Secondly, but more importantly, we do not know whether the Marsh I lesion always progresses at some future time or whether it can also regress like lymphocytic
insulitis in (female) NOD mice (40).
Functional IL-18 Is produced by primary pancreatic mouse islets and NIT-1 beta cells and participates in the progression towards destructive
insulitis. Horm Res 2002;57:94-104.
The presence of DRB1*04-DQB1*0302 and DRB1*03 among human leukocyte antigen (HLA) class II haplotypes in at least 90% of the individuals with the disease, detection of autoreactive anti-islet antigen specific T cells in the circulation of new onset or prediabetic individuals, demonstration of lymphocyte infiltration in the islet cells during the development of
insulitis and increased predisposition to Addison's disease and celiac disease support the role of autoimmunity in the progression to T1D (2,3,4,5,6).
AG019 also preserved residual ?-cell function, halted
insulitis progression and increased the frequency of regulatory T cells.
In the NOD mouse,
insulitis occurs at 3-4 weeks of age and is accompanied by infiltration of islets by CD4 and CD8 lymphocytes, resulting in cytotoxicity and [beta] cell destruction with the onset of overt diabetes at around 18 weeks.
Regarding the study of mechanisms, an in vivo study demonstrated that methimazole-induced hypothyroidism promotes immune cell infiltration into pancreatic islets of female rabbits, which could be inducing pancreatitis and
insulitis [79].
evaluated a spontaneous autoimmune diabetes model and showed that IL-17A and IL-17F expressions in islets are related to
insulitis in NOD mice.
Antigen-based studies in mice have demonstrated that DD are ineffective for tolerance induction when applied as peptide therapy in NOD mice with progressive
insulitis, and emerging data suggest that use of nontargeted determinants may allow better priming of naive T cells into regulatory function if treatment is initiated after the autoimmune process is well-established [26].
Immunohistochemical characterization of monocytes-macrophages and dendritic cells involved in the initiation of the
insulitis and [beta]-cell destruction in NOD mice.
The role of inflammation in
insulitis and [beta]-cell loss in type 1 diabetes.
investigated whether BV can prevent
insulitis and the development of diabetes in nonobese diabetic (NOD) female mice that have been subdivided into control (n = 24) and BV (n = 24) treated groups [20].
Nygaard, "Long-term bisphenol A exposure accelerates
insulitis development in diabetes-prone NOD mice," Immunopharmacology and Immunotoxicology, vol.
