Science Immunology

The PDF file includes:

  • Fig. S1. Recovery from EAE requires functional autophagy in the myeloid but not in the T cell compartment.
  • Fig. S2. Atg7 and Ulk1 deficiency in microglia affect noncanonical and canonical autophagy, respectively.
  • Fig. S3. Atg7 deficiency induces alterations in microglial transcriptome during EAE.
  • Fig. S4. Atg7 deficiency in microglia increases T cell proliferation and polarization to an inflammatory phenotype.
  • Fig. S5. Gene set enrichment analysis.
  • Fig. S6. Atg7-deficient microglia have impaired scavenger receptor recirculation associated with increased inflammation and a reduced myelinating oligodendrocyte population in EAE.
  • Fig. S7. Late-stage EAE is characterized by extensive tissue destruction and signs of increase in inflammation in mice with Atg7-deficient microglia.
  • Fig. S8. Trehalose boosts EAE recovery and decreases immune infiltration in aged mice.
  • Fig. S9. Gating strategy for defining cell populations by flow cytometry.

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Other Supplementary Material for this manuscript includes the following:

  • Table S1 (Microsoft Excel format). RNA-sequencing data.
  • Table S2 (Microsoft Excel format). IPA, ORA, and REViGO analysis.
  • Table S3 (Microsoft Excel format). Genes shared among homeostatic or pathogenic gene sets.
  • Table S4 (Microsoft Excel format). RNA sequencing data.
  • Table S5 (Microsoft Excel format). Technical data file.
  • Table S6 (Microsoft Excel format). Raw data.
  • Movie S1 (.mp4 format). Accumulation of phagocytosed myelin in Atg7fl/fl Cx3cr1CreERT2 microglia.
  • Movie S2 (.mp4 format). Accumulation of myelin-containing phagosomes in microglia of aged mice.