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Type 1 diabetes mellitus (T1DM) is an autoimmune disease characterized by the loss of pancreatic beta cells. Clinical symptoms include hyperglycemia, inflammation as well as insulin deficiency. Two significant factors may increase the risk of this disease: - genetics and environment. Pancreatic islet cells contain glial cells called peri-islet Schwann cells (pSCs) which express glial fibrillary acidic protein (GFAP), a marker for central and peripheral glial cells. T1DM causes tissue destruction extending beyond islets to include glial cells. Gliosis can be observed in pre-diabetes prior to the loss of the islets. Non-obese diabetic (NOD) mouse is a widely studied animal model of T1DM. Nucleotide-binding domain leucine-rich repeat- containing receptors (NLRs) belongs to the innate immunity receptors. NLRs subtype-Nlrx1 located in mitochondria, is a unique receptor that acts as a negative regulator of inflammation in autoimmune disease. The focus of this study was to evaluate the hypothesis of whether Nlrx1 can decrease glial inflammation and delay gliosis in a pre-insulitis stage in NOD mice. The hypothesis was addressed by assessing the role of Nlrx1 in gliosis in the central nervous system (CNS) and peripheral nervous system (PNS). In this study, we used female wild-type and Nlrx1-/- NOD mice groups in order to analyse role of Nlrx1. Since this study is focused on the progression of gliosis during aging, we used NOD mice at three different ages, including 3, 8, and 13 weeks of age. Intending to evaluate gliosis progression during the pre-insulitis stage in NOD mice, we quantified GFAP which is expressed in pSCs. Moreover, we conducted quantification of GFAP expression in astrocytes as well to observe an association between CNS and pSCs gliosis. Using Nlrx1 Knockout (KO) mice, this study revealed that GFAP expression increased with aging and reached a maximum level at 8 weeks of age. The presence of Nlrx1 present an efficiency in reducing gliosis during