Selective autophagy impedes KSHV entry after recruiting the membrane damage sensor galectin-8 to virus-containing endosomes.

Kaposi sarcoma-associated herpesvirus (KSHV) is an oncogenic γ-herpesvirus. Autophagy during KSHV entry has remained unexplored. We show that LC3 lipidation as a hallmark of autophagy is induced shortly after KSHV entry.

Analysis of LC3-Associated Phagocytosis and Antigen Presentation in Macrophages and B Cells.

Canonical autophagy and the non-canonical autophagy pathway LC3-associated phagocytosis (LAP) play crucial roles in the immune system by processing antigens for major histocompatibility complex (MHC) class II restricted presentation to CD4 T cells. Recent studies offer insight into the relationship between LAP, autophagy, and antigen processing in macrophages and dendritic cells; however their involvement during antigen processing in B cells is less well understood.In this chapter, we describe how to monitor, manipulate, and understand the role of LAP and classical autophagy during MHC-restricted antigen presentation by human monocyte-derived macrophages as well as in B cell lymphoblastoid cell lines (LCLs).

Modulation of Emotional Conflict Processing by High-Definition Transcranial Direct Current Stimulation (HD-TDCS).

Cognitive control is characterized by selective attention to relevant stimuli while irrelevant, distracting stimuli are inhibited. While the classical color-word Stroop task was implemented to investigate the processes of cognitive control, a variant of it-the face-word Stroop task-allows for directly investigating processes of emotional conflict control. It is thought that the prefrontal cortex (PFC) is especially involved in processes of cognitive control, while the rostral cingulate is mainly associated with the resolution of emotional conflict.

Tumor necrosis factor causes persistent sensitization of joint nociceptors to mechanical stimuli in rats.

Objective: During inflammation in the joint, normal joint movements are usually painful. A neuronal mechanism for this form of mechanical hyperalgesia is the persistent sensitization of joint nociceptors to mechanical stimuli. Because tumor necrosis factor (TNF) is a major mediator of joint inflammation, we undertook the present study both to explore the potential of TNF to sensitize joint nociceptors to mechanical stimuli and to address the cellular mechanism involved.