Feed aggregator

Title: NK cells in host immunity

Abstract: Immunological memory is a hallmark feature of the mammalian adaptive immune response and essential for prolonged host control of pathogens. Although these features are attributed to T and B cells, previous work has demonstrated that natural killer (NK) cells, which have traditionally been categorized as a component of innate immunity, also possess the ability to undergo clonal proliferation and generate memory in response to pathogens. Here, we seek to understand and dissect novel molecular pathways that underlie these “adaptive” NK cell responses during cytomegalovirus infection. Our findings uncover a previously unrecognized, host protective role for Wnt signaling in NK cell-mediated antiviral immunity, with implications for the design of novel NK cell therapies.

Bio: Joseph Sun received his PhD in immunology in 2005, having trained with Mike Bevan in CD8 + T cell memory as a graduate student at the University of Washington. As a postdoc with Lewis Lanier at UCSF from 2006-2010, he discovered that natural killer cells possess adaptive immune features including clonal expansion and long-lived memory following viral infection. He was recruited to Memorial Sloan Kettering Cancer Center in 2010 by Jim Allison, and his lab has been interested in defining the underlying epigenetic, transcriptional, and metabolic signals that govern innate and adaptive lymphocyte responses in host defense against pathogens and cancer.

Hosts Dr Tim Halim, CRUK & Dr Virginia Pedicord, CITIID

• Speaker: Dr Joseph Sun, Cornell/Memorial Sloan Kettering Cancer Center
• Thursday 19 March 2026, 16:00-17:00
• Venue: Lecture Theatre, Jeffrey Cheah Biomedical Centre, Cambridge Biomedical Campus.
• Series: Cambridge Immunology Network Seminar Series; organiser: Liat Churley.

Add to your calendar or Include in your list

This Cambridge Immunology Network Seminar will take place on Thursday 12 March 2026, starting at 4:00pm, in the Ground Floor Lecture Theatre, Jeffrey Cheah Biomedical Centre (JCBC)

Speaker: Professor Salim Khakoo, Professor of Hepatology, Southampton University

Title: NK cell receptors: on with the old and in with the new

Abstract: Natural killer (NK) cells play a fundamental role in the immune response to viruses and cancer. As part of the innate immune system, on an evolutionary scale, they are considered to be relatively ancient. However, in addition to highly conserved receptors they also express a class of receptors (the killer cell immunoglobulin-like receptors) that are rapidly evolving. These receptors have MHC class I ligands and are associated with many different diseases process. They recognize peptides derived from both viruses and cancer. Interactions with viruses may have driven the selection of KIR , but recognition of cancer also provides a potential therapeutic opportunity.

Host: Professor Francesco Colucci, School of Clinical Medicine, University of Cambridge

Refreshments will be available following the seminar.

• Speaker: Professor Salim Khakoo, Professor of Hepatology, Southampton University
• Thursday 12 March 2026, 16:00-17:00
• Venue: Lecture Theatre, Jeffrey Cheah Biomedical Centre, Cambridge Biomedical Campus.
• Series: Cambridge Immunology Network Seminar Series; organiser: Liat Churley.

Add to your calendar or Include in your list

Nat Rev Urol. 2026 Feb 26. doi: 10.1038/s41585-026-01130-1. Online ahead of print.

ABSTRACT

Bacterial urinary tract infections (UTIs) are prevalent in childhood and adolescence. Paediatric UTIs present unique challenges with respect to diagnosis, prevention and management, and the potential for adverse sequelae. Uropathogenic Escherichia coli (UPEC) accounts for the majority of UTIs and is the best studied uropathogen. Novel discoveries have advanced our understanding of host-pathogen interactions, cellular and molecular mechanisms of host defence, and risk factors for UTI recurrence. Emerging evidence also highlights an association of the gut, vaginal and urinary microbiota in influencing UTI risk and recurrence. Yet, key knowledge gaps persist regarding UTI pathogenesis, host susceptibility, optimal diagnostic and management strategies and prevention of UTI recurrence and sequelae, especially in paediatric populations. The development of standardized clinical pathways offers an opportunity to improve care consistency and outcomes by integrating evidence-based practices into routine management. As technologies evolve and understanding deepens, future efforts must integrate host, microbial and clinical insights to optimize UTI prevention and treatment in paediatric populations.

PMID:41748741 | DOI:10.1038/s41585-026-01130-1

bioRxiv [Preprint]. 2026 Feb 11:2026.02.10.704860. doi: 10.64898/2026.02.10.704860.

ABSTRACT

Single-cell transcriptomic and proteomic technologies enable molecular profiling of immune cells at scale but provide limited access to cellular phenotypes shaped by spatial organisation, organelle architecture and cytoskeletal remodelling. Here we present TGlow, a scalable high-content imaging platform optimized for systematic single-cell phenotyping of primary human lymphocytes. TGlow integrates cyclic immunofluorescence, deep z-stack confocal imaging, and open-source data processing pipelines, including both classical and self-supervised vision transformer-based feature extraction, to jointly quantify cellular morphology, organelle organization, and immune activation states. Applied across over 400,000 primary human T cells spanning CD4+ activation time courses, drug perturbations, CRISPR knockouts and CD8+ T-cell exhaustion, TGlow resolves distinct and reproducible phenotypic states. We uncover dose-dependent and mechanism-specific drug phenotypes, such as defective endoplasmic reticulum polarisation under mycophenolic acid and tofacitinib. We show that mitochondrial clustering reveals activation- and cell-cycle-linked remodelling programs, CRISPR perturbations map gene-specific phenotypes that reposition cells along activation trajectories, and we identify a previously unrecognised collapse of cytoskeletal architecture in exhausted CD8+ T cells. TGlow provides a scalable framework for high-dimensional phenotyping of lymphocyte states advancing functional genomics, perturbation screening and population-level immune profiling by resolving the morphological and functional heterogeneity of lymphocytes and enabling systematic linkage of genetic and pharmacological perturbations to cellular function.

PMID:41726991 | PMC:PMC12918823 | DOI:10.64898/2026.02.10.704860

Pediatr Nephrol. 2026 Feb 20. doi: 10.1007/s00467-026-07166-0. Online ahead of print.

ABSTRACT

The imminent availability of multiple therapeutic complement inhibitors, which target different complement pathway components, could revolutionise treatment for a broad range of kidney diseases. However, the complexity of complement activity within and between kidney diseases, for which IgA nephropathy is an illustrative example, and the possible adverse effects of complement inhibition mean robust patient selection and stratification to appropriately targeted inhibitors will be needed to maximise this therapeutic opportunity. Despite promising candidates, novel biomarkers that stratify patients to targeted complement inhibition have not yet been validated for clinical practice.

PMID:41714421 | DOI:10.1007/s00467-026-07166-0

Am J Physiol Gastrointest Liver Physiol. 2026 Feb 12. doi: 10.1152/ajpgi.00447.2025. Online ahead of print.

ABSTRACT

The intestinal epithelium is a key component of the intestinal barrier, which is the largest and most complex barrier of the human body, regulating nutrients absorption while restricting the entry of harmful antigens. Breakdown of this barrier facilitates microbial and dietary antigenic translocation, triggering local immune system activation and inflammation. Although barrier alterations alone may not be sufficient to initiate disease, accumulating evidence highlights its critical role in the pathogenesis and progression of a wide range of gastrointestinal and systemic disorders. Early identification of intestinal epithelium and barrier alterations could enable timely therapeutic approaches. This systematic review provides an overview of current in vivo (both non-invasive and invasive) and ex vivo/in vitro approaches used to assess intestinal epithelial barrier alterations. Non-invasive in vivo approaches rely mainly on urinary detection of orally ingested probes, but their clinical utility is limited by lack of standardization and specificity. Circulating and fecal constitutive markers derived from the intestinal barrier, which reflect epithelial alterations, together with indicators of microbial translocation, provide complementary insights but remain insufficiently validated. Advanced invasive endoscopic modalities such as confocal laser endomicroscopy enable near-histologic, real-time visualization but are costly and largely used as research tools in specialist centers. In vitro, transepithelial electrical resistance assessment remains the reference standard, though novel technologies (including impedance spectroscopy and organic electrochemical transistors) offer enhanced sensitivity and resolution. Despite progress, major gaps remain, including the absence of a standardized definition of epithelial barrier breakdown, the lack of a practical diagnostic tool, methodological heterogeneity, unvalidated thresholds, and limited prospective validation.

PMID:41677575 | DOI:10.1152/ajpgi.00447.2025

This Cambridge Immunology Network Seminar will take place on Thursday 26 February 2026, starting at 4:00pm, in the Ground Floor Lecture Theatre, Jeffrey Cheah Biomedical Centre (JCBC)

Speaker: Professor Holm Uhlig, Director of the Centre for Human Genetics, University of Oxford

Short Bio: Professor Holm Uhlig investigates the genetic and immunologic basis of disorders associated with intestinal inflammation aiming to understand functional mechanisms that contribute to autoimmunity, tissue inflammation and disturbed barrier function. Holm has developed a strong focus on inborn errors of immunity and monogenic forms of inflammatory bowel disease. He is the Director of the Centre for Human Genetics, University of Oxford and Honorary Consultant in Paediatric Gastroenterology, Children’s Hospital Oxford.

Title: ‘Monogenic and autoimmune forms of inflammatory bowel disease – an emerging taxonomy’

Host: Arthur Kaser, Professor of Gastroenterology, Cambridge University

Refreshments will be available following the seminar.

• Speaker: Professor Holm Uhlig, Director of the Centre for Human Genetics, University of Oxford
• Thursday 26 February 2026, 16:00-17:00
• Venue: Lecture Theatre, Jeffrey Cheah Biomedical Centre, Cambridge Biomedical Campus.
• Series: Cambridge Immunology Network Seminar Series; organiser: Liat Churley.

Add to your calendar or Include in your list

This Cambridge Immunology Network Seminar will take place on Thursday 26th March 2026, starting at 4:00pm, in the Ground Floor Lecture Theatre, Jeffrey Cheah Biomedical Centre (JCBC)

Speaker: Professor Susanne Häußler, Head of Department of Molecular Bacteriology, Helmholtz Centre for Infection Research

Title: To be confirmed

Host: Aaron Weimann, VPD Heart and Lung Research Institute, Cambridge (on behalf of Professor Andres Floto)

Refreshments will be available following the seminar.

• Speaker: Prof Susanne Häußler, Head of Department of Molecular Bacteriology, Helmholtz Centre for Infection Research
• Thursday 26 March 2026, 16:00-17:00
• Venue: Lecture Theatre, Jeffrey Cheah Biomedical Centre, Cambridge Biomedical Campus.
• Series: Cambridge Immunology Network Seminar Series; organiser: Liat Churley.

Add to your calendar or Include in your list

Bio: Joseph Sun received his PhD in immunology in 2005, having trained with Mike Bevan in CD8 + T cell memory as a graduate student at the University of Washington. As a postdoc with Lewis Lanier at UCSF from 2006-2010, he discovered that natural killer cells possess adaptive immune features including clonal expansion and long-lived memory following viral infection. He was recruited to Memorial Sloan Kettering Cancer Center in 2010 by Jim Allison, and his lab has been interested in defining the underlying epigenetic, transcriptional, and metabolic signals that govern innate and adaptive lymphocyte responses in host defense against pathogens and cancer.

Title TBC

Hosts Dr Tim Halim, CRUK & Dr Virginia Pedicord, CITIID

• Speaker: Dr Joseph Sun, Cornell/ Memorial Sloan Kettering Cancer Center
• Thursday 19 March 2026, 16:00-17:00
• Venue: Lecture Theatre, Jeffrey Cheah Biomedical Centre, Cambridge Biomedical Campus.
• Series: Cambridge Immunology Network Seminar Series; organiser: Liat Churley.

Add to your calendar or Include in your list

This Cambridge Immunology Network Seminar will take place on Thursday 12 March 2026, starting at 4:00pm, in the Ground Floor Lecture Theatre, Jeffrey Cheah Biomedical Centre (JCBC)

Speaker: Professor Salim Khakoo, Professor of Hepatology, Southampton University

Title: TBC

Host: Professor Francesco Colucci, School of Clinical Medicine, University of Cambridge

Refreshments will be available following the seminar.

• Speaker: Professor Salim Khakoo, Professor of Hepatology, Southampton University
• Thursday 12 March 2026, 16:00-17:00
• Venue: Lecture Theatre, Jeffrey Cheah Biomedical Centre, Cambridge Biomedical Campus.
• Series: Cambridge Immunology Network Seminar Series; organiser: Liat Churley.

Add to your calendar or Include in your list

bioRxiv [Preprint]. 2026 Jan 14:2026.01.14.698769. doi: 10.64898/2026.01.14.698769.

ABSTRACT

Many E3 ubiquitin ligases recognize cognate degron motifs located at protein termini, but the paucity of bona fide substrates of N-degron and C-degron pathways hampers our understanding of their physiological significance. Here, by devising an expression screening approach to assess the effect of C-terminal "capping" on the stability of thousands of human proteins, we systematically identify a suite of full-length substrates harboring C-terminal degrons. Interrogating one leading candidate, ZMYND19, we characterize a C-degron pathway governed by the Muskelin substrate adaptor of the CTLH E3 ligase complex. Cell-to-cell variability in ZMYND19 stability uncovered conditional regulation, with CTLH-mediated degradation impaired by TNF-α stimulation but enhanced by mTOR inhibition. Parallel genetic and proteomic screens identified two poorly characterized proteins, AAMP and AEN, as additional substrates of the CTLHMuskelin C-degron pathway, leading us to define an essential role for AAMP in ribosome maturation through chaperone activity towards ribosomal protein uL16. Altogether, these data define a C-degron pathway through which the Muskelin substrate adaptor connects conditional regulation of the CTLH E3 ligase complex to control of ribosome biogenesis.

PMID:41648430 | PMC:PMC12871134 | DOI:10.64898/2026.01.14.698769

This Cambridge Immunology Network Seminar will take place on Thursday 12 February 2026, starting at 4:00pm, in the Ground Floor Lecture Theatre, Jeffrey Cheah Biomedical Centre (JCBC)

Speaker: Prof James Arnold, Professor and Head of Tumour Immunology Group, King’s College London

Title: ‘Harnessing the Tumour Microenvironment to Unlock CAR -T Cell Immunotherapy’

Host: Maike de la Roche, CRUK

Refreshments will be available following the seminar.

• Speaker: Prof James Arnold, Professor and Head of Tumour Immunology Group, King's College London
• Thursday 12 February 2026, 16:00-17:00
• Venue: Lecture Theatre, Jeffrey Cheah Biomedical Centre, Cambridge Biomedical Campus.
• Series: Cambridge Immunology Network Seminar Series; organiser: Liat Churley.

Add to your calendar or Include in your list

Nat Commun. 2026 Feb 3;17(1):714. doi: 10.1038/s41467-025-68264-5.

ABSTRACT

In Juvenile Idiopathic Arthritis (JIA), the most common childhood rheumatic disease, many patients also develop uveitis (JIA-uveitis), risking life-long vision loss. The mechanisms driving uveitis development in JIA remain understudied. Here, we demonstrate that peripheral blood CD19+IgD-CD27- double negative type 1 (DN1) B cells are elevated in JIA-uveitis compared to JIA patients without eye disease (JIA). The B cell receptor (BCR) repertoire was also more clonal and somatically hypermutated in JIA-uveitis and antigen-activated B cells infiltrated chronically inflamed JIA-uveitis eyes. Features of heightened B cell activation were recapitulated in experimental autoimmune uveoretinitis (EAU) and disrupting B and T cell interactions using monoclonal antibodies and transgenic mice suppresses uveitis. Together, these findings support a conceptual shift that uveitis is a primarily T cell driven disease and provide evidence for potential new therapeutic strategies that also consider B cells as drivers in disease pathology.

PMID:41633998 | DOI:10.1038/s41467-025-68264-5

Summary Venom derived cysteine-rich miniproteins (knottins) have potential as therapeutic agents to block ion channels but suffer from manufacturing difficulties, short half-lives and a lack of specificity. We have developed a novel molecular format wherein the CDR loop of an antibody has been replaced by a knottin. This format, termed a KnotBodyTM, combines the benefits of both scaffolds with the antibody gaining the functionality of a scaffold pre-disposed to the blockade of ion channels and the knottin enjoying the extended half-life and the additional specificity conferred by the antibody molecule. This presentation illustrates the generation of KnotBody molecules with a particular focus on the generation and optimisation of KnotBody inhibitors of the Kv1.3 channel , an important target affecting function of T effector memory cells.

Biography Affiliated Professor John McCafferty was one of the founders of Cambridge Antibody Technology (CAT) and a co-inventor of antibody phage display. In 2012 he formed IONTAS who generated multiple drug leads currently in clinical trial by partner companies. John also developed KnotBodyTM technology to address ion channels, an important target class which are under-served by biologics. He founded Maxion Therapeutics to take advantage of this drug development opportunity. Interspersed with company formation John has held academic positions at the Wellcome Trust Sanger Institute and is currently is an Affiliated professor at the Department of Medicine at the University of Cambridge

Host Prof Mark Wills, Department of Medicine

• Speaker: John McCafferty, Affiliated Professor, CTO and founder, Maxion Therapeutics, CITIID, Department of Medicine
• Thursday 05 March 2026, 16:00-17:00
• Venue: Lecture Theatre, Jeffrey Cheah Biomedical Centre, Cambridge Biomedical Campus.
• Series: Cambridge Immunology Network Seminar Series; organiser: Liat Churley.

Add to your calendar or Include in your list

This Cambridge Immunology Network Seminar will take place on Thursday 5 February 2026, starting at 4:00pm, in the Ground Floor Lecture Theatre, Jeffrey Cheah Biomedical Centre (JCBC)

Speaker: Prof Neil Brockdorff, Biochemistry, University of Oxford

Title: ‘Mechanisms of Xist RNA function in X chromosome Inactivation’

Host: Prof Yorgo Modis, CITIID , Department of Medicine

Refreshments will be available following the seminar.

• Speaker: Professor Neil Brockdorff, Biochemistry, University of Oxford
• Thursday 05 February 2026, 16:00-17:00
• Venue: Lecture Theatre, Jeffrey Cheah Biomedical Centre, Cambridge Biomedical Campus.
• Series: Cambridge Immunology Network Seminar Series; organiser: Liat Churley.

Add to your calendar or Include in your list

This Cambridge Immunology Network Seminar will take place on Thursday 12 February 2026, starting at 4:00pm, in the Ground Floor Lecture Theatre, Jeffrey Cheah Biomedical Centre (JCBC)

Speaker: Prof James Arnold, Professor and Head of Tumour Immunology Group, King’s College London

Title: To be confirmed

Host: Maike de la Roche, CRUK

Refreshments will be available following the seminar.

• Speaker: Prof James Arnold, Professor and Head of Tumour Immunology Group, King's College London
• Thursday 12 February 2026, 16:00-17:00
• Venue: Lecture Theatre, Jeffrey Cheah Biomedical Centre, Cambridge Biomedical Campus.
• Series: Cambridge Immunology Network Seminar Series; organiser: Liat Churley.

Add to your calendar or Include in your list

bioRxiv [Preprint]. 2026 Jan 10:2022.10.19.512842. doi: 10.1101/2022.10.19.512842.

ABSTRACT

Innate lymphoid cells (ILCs) are rare, tissue-resident innate lymphocytes that functionally mirror CD4+ T helper cell lineages but lack antigen receptors. Type 3 ILCs (ILC3s) are enriched in the gut, airways, and mucosal lymphoid tissues, where they regulate inflammation and promote barrier integrity. To define the regulatory architecture of primary human ILC3s, we map promoter-anchored chromosomal contacts using high-resolution, low-input Promoter Capture Hi-C (PCHi-C) in these cells alongside CD4+ T cells. By combining statistical detection with a PCHi-C-adapted Activity-by-Contact approach, we link promoters to distal regulatory elements, identifying hundreds of ILC3-specific contacts. We use these maps to connect genome-wide association study (GWAS) risk variants for Crohn's disease to target genes using multiCOGS, a Bayesian framework that integrates PCHi-C with summary-statistic imputation and multivariate fine-mapping. This analysis highlights both known and unanticipated candidates, including CLN3, a causal gene for the neurodevelopmental Batten disease. Using a mouse ILC3-like cell line, we show that Cln3 is downregulated upon cytokine stimulation, and Cln3 overexpression alters stimulation-induced transcriptional programmes and cytokine secretion. Extending this approach, we generate a catalogue of ILC3-linked risk genes for five additional autoimmune conditions and show that they are enriched for regulators of the ILC3 inflammatory response identified in a CRISPR interference screen. Together, these findings illuminate long-range gene control in ILC3s and prioritise known and newly implicated autoimmune risk genes with potential roles in this clinically important cell type.

PMID:41573945 | PMC:PMC12821085 | DOI:10.1101/2022.10.19.512842

Nat Commun. 2026 Jan 20;17(1):482. doi: 10.1038/s41467-026-68335-1.

ABSTRACT

The 2022 multi-country mpox (formerly monkeypox) outbreak, driven by mpox virus (MPXV) Clade IIb poses renewed threat to global public health. The cessation of smallpox vaccination has created large immunologically naïve cohorts, with uncertain implications for contemporary MPXV susceptibility. To assess whether residual vaccination-derived immunity influences exposure risk, we combine serological and phylodynamic analyses. Using a six-plex Luminex assay, we measure immunoglobulin G (IgG) binding to six MPXV antigens in 176 Nigerian adults comprising of 75 healthcare workers sampled in 2021 and 101 community volunteers sampled in 2023. At baseline, 24/176 (13.6%) were MPXV seropositive, predominantly born before 1980. Magnitude-breadth analysis scores were two-fold higher in pre-1980 cohort relative to post-1980 cohort. In 153 participants with follow-up samples (median 9 months), 5/153 (3%) showed evidence of exposure, with ≥2-fold increases in magnitude-breadth scores and antigen-specific responses against ≥4/6 antigens without reported clinical illness. Antigen-specific responses were strongest to B6R (11-fold), followed by M1R and A35R, with marked individual-level heterogeneity. Complementary phylodynamic reconstruction of 105 Nigerian MPXV genomes identified sporadic transmission against frequent dead-end infections. Together, these data show that residual smallpox immunity continues to shape mpox transmission and asymptomatic exposure contributes to under-detected spread, informing surveillance and targeted vaccination strategies.

PMID:41559051 | DOI:10.1038/s41467-026-68335-1

Summary: Venom derived cysteine-rich miniproteins (knottins) have potential as therapeutic agents to block ion channels but suffer from manufacturing difficulties, short half-lives and a lack of specificity. We have developed a novel molecular format wherein the CDR loop of an antibody has been replaced by a knottin. This format, termed a KnotBodyTM, combines the benefits of both scaffolds with the antibody gaining the functionality of a scaffold pre-disposed to the blockade of ion channels and the knottin enjoying the extended half-life and the additional specificity conferred by the antibody molecule. This presentation illustrates the generation of KnotBody molecules with a particular focus on the generation and optimisation of KnotBody inhibitors of the Kv1.3 channel , an important target affecting function of T effector memory cells.

Biography Affiliated professor John McCafferty was one of the founders of Cambridge Antibody Technology (CAT) and a co-inventor of antibody phage display. In 2012 he formed IONTAS who generated multiple drug leads currently in clinical trial by partner companies. John also developed KnotBodyTM technology to address ion channels, an important target class which are under-served by biologics. He founded Maxion Therapeutics to take advantage of this drug development opportunity. Interspersed with company formation John has held academic positions at the Wellcome Trust Sanger Institute and is currently is an Affiliated professor at the Department of Medicine at the University of Cambridge

Host Prof Mark Wills, Department of Medicine

• Speaker: John McCafferty, Affiliated Professor, CTO and founder, Maxion Therapeutics, CITIID, Department of Medicine
• Thursday 05 March 2026, 16:00-17:00
• Venue: Lecture Theatre, Jeffrey Cheah Biomedical Centre, Cambridge Biomedical Campus.
• Series: Cambridge Immunology Network Seminar Series; organiser: Liat Churley.

Add to your calendar or Include in your list

PLoS Pathog. 2026 Jan 16;22(1):e1013817. doi: 10.1371/journal.ppat.1013817. Online ahead of print.

ABSTRACT

Chronic HIV infection drives B cell dysfunction associated with the accumulation of tissue-like memory (TLMs) and activated memory B cells (MBCs) but decline in resting memory B cells. TLMs express multiple inhibitory receptors and lack response to soluble antigens. However, their origin and the mechanisms driving their expansion in HIV infection remain unclear. From bulk heavy chain BCR sequencing of MBC subsets from 5 PLWH with no detectable viremia, we hypothesized that TLMs (CD21- CD27- B cells) were significantly less mutated but also less diverse than other MBCs, suggesting an enrichment for innate-like B cells or that they belong to a less mature subset. Subsequent detailed multi-omics study of an immune response to a transient HIV viremia in an elite controller demonstrated a functional increase in Env-reactive IgG and MBCs with non-TLM phenotype. Single-cell RNA/BCR sequencing of PBMCs enriched for B cells revealed an orchestrated TNF-α response followed by interferon-α and -γresponses across all B cell subsets. This study provides new insights into multifaceted functional B cell response to transient HIV viremia and highlights TLM heterogeneity.

PMID:41544177 | DOI:10.1371/journal.ppat.1013817