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The SARS-CoV-2 virus has spread worldwide in the past year, killing millions and disrupting normal daily life for many more. Nature Immunology introduces a new series ‘Coping with COVID’, wherein researchers and public health experts from across the globe describe their responses to the COVID-19 pandemic.
To cope with the new situation during the pandemic, the Turkish people have united in the fight against SARS-CoV-2 with their healthcare workers, scientists and government. We are waiting for the global pandemic to end soon.
Early preparedness, contact tracing, isolation and testing, coupled with timely border closure, physical distancing and community adherence, have been key measures in controlling COVID-19 in Vietnam.
New Zealand has avoided the major health impacts of the SARS-CoV-2 pandemic due to a strict country-wide lockdown, the end-goal of which was elimination rather than mitigation and suppression. The New Zealand government’s use of scientific expertise, spanning public health, infectious diseases, genomics, modeling and immunology, has been one of the keys to the success of its SARS-CoV-2 elimination and control strategy.
From the onset of the SARS-CoV-2 pandemic and following the creation of the ‘Coronavirus Unit’, Argentinean scientists and technologists have contributed by leading basic and translational research initiatives, including developing diagnostic and serological kits, designing new therapeutic approaches, establishing epidemiological platforms, executing clinical trials and implementing social measures to protect the most vulnerable groups of the population.
The transition of Sub-Saharan Africans from rural settings and traditional plant-rich diets to urban settings and calorie-dense Westernized diets has led to specific shifts in serum metabolites and activates a heightened proinflammatory state in immune cells.
Brain tumors respire more oxygen, causing a hypoxic microenvironment that impairs innate γδ T cell–mediated antitumor activity. Reducing oxygen consumption by brain tumors or inhibiting hypoxia-inducible factor-1α in γδ T cells reinvigorates γδ T cell tumor-killing activity, leading to prolonged survival in brain-tumor-bearing mice.
New research demonstrates that γδ T cells recognize Plasmodium-infected erythrocytes via interaction of the T cell antigen receptor with the phosphoantigen sensor BTN3A1 and subsequently destroy infected cells through either cytotoxic molecule secretion or antibody-dependent phagocytosis.
IRGM1 is recognized as a master regulator of type I interferon responses against pathogens, while also protecting against autoimmune diseases. It has now been shown that IRGM1 controls autoinflammatory responses by modulating mitophagy flux.
Long-term pathogen and tumor control as well as checkpoint immunotherapies rely on ‘stem-like’ CD8+ T cells. New results uncover BACH2 as a key regulator of this subpopulation and solve an important piece of the puzzle.
An investigation of the molecular processes of mitochondrial reprogramming and metabolic stress in antigen-experienced T cells within tumor microenvironments reveals mechanisms responsible for T cell exhaustion and dysfunction and facilitates the development of new strategies for tumor immunotherapy.
The microbiome can affect susceptibility to developing asthma. Marsland and colleagues show that changes in the microbial population lead to enrichment of an l-tyrosine metabolite, p-cresol sulfate, which can protect mice against allergic inflammation.
Rapid urbanization can be associated with adverse health implications. de Mast and colleagues compare urban and rural Tanzanian populations using multi-omics and observe that urbanization is associated with an elevated but reversible inflammatory state.
The transcription factor IRF8 is required for both DC and monocyte differentiation from common myeloid progenitors. Tamura and colleagues identify an enhancer (+56 kb) in the Irf8 locus that regulates early myeloid lineage choice.
Fessler and colleagues report that loss of the IFN-γ-induced GTPase IRGM1 results in autoinflammatory disease. Deficient IRGM1 activity led to defective lysosomal maturation and impaired mitophagy, prompting the release of cytosolic mtDNA and thereby activating the cGAS–STING pathway.
Severe COVID-19 is characterized by hyperinflammation, and there is a need for accurate predictive biomarkers of progression. Lehuen et al. demonstrate that patients with severe COVID-19 show a dramatic loss of MAIT cells, and those that do remain are in a highly activated state.
Glioblastoma is one of the most intractable tumors and presents a hypoxic and immunologically cold microenvironment. Lee and colleagues demonstrate that normalizing oxygen tension unleashes γδ T cell anti-glioblastoma function.
Junqueira et al. show that human γδ T cells control erythrocytic Plasmodium falciparum infection by multiple mechanisms: antibody-dependent phagocytosis, cytotoxic-granule-mediated erythrocyte lysis and direct parasite killing.
IL-2 is a classic T cell growth factor. Huang and colleagues demonstrate, however, that chronic IL-2 stimulation leads to a new exhaustion pathway that impairs antitumor immune responses.
Tuoqi Wu and colleagues show that the transcriptional repressor BACH2 is required early after chronic viral infection to enforce a stem-like fate in activated CD8+ T cells. BACH2 acts to suppress genes that lead to the exhausted cell state.
Lymphocyte homing to the gut and Peyer’s patches requires expression of integrin α4β7. Ballet and colleagues report that B cell expression of CD22 is required to specifically retain surface expression of β7 integrin molecules, thereby promoting B cell retention in the gut and optimal gut mucosal antibody responses.