Innovative immunotherapies and emerging treatments in type 1 diabetes management

Type 1 diabetes mellitus (T1D) is a chronic autoimmune disease characterized by the selective destruction of pancreatic insulin-producing beta cells, primarily mediated by CD4+ and CD8+ T cells. This review comprehensively examines the latest advances in immunotherapeutic approaches to T1D, categorizing current strategies into four main groups: antigen-independent therapies, antigen-dependent therapies, beta cell therapies, and stem cell therapies. Antigen-independent strategies, such as antibody-based therapies (e.g., Abatacept and Teplizumab) and cytokine inhibitors (e.g., Anakinra and Etanercept), have shown potential in preserving beta cell function by modulating immune responses. Antigen-dependent strategies focus on inducing immune tolerance to specific beta cell antigens, with mixed results from clinical trials involving autoantigen vaccines like GAD65. Beta cell therapies, including islet transplantation, offer promising outcomes but face challenges related to immunosuppression and donor availability. Stem cell therapies, particularly using mesenchymal stem cells (MSCs) and autologous hematopoietic stem cells (HSCs), demonstrate potential in immune modulation and beta cell regeneration. Novel approaches, such as Chimeric Antigen Receptor (CAR)–Tregs therapy and JAK-STAT pathway inhibition, represent exciting areas of ongoing research. This comprehensive overview underscores the necessity of personalized therapeutic approaches and continued research to optimize existing therapies and explore new targets, ultimately aiming to improve outcomes and achieve a potential cure for T1D

Protective effect of honokiol on cadmium-induced liver injury in chickens

ABSTRACT: Cadmium (Cd), a highly toxic heavy metal in the environment, poses a significant threat to livestock and poultry farming. Honokiol (HNK), a Chinese herbal extract with potent antioxidant activity, acts through oxidative damage and inflammation. Cd induces oxidative stress and causes liver damage in animals. However, whether HNK can alleviate Cd-induced liver injury in chickens and its mechanism remains unclear. In this study, the 48 chickens were randomly allocated into 4 groups, control group, Cd group (70 mg/kg Cd), HNK group (200 mg/kg HNK) and Cd + HNK group (70 mg/kg Cd+200 mg/kg HNK). Results showed that HNK improved the Cd induced reduction in chicken body weight, liver weight, and liver coefficient. HNK recovered the Cd induced liver damaged through increased serum liver biochemical indexes, impaired liver oxidase activity and the disordered the expression level of antioxidant genes. HNK alleviated Cd induced pathological and ultrastructure damage of liver tissue and liver cell that leads apoptosis. HNK decreased Cd contents in the liver, Cd induced disturbances in the levels of trace elements such as iron, copper, zinc, manganese, and selenium. HNK attenuated the damage to the gap junction structure of chicken liver cells caused by Cd and reduced the impairment of oxidase activity and the expression level of antioxidant genes induced by Cd. In conclusion, HNK presents essential preventive measures and a novel pharmacological potential therapy against Cd induced liver injury. Our experiments show that HNK can be used as a new green feed additive in the poultry industry, which provides a theoretical basis for HNK to deal with the pollution caused by Cd in the poultry industry