Studies have confirmed that in a mouse model of T1DM, a large increase in glomerular and interstitial CD4+ and CD8+ T cells and deposition of immune complexes are found, local activated cytokine levels are increased to stimulate the activation of neighboring macrophages, and these complexes activate complement trigger inflammation and glomerulonephritis, leading to podocyte damage, thereby promoting the production of proteinuria [51, 52]. Here, CD8A is linked to type 1 diabetes mellitus.