B cells are precursors of antibody-producing cells. They are also professional antigen presenting cells (APCs) that can activate both CD4+ and CD8+ T cells through presentation of peptides in the context of major histocompatibility (MHC) class II and class I molecules, respectively. B cells are targets of the g-herpesvirus family like Epstein-Barr Virus (EBV) and Kaposi Sarcoma Herpesvirus (KSHV). This can lead to severe immune hyperactivation of primarily CD8+ T cells, exemplifying the superior ability of especially EBV infected B cells to expand these cytotoxic lymphocytes. Autophagy is a catabolic process executed through ATG (autophagy-related) molecules allowing the translocation of cytoplasmic material into lysosomes, after sequestration in double membrane vesicles. Autophagy is a master regulator of B cell biology. It allows memory B cell survival, long-lived plasma cell maintenance, and consequently immune homeostasis. The importance of autophagy in long-term B cell responses is illustrated by its necessity to maintain humoral protection against viruses like influenza. It also plays pathogenic roles contributing to continuous autoantibody production during systemic autoimmunity in mice. MHC class II presented peptides were initially thought to come mainly from endocytosis and phagocytosis, resulting in lysosomal degradation. More recently, autophagy has also been shown to generate MHC class II presented peptides. The contribution of autophagy in antigen processing of endogenous molecules onto MHC-II molecules is highly relevant for non-phagocytic cells such as B cells. One of the consortium partners was pioneer in the original discovery that autophagy generates MHC class II presented peptides. These initial studies showed that under some circumstances, intracellular antigens could be processed by the autophagy machinery for presentation to CD4+ T cells. Nevertheless, autophagy’s impact on antigen presentation by B cells has to date mainly been studied in vitro. The role of autophagy dependent antigen presentation by B cells in vivo is poorly known but it is highly probable that it allows to maintain CD4+ T cell activation but might dampen immune surveillance by cytotoxic T cells like in the case of EBV infection. Moreover, the role played by ATG molecules might be more complex that initially thought. Indeed, some endocytic processes use part of the autophagy machinery and are also involved in antigen presentation. Furthermore, they could be necessary for the entry of some viruses in target cells, or conversely to limit infection. Thus, dissecting the roles played by ATG molecules in B cells by using in vivo approaches and viral infection models is crucial. This issue will be addressed by (i) describing the functional role of the ATG machinery in endocytosis in B cells, including during g-herpesvirus entry, (ii) by characterizing in vivo the role played by ATG molecules in the germinal center (GC) reaction and antigen presentation, as well as by (iii) defining the impact of autophagy proteins on EBV infection and protective virus specific T cell priming in vivo.