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CD1 molecules present diverse lipid ligands to TCRs expressed by NKT cells. Rossjohn, Moody and colleagues show a unique form of autoreactivity with human CD1c molecules, whereby TCRs recognize a closed conformation of CD1c molecules, which are loaded with a diverse array of ‘headless’ glycolipids.
Mosquito salivary-gland extract can modulate the host immune response. Qi and colleagues show that the salivary factor LTRIN from Aedes aegypti facilitates the transmission of Zika virus by interfering with the lymphotoxin-β receptor.
A unique subset of T-bet-expressing B cells accumulates with aging and in autoimmunity. Pernis and colleagues show that dysregulation of the transcription factor IRF5 occurs after loss of the Rho GTPase–regulatory proteins DEF6 and SWAP-70 and leads to the premature generation of age-associated B cells.
The presentation of antigen by germinal-center B cells to follicular T cells engenders the process of antibody affinity maturation and humoral memory. Pierce and colleagues show that TLR9 signaling in B cells antagonizes B cell–mediated antigen presentation, which leads to the enhanced generation of short-lived plasma cells and the production of lower-affinity antibodies.
Both environmental factors and genetic factors influence human immunity. Albert and colleagues leverage data from the Milieu Intérieur Consortium to comprehensively describe the effects of lifestyle, environment and genetics on human innate and adaptive immunity.
Wang and colleagues show that the transcription factor Hoxb5, which is expressed in uncommitted hematopoietic progenitor cells but is absent from committed B cells and T cells, can reprogram pro-pre-B cells into functional early T cell lineage progenitors.
Regulatory T (Treg) cells have distinct transcriptional programs underpinning their suppressive functions. Benoist and colleagues use single-cell RNA-seq to describe the transcriptional landscape of Treg cells and the effects of T cell–receptor signaling.
Affinity maturation and positive selection occur in germinal centers. Turner and colleagues demonstrate that the RNA-binding protein PTBP1 serves an essential B cell–intrinsic role by regulating the abundance and alternate splicing of transcripts in germinal center B cells.
Polymorphisms in the autophagy protein Atg16l are associated with human inflammatory bowel disease. Murthy and colleagues demonstrate that atg16l is crucial to autophagocytic degradation of the innate adapter TRIF and thereby restrains pathological over-production of type I interferons.
Cancer can be associated with alterations in innate immunity. Gao et al. demonstrate that these alterations arise from immunomodulatory exosomes released by tumors, which then dampen the production of type I interferons by macrophages.
Crabtree and colleagues show that Aire has an intrinsic repressive function that restricts chromatin accessibility and restrains the amplitude of active transcription.
Yipp and colleagues report that depletion of B cells leads to the accumulation of aged polymorphonuclear cells in the lungs, which causes fibrotic interstitial lung disease.
Masopust and colleagues show that mucosal tissue-resident memory T cells proliferate in situ in response to local antigen and dominate the local recall response.
Mackay, Mueller and colleagues show that tissue-resident memory T cells proliferate in situ in response to local antigen and persist during subsequent antigen encounters.
The bacterial secondary messenger c-di-AMP can be sensed by cytosolic receptors to activate innate immunity. Fan and colleagues show the ER-associated protein ERAdP to be a high-affinity receptor for c-di-AMP, linking it to downstream inflammatory responses.
Klein and colleagues show, in a mouse model of West Nile virus–induced cognitive dysfunction, that neurogenesis is impaired by production of IL-1 from pro-inflammatory astrocytes.