ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
Engineered Dual-Function Antibody-Like Proteins to Combat SARS-CoV-2-Induced Immune Dysregulation and Inflammation.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
5 citing papers in PubMed.
- Article
- The primary cilium as a compartmentalized signaling hub in tissue immunity and homeostasis.Frontiers in cell and developmental biology · 2026Review
- Engineered Dual-Function Antibody-Like Proteins to Combat SARS-CoV-2-Induced Immune Dysregulation and Inflammation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- MIS-C pathogenesis: immune dysregulation & viral triggers.Frontiers in immunology · 2025Review
- Therapeutic antibody delivery: vector tools to boost efficacy and affordability.Frontiers in immunology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
Complement dysregulation and immune hyperactivation are pivotal factors contributing to the mortality associated with SARS-CoV-2 infection. Engineered Antibody-like proteins (ALPs) targeting the SARS-CoV-2 spike protein are engineered to address immune dysregulation in COVID-19. In this study, Lectifitin-36 and Lectifitin-41, two such ALPs, are developed using cDNA display technology. These ALPs demonstrate strong binding affinity for the spike protein and effectively inhibit its interaction with ACE2 and several C-type lectins, including MBL, DC-SIGN, and L-SIGN. Both in vitro and in vivo analyses reveal that Lectifitin-36 and Lectifitin-41 suppress complement activation via the lectin pathway, reduce neutrophil extracellular trap (NET) formation, and attenuate hyper-inflammatory responses. In mouse models, Lectifitin-36 and Lectifitin-41 significantly mitigate inflammation, NETosis, and lung tissue damage induced by the spike protein. These results suggest that these ALPs hold promise as therapeutic candidates for alleviating SARS-CoV-2-induced immune dysfunction, with the potential to reduce severe COVID-19 outcomes and long-term sequelae. This study underscores the therapeutic potential of targeting spike protein-mediated immune modulation as an innovative approach to combat COVID-19.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.