This JAMA Forum discusses the recent budget cuts to National Institutes of Health (NIH), the effects of these cuts on scientific research and health of individuals in the US, and the prospects for cha...

Aspergillus poses a threat to human health and food security as the planet gets warmer, allowing pathogens to thrive in new areas

MPO activates an immunometabolic rheostat to restrict the functional plasticity of macrophages in favor of proresolving properties.

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The local immunoregulatory mechanisms that safeguard the host from excessive lung infection inflammation remain unclear. Yeung, Yokota et al. uncover the essential role of nerve- and airway-associated...

Peroxisomes are vital but often overlooked metabolic organelles. We found that excessive interferon signaling remodeled macrophage peroxisomes. This loss of peroxisomes impaired inflammation resolutio...

Administration officials pressured NIH to avoid clear advice from the agency’s own lawyers to restart grant funding now.

Very early exposure to even a very small dose of herpes simplex virus (HSV) in infant mice can lead to cognitive decline later in life, according to findings from a new Dartmouth-led study, publish…

Defects in mitochondria are associated with a variety of human diseases and metabolic disorders (1). Inherited mitochondrial diseases, caused by mutations harbored in the mitochondrial genome (mtDNA) or in nuclear-encoded mitochondrial genes, lead to devastating neurodegenerative and cardiovascular disorders (2). They are also frequently associated with chronic inflammation and autoimmunity. Type I interferonopathies, for example, are often caused by mutations that result in aberrant release of mitochondrial nucleic acids and chronic engagement of cytosolic nucleic acid sensing (3–5). Consistent with important links between mitochondrial health and immune function, patients with mitochondrial mutations are prone to frequent viral and bacterial infections that are often severe (6, 7). They can also suffer from systemic inflammatory response syndrome caused by hyperinflammation in the absence of infection (8). Furthermore, human single nucleotide polymorphisms (SNPs) in mitochondrial genes have been shown to confer susceptibility to several bacterial pathogens, including Salmonella enterica serovar Typhi (9), Listeria monocytogenes (10), and Mycobacterium leprae (11). Despite clear connections between mitochondria and immunity, the mechanistic contributions of specific mitochondrial-associated mutations in driving susceptibility to infection remain unclear.

Our findings propose a causal relationship between reduced IL-6 signalling and lower risk of tuberculosis, akin to the effect seen in other IL-6 mediated diseases. This study suggests that IL-6 antago...