This was also true when using another inhibitor of MTOR (Torin-1) (Figure 4D-F). and may also contribute to our understanding of CD36-mediated autophagy in other cells as well as in B cell lymphomas that have been shown to express the receptor. Abbreviations: AICDA/AID: activation-induced cytidine deaminase; ATG5: autophagy Bilastine related 5; ATP: adenosine Bilastine triphosphate; BCR: B-cell receptor; CPG: unmethylated cytosine-guanosine; CQ: chloroquine; DC: dendritic cells; FOB: follicular B cells; GC: germinal center; Ig: immunoglobulin; LPS: lipopolysaccharide; MAP1LC3/LC3: microtubule-associated protein 1 light chain 3; MFI: mean fluorescence intensity; MZB: marginal zone B cells; NP-CGG: 4-hydroxy-3-nitrophenylacetyl-chicken gamma globulin; OCR: oxygen consumption rate; oxLDL: oxidized low-density lipoprotein; Bilastine PC: plasma cells; Rapa: rapamycin; SQSTM1/p62: sequestosome 1; SRBC: sheep reddish blood cells; Tfh: follicular helper T cells; TLR: toll-like receptor. knockout mice the IgM and IgG levels were slightly reduced in response to heat-killed . Since CD36 is involved in several mechanisms during immune activation, we here investigate the role of CD36 in B cells by using mice with genetic ablation of CD36 specifically in B cells. Our obtaining reveals that CD36 deficiency in B cells suppress plasma cell formation, class switching, proliferation, and metabolic activation. This was accompanied by fewer autophagosomes in B cells lacking CD36 and we found that the receptor colocalizes with LC3B during autophagy induction. This shows that pattern recognition connected to altered self is a part of autophagy adaption in B cells. Results CD36 controls differentiation, proliferation, and metabolic status of B cells To investigate the role of CD36 in B cell activation, we first decided the expression pattern on na? ve and activated B cell subsets from mice. CD36?has previously been shown to be highly expressed by MZB and we confirmed this using splenic B cells . We also found CD36 expression on other B cell Bilastine subsets including transitional type 1 (T1) cells, transitional type 2 (T2) cells, T2 marginal zone precursors (T2MZP) cells, GC B cells, and plasma cells (PC). We also found that in the PC population the highest expression was on IgM+ cells (Physique 1A and S1A-E). The basal expression of CD36 on FOB was low but it could be induced by activation with either TLR4 ligand (LPS), TLR9 agonist (CPG), or anti-CD40 +?IL4 (Determine 1B). Moreover, we observed that this increased CD36 expression was not only located on the cell surface but also detected intracellularly with circulation cytometry when cells were stimulated with LPS (Physique 1C). To confirm this, we performed immunofluorescence staining of CD36 on activated B cells and we found that CD36 was localized both around the cell membrane and intracellularly in a punctate pattern in LPS-stimulated splenic B cells (Physique 1D). Next, B cell activation was investigated using stimulated splenic B cells from WT and knockout (KO) mice KO mice cultured with LPS, CPG, or anti-CD40 +?IL4 for 3 d presented relative to unstimulated (uns). (C) MFI of surface (left) and intracellular RBX1 (right) CD36 staining in splenic B cells from WT and KO mice after LPS activation. (D) Confocal microscopy analysis of CD36 staining in splenic B cells stimulated with LPS. Image size 35?m 35?m. (E-G) The frequency of PCs derived from purified splenic B cells cultured for 3 d. (H-J) The bar charts showing the proliferation of splenic B cells from WT and KO mice stimulated with LPS, CPG, or anti-CD40 +?IL4 measured by cell trace violet (CTV) dilution. Data are representative of three impartial experiments. *P? ?0.05, **P? ?0.01 and ***P? ?0.001 (Mann-Whitney test) Since scavenger receptors are known to participate in many cellular functions and little is known of their function in B cells, especially intracellularly, we next used immunoprecipitation of CD36 and proteomic analysis of the binding partners to.