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First Nations peoples of Australia have disproportionate rates of chronic comorbidities such as diabetes and renal disease. A study of COVID vaccination in First Nations peoples reveals that perturbed antibody responses can occur in individuals with comorbidities in a way strongly associated with altered IgG glycosylation patterns.
Indigenous populations are disproportionately affected by COVID-19, but are rarely studied. An investigation of the immune response of Australian First Nations people to SARS-CoV-2 vaccination and infection shows a major effect of comorbidities.
The magnitude and quality of the germinal center response after vaccination decline with age. We found that T follicular helper (TFH) cells are enriched in the dark zone of germinal centers in aged mice, which impairs the expansion of the follicular dendritic cell network upon immunization and reduces antibody responses.
In mice and humans, changes in neutrophil phenotypes and functionality during aging aggravate thromboinflammation in ischemic brain injury and determine the pathology associated with strokes. In mice, inhibition of CXCL3 signaling and rejuvenation of bone marrow offer ways of restricting brain injury and improving stroke outcomes.
In this Review, Künzli and Masopust provide updates on our understanding of the biology of memory CD4+ T cells as well as key technological advances that facilitate their characterization.
Bystander activation that leads to expression of IL-9 in effector TH9 cells is induced by a TCR-independent, STAT-dependent mechanism and may represent a new strategy for therapeutic intervention to treat TH9-induced pathologies in vivo.
Deletion of TFAM, the master regulator of mitochondrial transcription and translation, limits germinal center reactions. Notably, TFAM affects several processes beyond bioenergetics, such as migration, signaling, somatic hypermutation and redox balance.
We engineered CD8+ T cells with two orthogonal cytokines for adoptive cell transfer into mice with solid tumors. These cells acquired a novel synthetic effector state that fully deviated from TOX+ canonical exhaustion and displayed improved anti-tumor effector functions.
New work from Udeochu, Amin, Huang, and colleagues provides mechanistic insights into how the tau protein engages the cGAS–STING pathway to elicit antiviral responses in Alzheimer’s disease. This signaling axis diminishes the MEF2C transcriptional network in neurons critical for maintaining cognitive function.
Many immune cell subsets move in an amoeboid fashion and do not require strong adhesive interactions with their surrounding when moving through interstitial tissue spaces. In stark contrast, we show that mast cells critically depend on integrin-mediated adhesion and interactions with the extracellular matrix to enable slow migration and site-specific positioning in tissues.
Orthogonal engineering of adoptively transferred CD8+ T cells to co-express two cytokines — an IL-2Rβ/γ-biased IL-2 variant and the proinflammatory alarmin IL-33 — induces an exhaustion-resistant synthetic cell state with potent anti-tumor efficacy in the absence of host pre-conditioning.
The US National Institute of Allergy and Infectious Diseases hosted a two-day virtual workshop on skin microbial communities and their interactions with the host immune system in health and disease. The aim of the workshop was to evaluate the current state of knowledge in the field and identify gaps, challenges, and future directions.
Regulatory T (Treg) cells respond to interferon-γ (IFNγ) during viral infection and polarize to a T helper (TH)1-like state. Such Treg cells possess effector functions, such as the production of IFNγ, yet remain stable and potently limit virus-specific effector T cell function, CD8+ T cell proliferation and the formation of central memory T cells.
We show a crucial protective function for T follicular helper (TFH)-like cells localized within granuloma-associated lymphoid tissue for Mycobacterium tuberculosis control in mouse models of tuberculosis. Antigen-specific B cells contribute to this strategic localization and the maturation of cytokine-producing TFH-like cells.
The adipose tissue is rich in immune cells. In this Review, the authors cover adipose tissue myeloid cells and how they control and respond to inflammation and pathology.
APLAID is a very rare autoinflammatory disease thought to be caused by mutations in PLCG2. A mouse model of APLAID recapitulates clinical features of the disease, and identifies a crucial function for G-CSF that might be targeted therapeutically.
The immune system is not immune to sex differences. New research now uncovers the molecular mechanisms that underlie sex-based differences during antiviral immune responses.
Mononuclear phagocyte proliferation is thought to be limited to myeloid progenitor cells and mature macrophages. However, availability within an interstitial macrophage niche permits the proliferation of monocytes in the lung before macrophage differentiation.
When an interstitial macrophage niche is empty, classical monocytes can proliferate locally in a manner that is restricted by the transcription factor MAFB, before undergoing differentiation into distinct macrophage subsets. These findings reveal a new function of monocytes and highlight the complex regulation of proliferation and differentiation during macrophage development.
