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O’Sullivan and colleagues show that liver-resident type 1 ILCs have enhanced protective effector responses to secondary challenge with mouse cytomegalovirus, dependent on the viral glycoprotein m12.
Cerebral ischemia activates innate immune responses in injured brain lesions. Andreasson and colleagues show TREM1 is upregulated after stroke and amplifies these proinflammatory responses by peripheral CD11b+ myeloid cells in both the ischemic brain and distally in the intestine.
The membrane tetraspan protein MS4A4A is expressed on tissue-resident and tumor-associated macrophages. Locati and colleagues show that MS4A4A colocalizes with the β-glucan receptor dectin-1 to enhance cytokine and reactive oxygen species production and to enhance NK cell–mediated control of tumor metastasis.
Systemic lupus erythematosus (SLE) is characterized by autoantibodies produced by pathogenic B cells. Boss, Sanz and colleagues show that SLE-associated epigenetic changes exist in gene regulatory programs in resting naive B cells, before their differentiation into antibody-producing plasma cells.
Innate lymphoid cells (ILCs) can exhibit considerable plasticity. Humbles and colleagues identify a subpopulation of ILC2s in humans that can convert to proinflammatory ILC3s with implications for human skin diseases.
IFN-λ has important innate immune system functions at mucosal surfaces, but its importance in adaptive immunity is largely unknown. Using an influenza infection model, Gale and colleagues demonstrate that IFN-λ is essential for effective adaptive cellular immunity in the lung.
Ginhoux and colleagues show that the priming of mouse hematopoietic progenitor cells toward the pDC lineage occurs at the common lymphoid progenitor stage.
Treg cells are essential for self-tolerance. Huseby and colleagues identify multiple de facto Treg cell self-peptides and show that Treg cells are exported from the thymus within a defined postnatal developmental window that is controlled by their increased negative selection.
Long-lived, self-renewing ‘progenitor-like’ CD8+ T cells can arise during chronic viral infection or in cancer. Wu and colleagues identify the transcription factor TOX as essential to endow ‘stemness’ and long-term persistence in the face of chronic infection.
Multiple genetic variants have been identified that influence the outcome of HIV infection. Carrington and colleagues investigate the mechanism of one of the strongest variants, rs1015164, and show that it influences expression of a lncRNA controlling CCR5 expression.
IL-15 has important functions in the activation and homeostasis of cytotoxic T lymphocytes (CTLs) and NK cells. Sun and colleagues demonstrate that the deubiquitinase Otub1 controls CTLs and NK cells in a cell-intrinsic manner by negatively regulating IL-15 signaling.
Many tumors evade immunosurveillance by down-modulating expression of antigen-processing machinery and MHC molecules. Yang et al. report triple-negative tumor cell expression of the lncRNA LINK-A enhances degradation of antigen peptide-loading complex molecules and intrinsic tumor suppressors, which contribute to tumor persistence.
High-energy diet triggers mild β cell proliferation to compensate for peripheral insulin resistance. Qi and colleagues show that TLR2 and TLR4 inhibit the diet-induced replication of β cells in mice and humans.
Cachexia manifests in cancer, chronic inflammation and infections. Bergthaler and colleagues show that CD8+ T cells mediate infection-associated cachexia in a manner dependent on T cell–intrinsic type I IFN signaling and antigen recognition.
Natural killer cells have important roles in virus and anti-cancer responses. Glimcher and colleagues demonstrate that a natural killer cell-intrinsic endoplasmic reticulum stress pathway is essential for their proper function.
Edelson and colleagues show that the transcription factor Bhlhe40 is required in a cell-intrinsic manner for the self-renewal and maintenance of large peritoneal macrophages, but not that of other tissue-resident macrophages.
HIV-1 target cells employ a number of factors that restrict the production of viral progeny. Liang and colleagues identify the cell membrane-localized metalloprotease TRABD2A as a previously unknown restriction factor that acts at the late phase of infection to degrade HIV-1 Gag polyprotein.
RIG-I is an RNA sensor and is required for effective antiviral immunity. Cao and colleagues demonstrate that the previously undescribed long noncoding RNA Lnczc3h7a serves an essential scaffolding role in supporting productive RIG-I signaling.
BCR signaling in naive B cells and in GC B cells differs. Shlomchik and colleagues report that GC B cells are ‘rewired’ in their Akt activation module, increasing p-T308 over p-S473, leading to increases of negative regulators of BCR signaling and ultimately higher thresholds for BCR activation.