Blocking CXCR2 can lead to a rapid decline in islet-specific CD8 T cells at early stages, which may not only suppress subsequent diabetes-induced T cell responses, but also suppress the subsequent development of diabetes.[101,102] Recently, decreased expression of Cxcr1 messenger ribonucleic acid was found in both neutrophils and CD4 T lymphocytes isolated from NOD mice compared to diabetes-resistant mice. Here, CD4 is linked to diabetes mellitus.