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Zhong et al. exploit allelic variations in mice to pinpoint the ‘heavy lifter’ transcription factor families governing the chromatin landscape of resting and activated T cells.
New data show that, compared with adults, children infected by SARS-CoV-2 preferentially activate pre-existing immunity to endemic common-cold coronaviruses that are cross-reactive with SARS-CoV-2, with potential implications for pediatric vaccine strategies.
Coronavirus-specific antibody and T cell responses were characterized in young children who had been naturally infected with SARS-CoV-2. Immune responses were focused against the spike protein, strong and stable in magnitude, and showed notable cross-reactivity with other human coronaviruses.
New research provides evidence of an impaired vitamin D gene signature in CD4+ T cells in patients with severe COVID-19. Mechanistically, it is shown that vitamin D alters the epigenetic landscape of CD4+ T cells, as well as inducing key transcription factors such as STAT3, BACH2 and JUN that reduce levels of IFN-γ and increase IL-10. These changes generate pro-resolving TH1 cells that may be beneficial in resolving or preventing severe COVID-19.
Chronic viral infections can trigger ineffective antibody responses. A new study shows that deletion of B cell-specific Moloney murine leukemia virus integration site 1 (BMI-1) from B cells restores protective antibodies during chronic infection.
Mitochondria regulate endoplasmic reticulum (ER) size and protein maturation in healthy cells by releasing aspartate, regenerating cytoplasmic NAD+ and ADP-ribosylating the ER stress sensor BiP. In the autoimmune disease rheumatoid arthritis, a deficiency in mitochondrial aspartate in T cells causes an increase in ER size and excess production of the inflammatory mediator tumor necrosis factor (TNF), driving tissue inflammation.
In patients with rheumatoid arthritis, a short supply of aspartate in the mitochondria can force the endoplasmic reticulum of T cells to generate transmembrane TNF, which in turn contributes to synovial inflammation.
Analysis of antibody responses in BCG intravenous vaccination against Mycobacterium tuberculosis in non-human primates show a potential protective role for IgM.
The extreme diversity of the human immune system, forged and maintained throughout evolutionary history, provides a potent defense against opportunistic pathogens. Liston and colleagues review the current state of play in the field, identify the key unknowns in the causality of immune variation and identify the multidisciplinary pathways toward an improved understanding.
Whether COVID-19 during pregnancy affects the health of children is unclear. Data now show that SARS-CoV-2 infection of mothers can prime the fetal immune response indirectly even when the virus does not infect the fetus.
When transformed cells emerge in an epithelium, their elevated class I MHC expression signals to normal neighboring epithelial cells, which respond by inducing their apical extrusion as a tumor-suppressive mechanism.
Thrombosis complicates SARS-CoV-2 infection and vaccination. Recent data are being used to identify the autoimmune antibody repertoires responsible for the excessive activation of coagulation and platelets.
On 27 ̶ 29 July 2021, the National Institute of Allergy and Infectious Diseases (NIAID) hosted a virtual workshop on the topic of secondary vaccine effects to discuss existing evidence, potential immunological mechanisms and associated public health implications.
During acute COVID-19, there is little correlation between the nose and blood in terms of antibodies or cytokines; instead, these factors are associated with nasal microbiota.
Conjugation of the ubiquitin-like protein ISG15 to targets (ISGylation) benefits antiviral defense. However, SARS-CoV-2 induces human macrophages to preferentially secrete ISG15 via its papain-like protease, and extracellular non-conjugated ISG15 acts as a cytokine to exacerbate SARS-CoV-2-triggered inflammation.
The retention of erythroid mitochondria, a feature associated with impairments in the ubiquitin–proteasome system, is detected in a subset of pediatric patients with lupus and is associated with the type I interferon pathway.
Infections are known to induce epigenetic rewiring in myeloid cells, a phenomenon known as trained immunity, which protects against re-infection. New data show that, in mice, trained immunity can be inherited, possibly by gametic DNA methylation and chromatin remodeling linked to immune traits.
In this Perspective, Spaan and colleagues propose a strategy for identifying, recruiting, and genetically analyzing individuals who are naturally resistant to SARS-CoV-2 infection.
Type I interferon response to systemic infections after head trauma or stroke impairs angiogenesis in injured tissues and may contribute to secondary neurological injury.
