Laryngeal Mucous Membrane Pemphigoid as an Immune-related Adverse Effect of Pembrolizumab Treatment.

Pembrolizumab is an immune checkpoint inhibitor (ICI) approved for multiple indications in a variety of malignancies. Although generally well tolerated, the potential for significant adverse effects, specifically immune related adverse effects (irAEs) needs to be taken into consideration. Several cases of bullous pemphigoid have been reported as a cutaneous adverse effect of ICIs since 2015, and there are recent reports of mucous membrane pemphigoid (MMP).

Early-life inflammation primes a T helper 2 cell-fibroblast niche in skin.

Inflammation early in life can prime the local immune milieu of peripheral tissues, which can cause lasting changes in immunological tone that confer disease protection or susceptibility. The cellular and molecular mechanisms that prompt changes in immune tone in many nonlymphoid tissues remain largely unknown. Here we find that time-limited neonatal inflammation induced by a transient reduction in neonatal regulatory T cells causes a dysregulation of subcutaneous tissue in mouse skin.

Keepin' it regulatory: Foxp3 gets a BAFfling SWItch.

A novel role for SWI/SNF complexes in tuning Foxp3 expression and activity in T.

Transcriptional control of non-apoptotic developmental cell death in C. elegans.

Programmed cell death is an essential aspect of animal development. Mutations in vertebrate genes that mediate apoptosis only mildly perturb development, suggesting that other cell death modes likely have important roles. Linker cell-type death (LCD) is a morphologically conserved cell death form operating during the development of Caenorhabditis elegans and vertebrates.

HSF-1 activates the ubiquitin proteasome system to promote non-apoptotic developmental cell death in C. elegans.

Apoptosis is a prominent metazoan cell death form. Yet, mutations in apoptosis regulators cause only minor defects in vertebrate development, suggesting that another developmental cell death mechanism exists. While some non-apoptotic programs have been molecularly characterized, none appear to control developmental cell culling.

Noncanonical cell death in the nematode Caenorhabditis elegans.

The nematode Caenorhabditis elegans has served as a fruitful setting for cell death research for over three decades. A conserved pathway of four genes, egl-1/BH3-only, ced-9/Bcl-2, ced-4/Apaf-1, and ced-3/caspase, coordinates most developmental cell deaths in C. elegans.