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Systemic lupus erythematosus is associated with neurological impairment. Here the authors show that exposure of hippocampal neurons to lupus autoantibodies in mice initiates a neuroinflammatory state sustained by continuous HMGB1:RAGE signaling that can be reversed with an ACE inhibitor.
In acknowledgment of Women’s History Month, I have drawn upon timeless concepts from Jane Jacobs’ seminal 1961 book The Death and Life of Great American Cities1 to describe emerging ideas in neuroimmunology and how we may collectively move the field forward.
Drivers of persistent symptoms after acute COVID-19 remain largely unknown. Alterations in immune function, iron homeostasis and dysregulated erythropoiesis are described as treatable correlates of post-acute sequelae of COVID-19.
Entering a new scientific field is difficult and daunting. Here I relate my personal journey as a fish immunologist and how neuroimmunologists welcomed me with open arms (and brains), giving me the sense of belonging that we all need as scientists.
A landmark study reveals how Kupffer cells, resident macrophages of the liver, can promote antitumor immunity. Central to this function is ID3, a Kupffer cell lineage-determining factor. The findings provide new insights into cancer therapy.
Since the discoveries of autoantibodies in neurological diseases, women have had a fascinating journey in neuroimmunology. At a time when groundbreaking advances are being made, let’s continue the conversation about women in science.
Smith and colleagues find that a multivariate signature of unresolved inflammation and altered iron homeostasis detected beyond 2 weeks following acute COVID-19 onset was the strongest early differentiator of those who report long COVID symptoms at 3–10 months.
Schäfer et al. discuss the application of computational methods that integrate single-cell and spatial multi-omics with existing biological knowledge to inform our understanding of immunological responses.
A study identifies an increase in the tissue-protective factor HB-EGF during the initial stage of multiple sclerosis (MS), which is actively turned off as the disease worsens.
Linnerbauer and colleagues find that HB-EGF produced by reactive astrocytes is protective during autoimmune neuroinflammation, but epigenetically suppressed during late stages.
Here the authors use positron emission tomography to visualize fibroblasts in patients with arthritis and combined with spatial transcriptomic data show that these cells undergo a phenotypic shift upon resolution of inflammation. A CD200+DKK3+ fibroblast subset promotes this resolution by inhibiting tumor necrosis factor and interleukin-17A.
Bacillus Calmette–Guérin (BCG) is the only available vaccine against tuberculosis. As well as being an effective vaccine against tuberculosis, BCG also provides off-target protection against various pathogens. Here, we report a mechanism for BCG-mediated cross-protection against influenza A virus (IAV), which requires a dialogue between the innate and adaptive immune memory systems.
In this study, we developed an adenoviral-vectored vaccine that targets the spike protein of BA.5 Omicron SARS-CoV-2. When nasally delivered in mice and hamsters, the vaccine stimulated mucosal antibody production and CD8+ T cell responses, and demonstrated protection against several SARS-CoV-2 strains, including the antigenically distant Omicron XBB.1.5 strain. Immune cell depletion studies showed that cross-reactive memory CD8+ T cells contribute to the cross-protection that is conferred by nasal vaccines against respiratory infection with antigenically shifted SARS-CoV-2 Omicron strains.