Decoding T cell senescence in cancer: Is revisiting required?

Senescence is an inherent cellular mechanism triggered as a response to stressful insults. It associates with several aspects of cancer progression and therapy. Senescent cells constitute a highly heterogeneous cellular population and their identification can be very challenging.

Potent induction of trained immunity by β-glucans.

cell wall component β-glucan has been extensively studied for its ability to induce epigenetic and functional reprogramming of innate immune cells, a process termed . We show that a high-complexity blend of two individual β-glucans from possesses strong bioactivity, resulting in an enhanced trained innate immune response by human primary monocytes. The training required the Dectin-1/CR3, TLR4, and MMR receptors, as well as the Raf-1, Syk, and PI3K downstream signaling molecules.

Decoding the Myeloid-Derived Suppressor Cells in Lymphoid Malignancies.

Myeloid-derived suppressor cells (MDSCs) are immature myeloid precursors which emerged as a potent regulator of the immune system, exerting suppressive properties in diverse disease settings. In regards to cancer, MDSCs have an established role in solid tumors; however, their contribution to immune regulation during hematologic malignancies and particularly in lymphomas remains ill-defined. Herein focused on lymphoma, we discuss the literature on MDSC cells in all histologic types, and we also refer to lessons learned by animal models of lymphoma.

Idiopathic thrombocytopenic purpura in childhood: twenty years of experience in a single center.

Background: Idiopathic thrombocytopenic purpura (ITP) is an autoimmune disorder with a variable clinical course.

Methods: A retrospective analysis was carried out of ITP patients presenting to a pediatric hematology-oncology department during a period of 20 years, with a focus on treatment and outcome.

Results: One hundred and twenty-four cases were recorded (mean patient age, 8.

The role of ghrelin, neuropeptide Y and leptin peptides in weight gain after deep brain stimulation for Parkinson's disease.

Background: The exact mechanism of weight gain (WG) after deep brain stimulation (DBS) of the subthalamic nucleus (STN) in patients with idiopathic Parkinson's disease remains unknown.

Objectives: To investigate a possible involvement of ghrelin, neuropeptide Y (NPY) and leptin in WG after DBS.

Methods: Twenty-three Parkinson patients were submitted for body composition measurements and blood sampling 3 days before, and 3 and 6 months after STN DBS.