Diffuse large B-cell lymphoma (DLBCL), the most common subtype of non-Hodgkin's lymphoma, is clinically heterogeneous: 40% of patients respond well to current therapy and have prolonged survival, whereas the remainder succumb to the disease. We proposed that this variability in natural history reflects unrecognized molecular heterogeneity in the tumours. Using DNA microarrays, we have conducted a systematic characterization of gene expression in B-cell malignancies. Here we show that there is diversity in gene expression among the tumours of DLBCL patients, apparently reflecting the variation in tumour proliferation rate, host response and differentiation state of the tumour. We identified two molecularly distinct forms of DLBCL which had gene expression patterns indicative of different stages of B-cell differentiation. One type expressed genes characteristic of germinal centre B cells ('germinal centre B-like DLBCL'); the second type expressed genes normally induced during in vitro activation of peripheral blood B cells ('activated B-like DLBCL'). Patients with germinal centre B-like DLBCL had a significantly better overall survival than those with activated B-like DLBCL. The molecular classification of tumours on the basis of gene expression can thus identify previously undetected and clinically significant subtypes of cancer.

Coronavirus disease 2019 (COVID-19) was first reported in Wuhan, China, in late December 2019 (refs 1-3). Since then, COVID-19 has spread rapidly worldwide and has become a global pandemic affecting >200 countries and territories, with an unprecedented effect not only on public health, but also social and economic activities. The exponential increase in the number of patients with COVID-19 in the past 6 months has overwhelmed health-care systems in numerous countries across the world. At present, preventive vaccines and prophylactic therapies for COVID-19 are not available. COVID-19 is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which is a member of the genus Betacoronavirus like the two other coronaviruses that have caused pandemic diseases (severe acute respiratory syndrome coronavirus (SARS-CoV) and Middle East respiratory syndrome coronavirus (MERS-CoV)) 1-4. As with SARS-CoV and MERS-CoV, SARS-CoV-2 causes a respiratory infection, which leads to viral pneumonia and acute respiratory distress syndrome (ARDS) in some patients 1. However, in addition to respiratory symptoms, uncontrolled SARS-CoV-2 infection can trigger a cytokine storm, whereby pro-inflammatory cytokines and chemokines such as tumour necrosis factor-α, IL-1β and IL-6 are overproduced by the immune system, resulting in multiorgan damage 5. Furthermore, COVID-19 causes coagulation abnormalities in a substantial proportion of patients, which can lead to thromboembolic events 6,7. The genomic sequence 1-3,8 and viral protein structure 9-11 of SARS-CoV-2 have been studied intensively since its emergence. To date, research shows that SARS-CoV-2 shares many biological features with SARS-CoV owing to 79.6% genomic sequence identity 1,2. In particular, both SARS-CoV and SARS-CoV-2 use the same system of cell entry, which is triggered by binding of the viral spike (S) protein to angiotensin-converting enzyme 2 (ACE2) on the surface of the host cell 4. Understanding the biological features of the virus will contribute to the development of diagnostic tests, vaccines and pharmacological therapies and can further our knowledge of tissue tropism. Early clinical data indicate that both the susceptibility to and the outcomes of COVID-19 are strongly associated with cardiovascular disease (CVD) 12-16. A high prevalence of pre-existing Acute respiratory distress syndrome (ArDs). A type of severe, acute respiratory failure characterized by bilateral pulmonary infiltrates and severe hypoxaemia that occurs as a result of illness or injury. Cytokine storm A form of severe immune reaction characterized by overproduction of cytokines and chemokines that can be triggered by a variety of factors such as infection and drugs.

The cytokine thymic stromal lymphopoietin (TSLP) has been linked to human allergic inflammatory diseases. We show here that TSLP expression was increased in the lungs of mice with antigen-induced asthma, whereas TSLP receptor-deficient mice had considerably attenuated disease. Lung-specific expression of a Tslp transgene induced airway inflammation and hyperreactivity characterized by T helper type 2 cytokines and increased immunoglobulin E. The lungs of Tslp-transgenic mice showed massive infiltration of leukocytes, goblet cell hyperplasia and subepithelial fibrosis. TSLP was capable of activating bone marrow-derived dendritic cells to upregulate costimulatory molecules and produce the T helper type 2 cell-attracting chemokine CCL17. These findings suggest that TSLP is an important factor necessary and sufficient for the initiation of allergic airway inflammation.

The maintenance of pregnancy relies on finely tuned immune adaptations. We demonstrate that these adaptations are precisely timed, reflecting an immune clock of pregnancy in women delivering at term. Using mass cytometry, the abundance and functional responses of all major immune cell subsets were quantified in serial blood samples collected throughout pregnancy. Cell signaling–based Elastic Net, a regularized regression method adapted from the elastic net algorithm, was developed to infer and prospectively validate a predictive model of interrelated immune events that accurately captures the chronology of pregnancy. Model components highlighted existing knowledge and revealed previously unreported biology, including a critical role for the interleukin-2–dependent STAT5ab signaling pathway in modulating T cell function during pregnancy. These findings unravel the precise timing of immunological events occurring during a term pregnancy and provide the analytical framework to identify immunological deviations implicated in pregnancy-related pathologies.

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