Immunology · SciDEX

What we know

1 active hypothesis in scope
8 open frontiers with evidence gaps
10 indexed papers in corpus

Funded

1 active mission

1 hypotheses in scope top ranked

30 open frontiers

0 in-flight debates

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Top hypotheses

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#1 Longitudinal clonal, cytokine, and single-cell trajectories can distinguish protective remodeling from pathological immunosenescence. 66% proposed mechanism

Open frontiers

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How do tissue-specific immune environments affect TREM2 therapeutic strategies across different organs?

The cardiac-inspired hypothesis assumes TREM2 mechanisms translate between heart and brain, but the skeptic highlighted fundamental differences in immune environments. This knowledge gap affects cross-tissue therapeutic extrapolation. Source: Debate session sess_SDA-2026-04-06-gap-001 (Analysis: SDA-2026-04-06-gap-001)

priority 70%Do different priming stimuli require distinct therapeutic approaches or share common epigenetic pathways?

The skeptic proposed that epigenetic modifiers should work equally well regardless of initial priming stimulus if the hypothesis is correct. This fundamental question about pathway convergence versus stimulus-specific responses remains unresolved. Source: Debate session sess_SDA-2026-04-04-gap-20260404-microglial-priming-early-ad (Analysis: SDA-2026-04-04-gap-20260404-microglial-priming-early-ad)

priority 75%Why do peripheral tissue TREM2 functions fail to predict brain-specific therapeutic outcomes?

Evidence from liver and cardiac tissues was cited but the Skeptic noted these may not translate to brain pathophysiology. The molecular basis for this tissue-specific divergence remains unexplored. Source: Debate session sess_SDA-2026-04-10-trem2-ad (Analysis: trem2-ad)

priority 80%Which microbiome-derived metabolites directly modulate NLRP3 inflammasome activation in microglia?

The synthesis identified inflammasome targeting as high-priority but specific bacterial metabolites that regulate NLRP3 in brain tissue were not characterized. This knowledge gap prevents precision microbiome interventions. Source: Debate session sess_sda-2026-04-01-gap-20260401-225149 (Analysis: sda-2026-04-01-gap-20260401-225149)

priority 75%Which complement activation pathway predominates in different myelopathy etiologies despite convergent C5a signaling?

The complement hypothesis assumed convergence on C5a/C5aR1 but didn't address whether classical, alternative, or lectin pathways drive activation in different etiologies. This mechanistic gap affects upstream therapeutic targeting and biomarker development strategies. Source: Debate session sess_SDA-2026-04-08-gap-pubmed-20260406-062111-db808ee9 (Analysis: SDA-2026-04-08-gap-pubmed-20260406-062111-db808ee9)

priority 75%Do compensation mechanisms upregulate alternative cytokine pathways when IL-1α is blocked in neuroinflammation?

The skeptic raised concerns that IL-1α blockade may trigger compensatory upregulation of IL-1β, IL-18, or TLR signaling pathways. This potential for pathway redundancy could undermine single-target therapeutic approaches but has not been systematically investigated. Source: Debate session sess_sda-2026-04-01-gap-009 (Analysis: sda-2026-04-01-gap-009)

priority 75%Do microglia metabolic states directly control synaptic engulfment capacity independent of other functions?

The metabolic reprogramming hypothesis assumes pruning activity can be selectively modulated while preserving protective functions, but this functional dissociation hasn't been demonstrated. The debate noted this as having 'highest feasibility' yet acknowledged 'essential function risks' remain uncharacterized. Source: Debate session sess_sda-2026-04-01-gap-v2-691b42f1 (Analysis: sda-2026-04-01-gap-v2-691b42f1)

priority 80%How do NLRP3 inflammasome and mitophagy pathways mechanistically interact in microglia?

The highest-ranked hypothesis proposed NLRP3/mitophagy coupling modulation, but the specific molecular crosstalk mechanisms between these pathways in microglial cells remain undefined. Understanding this interaction is essential for targeted intervention. Source: Debate session sess_SDA-2026-04-03-gap-immune-atlas-neuroinflam-20260402 (Analysis: SDA-2026-04-03-gap-immune-atlas-neuroinflam-20260402)

priority 73%

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shield Immunology 120.0k budget · active

Recent literature

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Unifying researchers and clinicians to eliminate ex vivo artifacts in human immune system studies Immunology tackled the issue of blood samples changing over time
The function and regulation of TET2 in innate immunity and inflammation. Immunology, Institute of Immunology, Navy Military Me
Human Inborn Errors of Immunity: 2022 Update on the Classification from the International Union of Immunological Societies Expert Committee immunological mechanisms of disease pathogenesis, thereby simultane
B cells orchestrate tolerance to the neuromyelitis optica autoantigen AQP4. Immunology, Faculty of Medicine, Ludwig-Maximilians-University Mun
Immunity to <scp>SARS‐CoV</scp>‐2 infection* immunology provided the foundation for these advances and for the r
Omega-3 polyunsaturated fatty acids protect against inflammation through production of LOX and CYP450 lipid mediators: relevance for major depression and for human hippocampal neurogenesis. Immunology Laboratory, Institute of Psychiatry, Psychology and Neu
A humanised ACE2, TMPRSS2, and FCGRT mouse model reveals the protective efficacy of anti-receptor binding domain antibodies elicited by SARS-CoV-2 hybrid immunity. Immunology, La Jolla, CA, 92037, USA. (2)Center for Vaccine
NPM1 inhibits tumoral antigen presentation to promote immune evasion and tumor progression. Immunology, Center for Immunotherapy, Institute of Basic Medicine,
Abstract 1071: Online resources from the Allen Institute for Immunology: longitudinal profiling of multiple myeloma treatment and the Human Immune System Explorer platform Immunology was founded in 2018 to deeply profile the human
CD161 defines a transcriptional and functional phenotype across distinct human T cell lineages. Immunology, Stanford University, Stanford, CA 94305, USA; Agency f

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