Modulatory effect of interleukin-2 loaded chitosan nano sphere on regulatory T cell activity in streptozotocin-induced diabetic mice.

Objective: The current study aimed to assess the modulating effect of IL-2 encapsulated chitosan-nanoparticles (CSNPs) on the function of Treg cells through induction of type 1 diabetes (T1D). Treg cell function was monitored by the forkhead box P3 (FoxP3) and transforming growth factor beta (TGFβ) levels, correlating them with blood glucose and serum insulin levels.

Materials And Methods: In this case-control study, a low dose of IL-2 (free and chitosan-loaded) was injected into a diabetic mice group.

Low-dose interleukin-2-loaded nanoparticle effect on NK and T-reg cell expression in experimentally induced type 1 diabetes mellitus.

Introduction: Type 1 diabetes mellitus is an autoimmune disorder characterized by inflammatory damage to pancreatic β cells resulting in loss of insulin secretion. In autoimmune type 1 diabetes mellitus (T1D) natural killer cells (NK) initiate pancreatic islets cell lyses in autoimmune T1D. Loss of T regulatory cells (Treg) at disease onset facilitates the activation and accumulation of NKs in the pancreatic microenvironment.

Concanavalin-A as a Model for Induction of Murine Autoimmune Hepatitis: Role of TNF-α and NF-κβ During The Acute Phase.

Autoimmune hepatitis (AIH) is a heterogeneous immune-mediated chronic liver disease affecting children and adults. It is important to rely on a specific animal model to study the hepatic changes and to evaluate the roles played by pro-inflammatory cytokines such as tumor necrosis factor alpha "TNF-α" and transcription factors such as nuclear factor kappa-light-chain-enhancer of activated B cells "NF-κβ" in the pathogenesis and outcome of the disease. This will help to identify specific targets for treatment of AIH.

Effect of low dose IL-2 loaded chitosan nanoparticles on natural killer and regulatory T cell expression in experimentally induced autoimmune type 1 diabetes mellitus.

Introduction: Natural killer cells (NK) initiate pancreatic islets cell lyses in autoimmune type 1 diabetes mellitus (T1D). Loss of T regulatory cells (Treg) at disease onset facilitates activation and accumulation of NKs in the pancreatic microenvironment. A proper low dose interleukin 2 (IL-2) could enhance Tregs and enforce control and regulation of pro-inflammatory NKs.