A Mini-Review of Current Treatment Approaches and Gene Therapy as Potential Interventions for Diabetes Mellitus Types 1.

Diabetes mellitus type 1 is a chronic condition characterized by the loss or dysfunction of ß-cells in the pancreas, resulting in insufficient insulin production. This mini-review examines current treatment approaches and explores the potential of gene therapy as interventions for type 1 diabetes mellitus. The discussed strategies include ß-cell sensitization, ß-cell regeneration from various cell sources, stem cell therapies, and the promotion of ß-cell replication. The article emphasizes the importance of understanding the pathways involved in ß-cell proliferation and the factors influencing their replication. Stem cell therapies, particularly using embryonic stem cells and induced pluripotent stem cells, hold promise for generating ß-cells and replacing damaged or lost cells. Additionally, gene therapy offers a novel approach by manipulating genes involved in insulin production and glucose metabolism. However, ethical considerations, tumorigenic risks, and the translation of these therapies into clinical trials pose challenges. Nonetheless, the ongoing research and advancements in these areas provide hope for improved management and treatment of type 1 diabetes mellitus.

IL-23 plasma level measurement in relapsing remitting multiple sclerosis (RRMS) patients compared to healthy subjects.

BACKGROUND: Multiple sclerosis (MS) is a chronic neuroinflammatory disease with unknown etiology and variable clinical evolution. Interleukin-23 (IL-23), a member of the IL-12 cytokine family is a heterodimeric cytokine composed of the IL-12p40 subunit, and with a novel p19 subunit, its ability to enhance the expansion of T helper type 17 (Th17) cells indicates the responsibility for many of the inflammatory autoimmune responses. OBJECTIVE: The objective of the project is to measure IL-23 level in plasma of multiple sclerosis (MS) patients in comparison with healthy control subjects. METHODS: In a case-control study, plasma was collected from healthy subjects as control group (n = 40) and patients with relapsing remitting multiple sclerosis (RRMS) (n = 40). The plasma level of IL-23 was assessed by ELISA method. Statistical analysis was performed with SPSS (Ver. 16). RESULTS: Plasma level of IL-23 in MS patients was significantly increased compared to control subjects (p Value < 0.001). CONCLUSIONS: Our findings revealed the increased IL-23 level in patients' group. In conclusion, the inhibition of IL-23 might be a novel and promising therapeutic strategy, especially in the therapy of autoimmune inflammatory diseases. IL-23 plays a pivotal role in development of MS and might be a specific marker and therapeutic target for MS.