tissue damage in a chronic inflammatory context. Toso exhibited its B cell-inherent immunoregulatory function by negatively controlling the pool of IL-10-competent B1 and B2 B cells, which were characterized by a high degree of self-reactivity and were shown to mediate immunosuppressive activity on inflammatory T cell responses in vivo. Our results indicate that Toso is involved in the differentiation/maintenance of regulatory B cells by fine-tuning B cell receptor activation thresholds. Furthermore, we showed that during influenza A-induced pulmonary inflammation, the application of Toso-specific antibodies selectively induced IL-10-competent B cells at the site of inflammation and resulted in decreased proinflammatory cytokine production by lung T cells. These findings suggest that Toso may serve as a novel therapeutic target to dampen pathogenic T cell responses via the modulation of IL-10-competent regulatory B cells. [ABSTRACT FROM AUTHOR]