Loss of BECN1 changes what B cells target and how they present antigens without stopping autophagosome formation

In BECN1-deficient human B lymphoblastoid cell lines, autophagosome formation remained intact despite the absence of BECN1.

• Autophagic flux can still be induced in BECN1-deficient cell lines during nutrient starvation or MTOR inhibition.
• The composition of autophagosomal cargo is significantly different between BECN1-deficient and control cell lines.
• Autophagosomes in BECN1-deficient cells preferentially form at the endoplasmic reticulum rather than at endosomes or lysosomes.
• Incorporation of endosomal TLR3 into autophagosomes is less frequent in BECN1-deficient cells.
• Proteins associated with the endoplasmic reticulum's peptide loading complex for MHC class I antigen presentation are enriched in autophagosomes from BECN1-deficient cells.
• A reduced detection of BECN1-deficient cells by T cells may occur due to alterations in cargo selection.

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