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Aifantis and colleagues identify the E3 ubiquitin ligase SPOP as a negative regulator of ‘emergency hematopoiesis’ in bone marrow hematopoietic stem progenitor cells.
Loss of the transcription factor Foxp3 impairs Treg cell development and immune homeostasis. Chatila and colleagues use a series of Foxp3 mutants to show that its disruption results in altered Treg cell metabolism and loss of regulation, which are rescuable by metabolic manipulation.
Horng and colleagues show that mitochondrial glycerol-3-phosphate dehydrogenase, a component of the glycerol phosphate shuttle, modulates a shift from inflammation to immunosuppression in activated macrophages.
NK cells recognize class I and stress-associated ligands. Altfeld and colleagues identify the NK cell receptor NKp44 as directly interacting with the class II HLA-DP in a partially peptide-dependent manner and with functional consequences for NK cell activity.
PD-1 blockade can enhance antitumor responses in a subset of cases. Khleif and colleagues demonstrate that PD-1 blockade in the context of suboptimal T cell activation engenders a state of non-responsiveness but not when there is strong stimulation by vaccination.
HIV infection results in T cell dysfunction. Kaufmann and colleagues demonstrate that HIV infection results in an alterated differentation of HIV-specific CD4+ T cells that is only partially reversed by antiretroviral therapy and generation of dysfunctional T cells with a follicular helper-like phenotype.
Treg cells obstruct effective anticancer responses. Lee and colleagues describe a Treg cell biomarker signature that is strongly associated with enhanced suppression and progression of human breast cancer.
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.
Much about the kidney-resident immune populations is a black box. Hacohen and colleagues use single cell RNA sequencing of kidney, skin and urine from lupus nephritis patients to describe the transcriptional state of the immune cells present in each compartment.