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The immune system needs to tailor its responses according to the threat level. Lemaitre and colleagues (p 1150; News and Views by Tomé-Poderti and Saleh, p 1138) identify a novel version of the peptidoglycan receptor PGRP-LC in flies and demonstrate that this 'tunes' immune responses according to challenge with live (threatening) bacteria or dead (harmless) bacteria. The original image by Claudine Neyenis shows a section through fat-body cells expressing a mutant form of the receptor (green). Artwork by Lewis Long.
CD1a on Langerhans cells in the epidermis is the lipid receptor for the plant-derived allergen urushiol and self lipids and is a key amplifier of inflammatory responses in urushiol-induced contact dermatitis as well as in psoriasis.
Follicular helper T cells (TFH cells) sequentially acquire the potential to secrete interleukin 21 (IL-21) and IL-4. The shift from secretion of IL-21 to that of IL-4 modifies the nature of the 'help' signals delivered by TFH cells to germinal center (GC) B cells.
New findings show that the NLRP3 inflammasome is inactivated by disassembly of the inflammasome mediated by the kinase PKA and that this regulation might be negated in NLRP3-gain-of-function diseases.
The Drosophila immune system distinguishes live, and potentially harmful, bacteria from harmless dead bacteria through the use of a splice variant of the receptor PGRP-LC.
In this Review, Chen and colleagues discuss recent advances in understanding of the cGAS–STING pathway, focusing on the regulatory mechanisms and roles of this pathway in heath and disease.
The immune system tailors its responses according to the level of threat. Lemaitre and colleagues identify a novel version of the peptidoglycan receptor PGRP-LC and demonstrate that it tunes immune responses to live (threatening) or dead (harmless) bacteria.
Human Langerhans cells express CD1a, but those in mice do not, which makes determination of its function on these cells challenging in vivo. Through the use of a transgenic mouse that expresses CD1a, Winau and colleagues demonstrate that Langerhans cells use CD1a to present contact allergens and self lipid antigens and thereby worsen inflammatory skin conditions.
CD8α+ DCs are specialized at cross-presentation, but the mechanisms that bestow this ability have not been fully characterized. Cao and colleagues show that the lectin Siglec-G negatively regulates cross-presentation and that its expression is lower in CD8α+ DCs.
Dysregulated inflammasome activation is associated with auto-inflammatory diseases. Chadee and colleagues show that prostaglandin E2 triggers rapid inhibition of the inflammasome component NLRP3 by the kinase PKA. Patients with the inflammatory disease CAPS who have mutations in NLPR3 escape this negative regulation.
B cells and follicular helper T cells in B cell follicles can act as important reservoirs for chronic infection by viruses such as HIV or EBV. Yu and colleagues show that a specialized subpopulation of cytotoxic T cells can enter the B cell follicles to eliminate such virus-infected cells.
Craft and colleagues show that follicular helper T cells progress through transcriptionally and functionally distinct stages that provide specific signals for germinal center regulation.
Holländer and colleagues provide a map of genes that are direct targets of the transcription factor Foxn1 in thymic epithelial cells and show that Foxn1 controls genes encoding products involved in thymocyte development, antigen processing and thymocyte selection.
Boss and colleagues provide mechanistic insight into cell-division-coupled transcriptional and epigenetic reprogramming events during plasma cell differentiation.
Immunologic memory promotes faster and more-efficient responses after re-exposure to pathogens. Ahmed and colleagues characterize a subset of human B cells that arise after vaccination against or exposure to influenza or Ebola virus and contribute to the memory cell pool.