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Khor, B.

Publications and source records attributed to Khor, B..

4 recordsLinked to original sources

ORION: An agentic reasoning construct for the analysis of complex human immune profiling

The capacity to generate high-dimensional biological datasets has outpaced the ability to interpret them. Technologies such as phage immunoprecipitation and sequencing (PhIP-seq) enable proteome-scale profiling of antibody repertoires, but interpreting thousands of enriched peptides into mechanistic hypotheses remains a labor-intensive bottleneck requiring expert synthesis of statistics, literature, and domain knowledge. Here we describe ORION (Omics Reasoning & Interpretation Orchestrator), a multi-agent framework that uses reasoning-capable large language models to perform end-to-end analysis of complex immune profiling data. ORION integrates statistical analysis, machine learning, and automated literature review into a single structured workflow, producing results that are reproducible and fully traceable. Applied to a published PhIP-seq dataset from autoimmune polyendocrine syndrome type 1 (APS-1), ORION recovered the canonical autoantibody signature in approximately two hours, closely recapitulating an analysis that originally required one to two months of manual effort. To test hypothesis-generation capacity on previously unseen data, we applied ORION to a novel PhIP-seq dataset from individuals with Down syndrome, for which no proteome-wide autoantibody reference exists. ORION distinguished disease from control samples with high accuracy, prioritized candidate autoantibody targets, and organized them into biologically coherent groups spanning immune, gut, and neuronal programs, generating testable hypotheses for experimental follow-up. These results demonstrate that agentic AI systems can compress the analysis of complex immune profiling data from weeks to hours, allowing scientists to redirect their time toward the fundamental biology.

bioinformatics↗

Permutational immune analysis reveals architectural similarities between inflammaging, Down syndrome and autoimmunity

People with Down syndrome show cellular and clinical features of dysregulated aging of the immune system, including naive-memory shift in the T cell compartment and increased incidence of autoimmunity. However, a quantitative understanding of how various immune compartments change with age in Down syndrome remains lacking. Here we performed deep immunophenotyping of a cohort of individuals with Down syndrome across the lifespan, selecting for individuals not affected by autoimmunity. We simultaneously interrogated age- and sex-matched healthy neurotypical controls and people with type 1 diabetes, as a representative autoimmune disease. We built a new analytical software, IMPACD, that enabled us to rapidly identify many features of immune dysregulation in Down syndrome that are recapitulated in other autoimmune diseases. We found significant quantitative and qualitative dysregulation of naive CD4+ and CD8+ T cells in Down syndrome and identified IL-6 as a candidate driver of some of these changes, thus extending the consideration of immunopathologic cytokines in Down syndrome beyond interferons. Notably, we successfully used immune cellular composition to generate three quantitative models of aging (i.e. immune clocks) trained on control subjects. All three immune clocks demonstrated significantly advanced immune aging in people with Down syndrome. Notably, one of these clocks, informed by Down syndrome-relevant biology, also showed advanced immune aging in people with type 1 diabetes. Together, our findings demonstrate a novel approach to studying immune aging in Down syndrome which may have implications in the context of other autoimmune diseases. One Sentence SummaryPermutational analysis of immune landscape reveals advanced immune aging in people with Down syndrome and in people with type 1 diabetes.

immunology↗

Tonic interferon restricts pathogenic IL-17-driven inflammatory disease via balancing the microbiome

Maintenance of immune homeostasis involves a synergistic relationship between the host and the microbiome. Canonical interferon (IFN) signaling controls responses to acute microbial infection, through engagement of the STAT1 transcription factor. However, the contribution of tonic levels of IFN to immune homeostasis in absence of acute infection remains largely unexplored. We report that STAT1 KO mice spontaneously developed an inflammatory disease marked by myeloid hyperplasia and splenic accumulation of hematopoietic stem cells. Moreover, these animals developed inflammatory bowel disease. Profiling gut bacteria revealed a profound dysbiosis in absence of tonic IFN signaling, which triggered expansion of TH17 cells and loss of splenic Treg cells. Resolution of dysbiosis by antibiotic treatment averted the TH17 bias, and blocking IL17 signaling prevented myeloid expansion and splenic stem cell accumulation. Thus, tonic IFNs regulate gut microbial ecology, which is crucial for maintaining physiologic immune homeostasis and preventing inflammation.

immunology↗

DCA promotes a novel tolerogenic program in CD4+ T cells by inhibiting CDK8

Immune health requires innate and adaptive immune cells to engage precisely balanced pro- and anti-inflammatory forces. We employ the concept of chemical immunophenotypes to classify small molecules functionally or mechanistically according to their patterns of effects on primary innate and adaptive immune cells. The high-specificity, low-toxicity cyclin dependent kinase 8 (CDK8) inhibitor DCA exerts a distinct tolerogenic profile in both innate and adaptive immune cells. DCA promotes Treg and Th2 differentiation, while inhibiting Th1 and Th17 differentiation, in both murine and human cells. This unique chemical immunophenotype led to mechanistic studies showing that DCA promotes Treg differentiation in part by regulating a previously undescribed CDK8-GATA3-FOXP3 pathway that regulates early pathways of Foxp3 expression. These results highlight previously unappreciated links between Treg and Th2 differentiation and extend our understanding of the transcription factors that regulate Treg differentiation and their temporal sequencing. These findings have significant implications for future mechanistic and translational studies of CDK8 and CDK8 inhibitors.

immunology↗