Few Layer Graphene Does Not Affect Cellular Homeostasis of Mouse Macrophages.

Graphene-related materials (GRMs) are widely used in various applications due to their unique properties. A growing number of reports describe the impact of different carbon nanomaterials, including graphene oxide (GO), reduced GO (rGO), and carbon nanotubes (CNT), on immune cells, but there is still a very limited number of studies on graphene. In this work, we investigated the biological responses of few layer graphene (FLG) on mouse macrophages (bone marrow derived macrophages, BMDMs), which are part of the first line of defense in innate immunity.

Few layer graphene does not affect the function and the autophagic activity of primary lymphocytes.

Carbon-based nanomaterials represent a new tool in future medical applications. Thus, focusing on the evaluation of the degree of their safety has been growing in the last years. In this study we were particularly interested in understanding the impact of few layer graphene (FLG) on primary murine lymphocytes.

"Ultramixing": A Simple and Effective Method To Obtain Controlled and Stable Dispersions of Graphene Oxide in Cell Culture Media.

The last decade has seen an increase in the application of graphene oxide (GO) in the biomedical field. GO has been successfully exploited for its ability to deliver many kinds of drugs into target cells. However, GO toxicity assessment is still controversial.

ATG5 is required for B cell polarization and presentation of particulate antigens.

The involvement of macroautophagy/autophagy proteins in B-cell receptor (BCR) trafficking, although suspected, is not well understood. We show that ATG5 (autophagy related 5) contributes to BCR polarization after stimulation and internalization into LAMP1 (lysosomal-associated membrane protein 1) and major histocompatibility complex class II (MHC-II) compartments. BCR polarization is crucial in the context of immobilized antigen processing.

CD4 T cell autophagy is integral to memory maintenance.

Studies of mice deficient for autophagy in T cells since thymic development, concluded that autophagy is integral to mature T cell homeostasis. Basal survival and functional impairments in vivo, limited the use of these models to delineate the role of autophagy during the immune response. We generated Atg5 distal Lck (dLck)-cre mice, with deletion of autophagy only at a mature stage.

[Autophagy in T and B cell homeostasis: recycling for sustainable growth].

Macroautophagy often abbreviated by "autophagy" is an intracellular degradation mechanism linked to lysosomal activity. Autophagy is conserved from yeast to mammals and plays a role in the response to energetic stress and in organelle homeostasis. Autophagy is also involved in the regulation of immunity, in particular in the adaptive immune response, which involves B and T lymphocytes.

Autophagy is dispensable for B-cell development but essential for humoral autoimmune responses.

To gain new insight into the role of B-cell autophagy, we generated two novel mouse models deficient for the autophagy-related gene (Atg)5, one from the outset pro-B cell stage (Atg5(f/-) Mb1 cre) and the other in mature B cells only (Atg5(f/-) CD21 cre). We show that autophagy is dispensable for pro- to pre-B cell transition, but necessary at a basal level to maintain normal numbers of peripheral B cells. It appears non-essential for B-cell activation under B-cell receptor stimulation but required for their survival after lipopolysaccharide stimulation that drives plasmablast differentiation and for specific IgM production after immunization.