Biological functions of extracellular vesicles from mammalian cells.

Extracellular vesicles (EVs) are enclosed by a phospholipid bilayer and can be secreted by most types of cells. EVs deliver cargo from the secreting cell into the cytoplasm of recipient cells, influencing the function of the recipient cells. EVs are attracting increasing attention from a broad range of clinicians and scientists due to their ability to promote or inhibit various physiological pathways or pathological conditions.

Sex-dependent expression levels of VAV1 and P2X7 in PBMC of multiple sclerosis patients.

Multiple sclerosis (MS) is an inflammatory autoimmune disorder of the central nervous system and the leading cause of progressive neurological disability in young adults. It decreases the patient's lifespan by about 10 years and affects women more than men. No medication entirely restricts or reverses neurological degradation.

P2X7 purinergic receptor plays a critical role in maintaining T-cell homeostasis and preventing lupus pathogenesis.

The severe lymphoproliferative and lupus diseases developed by MRL/ mice depend on interactions between the Fas mutation and MRL genetic background. Thus, the Fas mutation causes limited disease in C57BL/6 mice. We previously found that accumulating B220 CD4CD8 double negative (DN) T cells in MRL/ mice show defective P2X7 receptor ( P2X7)-induced cellular functions, suggesting that P2X7 contributes to T-cell homeostasis, along with Fas.

The ins and outs of T cell signaling.

This special edition summarizes major advances in our understanding of signaling by T lymphocytes. T cell interactions with antigen-presenting cells (APCs) and other immune cells are characterized by changes in T cell adhesion and major rearrangements of the actin cytoskeleton. This issue describes some of the mediators of these changes both within the T cells and on the T cell surface.

Scaling the tips of the ALPS.

This special issue contains four review articles that describe advances in analysis of mutations responsible for the autoimmune lymphoproliferative syndrome (ALPS). This disease is triggered by a family of mutations in genes involved in the extrinsic apoptotic pathway such as FAS, FASL and CASP10. Advances in sequencing technology have enabled extended genetic testing of patients with various defects in alternative biological have pathways that can cause ALPS-like syndromes.