The selective destruction of pancreatic β-cells causes type 1 diabetes mellitus (T1DM), and CD8+ T cells, which include cytotoxic T cells, are key in this process. Now a study by Mark Peakman and colleagues shows that changes in the number of β-cell-specific effector memory T cells expressing CD57 reflect changes in levels of C-peptide (a surrogate marker for insulin levels) in patients with T1DM.

Previous studies have established that large numbers of CD8+ T cells are present in the pancreatic islets of patients with T1DM. The CD8+ T cells found in these islets recognize β-cell antigens; however, the relationship between CD8+ T cells and β-cell function is unknown, leading Peakman and his team to investigate this link.

In the current study, the researchers used samples of peripheral blood mononuclear cells from 38 patients with T1DM (aged 6–34 years), who were followed up for 2 years. An initial characterization of the different T cell populations in the patient samples showed that the subset of β-cell-specific T cells were largely composed of effector memory T cells expressing the terminal differentiation marker CD57.

Next, Peakman and colleagues analysed the levels of C-peptide in relation to the number of CD57+ effector memory CD8+ T cells and found a positive correlation. The results suggest that the numbers of these T cells correspond to changes in β-cell function. Additionally, the researchers found that this positive correlation is more marked in children who are <12 years of age.

Finally, the researchers compared the transcription profiles of effector memory CD8+ T cells with and without CD57 expression and found that CD57+ cells show increased expression of genes related to cytotoxicity. The data suggest that the β-cell-specific CD57+ effector memory CD8+ T cells have increased cytotoxicity and are capable of causing β-cell destruction. Therefore, changes in circulating CD57+ effector memory CD8+ T cells can be used to monitor the health of pancreatic islets.