Role of alpha-synuclein in autophagy modulation of primary human T lymphocytes

T. Colasanti, M. Vomero, C. Alessandri, C. Barbati, A. Maselli, C. Camperio, F. Conti, A. Tinari, C. Carlo-Stella, L. Tuosto, D. Benincasa, G. Valesini, W. Malorni, M. Pierdominici, E. Ortona

Research output: Contribution to journalArticlepeer-review


It has been demonstrated that α-synuclein can aggregate and contribute to the pathogenesis of some neurodegenerative diseases and it is capable of hindering autophagy in neuronal cells. Here, we investigated the implication of α-synuclein in the autophagy process in primary human T lymphocytes. We provide evidence that: (i) knocking down of the α-synuclein gene resulted in increased autophagy, (ii) autophagy induction by energy deprivation was associated with a significant decrease of α-synuclein levels, (iii) autophagy inhibition by 3-methyladenine or by ATG5 knocking down led to a significant increase of α-synuclein levels, and (iv) autophagy impairment, constitutive in T lymphocytes from patients with systemic lupus erythematosus, was associated with abnormal accumulation of α-synuclein aggregates. These results suggest that α-synuclein could be considered as an autophagy-related marker of peripheral blood lymphocytes, potentially suitable for use in the clinical practice.

Original languageEnglish
Article numbere1265
JournalCell Death and Disease
Publication statusPublished - May 29 2014


  • autophagy
  • lymphoma
  • systemic lupus erythematosus
  • T lymphocytes
  • α-synuclein

ASJC Scopus subject areas

  • Cell Biology
  • Immunology
  • Cancer Research
  • Cellular and Molecular Neuroscience
  • Medicine(all)


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