Autophagy-related gene16L2, a potential serum biomarker of multiple sclerosis evaluated by bead-based proteomic technology

• Serum of Multiple sclerosis (MS) patients were evaluated by bead-based proteomic technology.
• Decreased levels of Atg16L2 in MS patients compared to controls were found.
• We further validated the decreased Atg16L2 by immunoblotting and real-time PCR.
• Decreased Atg16L2 may affect autophagy of T cells and contribute to MS relapse.

Multiple sclerosis (MS) is an autoimmune disease characterized by neuroinflammation and demyelination that are mediated by T cells. The prolonged survival of autoreactive T cells acts as a primary event to trigger an inflammatory cascade that mediates myelin loss and clinical relapse in MS. Recently, T cell survival has been shown to be modulated by the autophagy-related gene (Atg). In the present study, we performed bead fractionation/matrix-assisted laser desorption/ionization time-of-flight (MALDI-TOF) mass spectrometry analyses using serum from 54 MS patients and 55 healthy controls. Eleven peptides were significantly different between the two groups with one being identified as a fragment of Atg16L2. Then the decreased levels of Atg16L2 peptides in MS patients were validated by immunoblotting and real-time PCR. As the Atg12-Atg5·Atg16 multimeric complex plays an essential role in autophagy, our results suggest that Atg16L2 may play an important role in autophagy of T cells and serve as a potential biomarker to predict clinical relapse of MS.