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Comprehensive analysis of specific and cross-reactive SARS-CoV-2 epitopes reveals functional T cell responses against specific viral regions in essentially all convalescent individuals and a majority of unexposed donors, demonstrating that cross-reactive responses to COVID-19 are widespread.
The natural variability of CRELD1 expression identified in comprehensive data sets from healthy individuals helps predict and establish its role in regulating T cell homeostasis.
A subset of neutrophils with an immature phenotype confers neuroprotection in traumatic optic nerve and spinal cord injury. This study identifies a new target population of cells for therapeutic strategies to induce neural regeneration during injury.
An exaggerated extrafollicular B cell response characteristic of active systemic lupus erythematosus also characterizes the B cell response to SARS-CoV-2 in those with severe COVID-19.
The presence of central memory precursor cells during the acute response to cytomegalovirus infection is the best predictor of whether a T cell family will contribute to the inflationary memory pool.
In contrast with the classical dogma that the pathways generating either memory or ‘exhausted’ T cells are strictly segregated, data now identify a clonally distinct hybrid memory T cell subpopulation with an exhausted phenotype.
The lung endothelial cell–derived angiocrine Rspondin3 activates Wnt–β-catenin signaling in interstitial macrophages, leading to a metabolic–epigenetic reprogramming of interstitial macrophages that drives anti-inflammatory responses and attenuates endotoxin-induced lung injury.
Two studies reveal a role for the transcriptional regulator BATF3 as a T cell–intrinsic factor mediating effective memory responses. This finding opens future avenues of investigation and opportunities to enhance cellular immunotherapy.
The mechanisms that drive responses to PD-1-blocking immunotherapy in some but not all patients have been puzzling. A new study suggests that the balance of PD-1 expression levels between CD8+ T cells and Treg cells might provide an answer.
The activation of the Notch4–Wnt–GDF15 axis in induced regulatory T (Treg cells) dampens their immunoregulatory function and turns them into TH2 and TH17 cytokine producers, allowing them to maintain ongoing allergic asthma.
Cytokines are well-known mediators of the immune response, but, recently, pleiotropic roles in the central nervous system have started to be uncovered. It is now shown that IL-17 directly modulates fear behavior in mice.
Comprehensive mapping reveals that functional CD4+ and CD8+ T cells targeting multiple regions of SARS-CoV-2 are maintained in the resolution phase of both mild and severe COVID-19, and their magnitude correlates with the antibody response.
Costimulatory blockade via the CTLA-4–Ig fusion protein abatacept is beneficial in patients with early-onset type 1 diabetes, but some individuals benefit more than others. A new study reports that the pretreatment abundance of T follicular helper (TFH) cells could predict clinical responses to abatacept.
To trigger an adequate humoral immune response while ensuring self-tolerance, B cell activation is tightly controlled. A new study indicates that an NR4A-enforced built-in brake fine-tunes the early phase of transcriptional reprogramming induced by BCR stimulation.
A vicious cycle, linking obesity with chronic inflammation, fuels the development and exacerbation of metabolic syndrome and other disorders. Modulation of mitochondrial energy metabolism via interleukin-1β signaling establishes a runaway positive-feedback loop that brings about and reinforces the sequelae of a high-fat diet.
New studies suggest that NKG7 is essential for NK and CD8+ T cell cytotoxic degranulation and CD4+ T cell activation and proinflammatory responses. While the mechanism is yet to be determined, the functional relevance is exciting and opens the possibility of a new target for cellular immunotherapies.
The combination of single-cell RNA-seq and in vivo CRISPR–Cas9 screens reveal a new circuit that directs germinal center B cells toward a memory B cell phenotype during viral infection.
Group 2 innate lymphoid cells (ILC2s) closely intersect with antitumor immunity. A new study describes how activation of lung-resident ILC2s orchestrates the suppression of natural killer cell–mediated innate antitumor immunity via an eosinophil-mediated metabolic mechanism.
Durable responses to immunotherapy require the development of robust CD8+ T cell memory. A new study indicates that NRP1 differs from other checkpoint receptors as it functions as a checkpoint for the generation of memory.
A complex formed by the chemokine CXCL10 and commensal skin microbiota–derived DNA is a crucial component that triggers type I IFN responses to facilitate skin repair.
