Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain
the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in
Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles
and JavaScript.
In this Focus Review, Bar-Or and colleagues discuss the latest evidence that B cells play an important antibody-independent role in multiple sclerosis and the prospects this holds for therapeutic intervention.
The cytokine IL-17F constrains the growth of immunoregulatory Clostridium cluster XIVa species and represents a potential therapeutic target for the treatment of inflammatory bowel disease.
Tumor-associated natural killer cells have elevated expression of the checkpoint inhibitory receptor TIGIT. Monoclonal antibody–mediated blockade targeting TIGIT unleashes the anti-tumor activity of both natural killer cells and T cells in preclinical mouse models and efficiently delays tumor growth.
Naive T cells migrate rapidly through the lymph node. A high-resolution look at the chemokine receptor CCR7 and integrin LFA-1 reveals that T cells remain highly responsive to their microenvironment via instantaneous tuning of chemokine-regulated actin flow and integrin-regulated adhesion.
Human affinity-matured antibodies to Klebsiella pneumoniae lipopolysaccharide O-antigen have different patterns of glycan fine specificity without being polyreactive. These antibodies might constitute an important mechanism for homeostatic control of the intestinal microbiome.
Tuberculous meningitis is a serious, life-threatening disease affecting vulnerable populations, including HIV-infected individuals and young children. The US National Institutes of Health convened a workshop to identify knowledge gaps in the molecular and immunopathogenic mechanisms of tuberculous meningitis and to develop a roadmap for basic and translational research that could guide clinical studies.
The metabolic master regulator mTORC1 is shown to promote alternative macrophage activation via Semaphorin 6D reverse signaling and reprogramming of lipid metabolism.
Tissue-resident memory T cells provide immunological protection in peripheral tissues. Amsen et al. discuss the role of these cells in the context of anti-tumor immunity.
γδ T cells accumulate with age in adipose tissue and produce the cytokine IL-17, which controls the homeostasis of regulatory T cells and adaptive thermogenesis. Thus, maintenance of core body temperature unexpectedly relies on these adipose tissue–resident γδ17 T cells.
Myeloid cells exhibit different inflammatory phenotypes after brain injury, yet the relative mechanistic roles for these diverse cell types in post-traumatic tissue damage and repair remain controversial.
Evasion of the immune system and global activation of the immune system are hallmarks of human immunodeficiency virus (HIV) infection. Studies reveal that macrophages might be responsible for HIV-associated pathogenesis via resistance to killing and induction of chronic inflammation.
The role of the transcription factor c-Maf varies in different CD4+ T cell subsets and can be associated with either pro-inflammatory activity or anti-inflammatory activity, depending on the cell context.
The activating natural killer cell receptor NKG2C can specifically recognize peptides derived from the cytomegalovirus protein UL40 in the context of HLA-E. This drives the expansion of a population of adaptive NKG2C+ natural killer cells.
Autoreactive T cells exclusively recognize the roof of the binding groove of the antigen-presenting molecule CD1c after it has caved in on short headless self lipids.
SWAP-70 and DEF6 prevent the cytokine IL-21–induced transcription factor IRF5 from binding to DNA and recruiting the transcription factor T-bet and thereby diminish the activation of age-associated B cells.
Systemic exposure to dietary and microbial components induces long-lasting epigenetic and metabolic changes in myeloid precursor cells, which results in enhanced proinflammatory and anti-microbial responses of mononuclear phagocytes after challenge with related or unrelated stimuli.
IL-33 is a mediator of allergic inflammation and is localized in mucosal tissues to respond rapidly to environmental insults. These include allergens themselves, which can directly activate IL-33 through their intrinsic proteolytic activity.
The sensing of viable pathogens by the receptor TLR8 on human monocytes provides key signals that initiate the differentiation of naive CD4+ T cells into follicular helper T cells. Targeting TLR8 might represent a novel approach for improving immunity following vaccination.
