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Shulman and colleagues show that in Peyer’s patches, in contrast to lymph nodes and spleen, T cells predominantly promoted expansion of B cells without clonal selection during pre-germinal centre events.
Members of the SLAM family of receptors promote the progression of invariant natural killer T cells through the thymic maturation process and facilitate proper host responses to exogenous lipid antigen through the recruitment and activity of SAP–Fyn and SHP-1, respectively.
Recent studies indicate that macrophages utilize NAD+-biosynthetic pathways to control inflammation and cell survival during the immune response and aging.
The identification of T cells recognizing antigen has historically depended on live-cell imaging. Through the use of neural network–based image analysis, T cell–priming events can now be identified in fixed archival tissues.
Inflammasomes have been reported to function in a wide variety of innate immune cells; however, their activity now seems to be more restricted than previously thought.
The skin and intestine are unique environments at the front line of the immune system. Powrie and colleagues review the distinctive adaptations acquired by regulatory T cells at these barrier surfaces.
Dendritic cells (DCs) have been suggested to express a functional NLRP3 inflammasome. Gerlic and colleagues demonstrate, however, that bone marrow–derived DCs completely lack NLRP3 inflammasome activity and that the bulk of splenic DCs lack or have only minimal activity.
The central nervous system meninges have a dense network of yolk sac–derived macrophages that serve a sentinel role. McGavern and colleagues show that this meningeal niche is replenished by bone marrow–derived inflammatory monocytes, which alters meningeal immune reactions after subsequent immune challenge.
Macrophages can shift their cellular metabolism in response to tissue cues and infection. Pearce and colleagues show that lipopolysaccharide-activated ‘inflammatory’ macrophages become depleted of NAD+ pools and require the salvage-pathway enzyme NAMPT to sustain cellular redox balance.
Removal of damaged mitochondria maintains cellular homeostasis and regulates inflammation. Qian and colleagues describe a mechanism by which intracellular bacteria such as Listeria can elicit mitophagy to enable their survival.
Veillette and colleagues show that receptors of the SLAM family promote the development of iNKT cells by reducing the strength of the TCR signal after positive selection.
The cytokine IL-6 controls the survival, proliferation and effector functions of lymphocytes. Jones and colleagues show that activation of CD4+ T cells leads to suppression of STAT1 activation by tyrosine phosphatases and changes the effector characteristics of memory CD4+ T cells in response to IL-6.
An intricately linked homeostasis exists between the gut microbiome and host immune system. Scheffold and colleagues show that intestinal Treg cells upregulate the transcription factor c-Maf in response to specific signals from the gut microenvironment to establish host–microbiota homeostasis.
Shulman and colleagues show that in contrast to events in lymph nodes and spleen, in Peyer’s patches, T cells promote B cell expansion without clonal selection during pre-germinal center events.
Interferon-stimulated genes (ISGs) are a key component of the antiviral response. Pichlmair and colleagues generate a comprehensive ISG interactome that sheds light on their functions in antiviral responses.
It remains difficult to distinguish cognate APC–T cell interactions in human tissue sections. Clark and colleagues have developed an imaging–machine-learning pipeline that uses deep convolutional and tuned neural networks to identify the combination of distance and cell-shape features that can discriminate between bystander human APC–T cell interactions and cognate interactions in situ.