“Diabetes mellitus type 1 is an autoimmune disease which is characterized by the destruction of the pancreatic beta cells that produce insulin by immune cells T lymphocytes and macrophages that invading the islets of Langerhans”. A polyprotein called NLRP3 contributes significantly to the inflammation process in the body. Complex protein known as the nucleotide-binding domain, leucine-rich containing family, pyrin domain containing-3 inflammasome that is very important to the process of inflammation. It is made up of the proteins Procaspase-1, NLRP3, and ASC, and its function is to identify pathogens. When a cell is presented with a pathogen-associated molecular pattern, further recognized as a PAMP, or a damage-associated molecular pattern, further recognized as a DAMP, the cell's immune response is triggered (DAMP), the NLRP3 inflammasome is triggered. Caspase-1, when activated, catalysis the conversion of inactive forms of pro-inflammatory cytokines and interleukins (IL-1 and IL-18) into their active metabolic forms, which in turn promotes inflammation. The pathophysiology of type 1 diabetes is affected by the involvement of the NLRP3 inflammasome and also NLRP3 is associated with vast scope of inflammation and immunological conditions. Once immune cells employ Toll-like receptors (TLRs) to identify particular pathogens or endogenous alarm signals, IL-1b is generated as a first-stage indicator of illness. One of the distinguishing features of type 1 diabetes is that auto-reactive T lymphocytes are the cause of the beta cells found in the pancreas that are responsible for insulin production being destroyed. Also, IL-1beta kills beta-cells directly and sends out an inflammatory signal during the disease's initial phases. Those who have just been diagnosed with diabetes mellitus or who have been living with the condition for a long time have increased levels of IL-1b, although treatment may bring these levels down. Moreover, the decreased expression of IL-1RA in islets from donors who did not have diabetes who were subjected to sera from type 1 diabetes patients causes beta-cells that produce insulin to become dysfunctional and eventually die. This further increases the creation of IL-1 beta, which is harmful to beta-cells.