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Restriction factors are host cell proteins that inhibit retroviral infection. A new study using mutants of human HIV-1 restriction factor SAMHD1 suggests that it inhibits infection through degradation of viral RNA rather than through its dNTPase activity as previously suggested.
The search for cells that can regenerate lung tissue has been fueled by the need for improved clinical therapies for treatment of lung injury or degenerative lung diseases. Emerging techniques are allowing the identification of putative stem and progenitor cells in the lung and the understanding of the molecular mechanisms regulating lung development and regeneration.
Our understanding of stem cell biology is increasing, but the translation of this knowledge into regenerative medicine therapies for aged or diseased tissues is proving challenging. In this Perspective, four experts in the field discuss strategies for overcoming the major hurdles facing the translational regenerative field.
Diamond-Blackfan anemia (DBA) is an inherited hypoplastic anemia characterized by impaired production of erythroid cells, and it is caused by inactivating mutations in ribosomal protein genes in more than half of all cases. A new study in human cells demonstrates that reduced translation of the transcription factor GATA1, as a consequence of ribosomal protein haploinsufficiency, is a crucial factor in mediating the erythroid defect found in DBA (pages 748–753).
Stress has long been thought to be a major contributing factor to cardiovascular disease, although little is known about the underlying cellular mechanisms. A new study in humans and mice suggests that chronic stress promotes hematopoietic stem cell proliferation in bone marrow, leading to increased leukocyte production, circulation and recruitment to the vasculature (pages 754–758).
Leptin deficiency, which is associated with type 1 diabetes, is a critical factor in the pathophysiology of this disease, a new study in rats shows. The lack of this hormone triggers a cascade of neuroendocrine events that affect adipose tissue and the liver, resulting in hyperglycemia and ketoacidosis (pages 759–763).
Barth syndrome is a rare X-linked genetic disorder caused by mutations in the tafazzin (TAZ) gene that result in dilated cardiomyopathy, skeletal myopathy and neutropenia. Tafazzin has a mitochondrial function, and a new study using cardiomyocytes derived from induced pluripotent stem cells (iPSCs) from humans with Barth syndrome identifies increased mitochondrial reactive oxygen species (ROS) production as a key intermediate causing cardiac contractile dysfunction (pages 616–623).
Regulatory B cells exert an immunosuppressive role by secreting the cytokine interleukin-10 (IL-10). Two studies have now identified B cell–derived IL-35 as both an inducer and a mediator of regulatory B cell function. IL-35 switched off inflammation in mouse models of autoimmunity, whereas its absence in B cells in mice enhanced survival after Salmonella enterica serovar Typhimurium infection. IL-35 could therefore be targeted for treating human autoimmune and infectious disease.
A new study in infants shows that broadly neutralizing antibodies (bNAbs) against HIV can be found early in life, demonstrating for the first time that these antibodies can be induced by the infant immune system.
Although hematological cancers are genomically unstable, the mechanisms by which they evade DNA damage–induced cell death are largely unknown. A current study has revealed that the Hippo signaling pathway transcriptional regulator YAP1 activates an ABL1/p73-mediated proapoptotic effect in response to DNA damage, suggesting that YAP1 has a tumor suppressor function and that the Hippo pathway is a potential therapeutic target in human cancers.
Age-related cognitive decline occurs in many mammals, including humans, resulting from a decline in hippocampal function, and it is associated with reduced synaptic plasticity in hippocampal circuits. In this issue of Nature Medicine, a new study shows that cognitive impairment observed in aged mice is largely reversible following exposure to the blood of young mice.
The function of the innate immune system is suppressed in patients with acutely decompensated cirrhosis and predisposes these patients to bacterial infections. A new study shows that increased synthesis of the immunosuppressive prostaglandin PGE2 by circulating monocytes and resident macrophages and impaired hepatic synthesis of human serum albumin (HSA) are major contributors to immune suppression in cirrhosis (pages 518–523). The authors' data suggests a new avenue for therapy in acute decompensation of cirrhosis.
A new antiviral capacity for matrix metalloproteinase 12 (MMP-12) adds to our expanding understanding of matrix metalloproteinase biology, from matrix remodeling to host defense, in this issue of Nature Medicine (pages 493–502). Marchant et al. show that following viral infection, macrophages secrete MMP-12, which regulates antiviral immunity both as a transcription factor for IκBα, leading to interferon-α (IFN-α) secretion, and later by degrading extracellular IFN-α, resolving inflammation.
Central nervous system (CNS) control of systemic nutrient homeostasis is a crucial but poorly understood metabolic regulatory axis. A new study (484–492) shows that rat insulin promoter (RIP)-expressing neurons in the hypothalamus regulate peripheral metabolic responses to both normal and high-fat diets through anti-inflammatory effects mediated by vagal innervation of the spleen.
As babies leave their mothers' wombs, they are colonized by commensal bacteria. A new study shows that these microbes in a newborn's gut can promote an increase in circulating neutrophils that can guard the body from infections. Altering a neonate's gut microbiota with perinatal antibiotic treatment can impair neutrophils, leaving the newborn vulnerable to attack by harmful bacteria (pages 524–530).
