ArticleImmunologic research2026
Lewis Y (Le
Article in Immunologic research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Leprosy is characterized by a complex inflammatory microenvironment in which host-related factors play a decisive role in disease progression. However, the contribution of tissue glycans to inflammatory remodeling remains poorly understood. In this study, we investigated the expression of Lewis blood group antigens in skin biopsies from patients with different clinical forms of leprosy in the Brazilian Amazon, a region marked by persistent hyperendemic transmission. Using immunohistochemistry, we demonstrate that the difucosylated epitope Lewis Y (Ley) is preferentially expressed in inflamed lesions, particularly in endothelial cells, histiocytes, lymphocytes, and neural structures, while being absent in healthy skin. Quantitative and spatial analyses revealed that Ley displays the broadest and most intense expression pattern among the investigated Lewis antigens, whereas Lewis X (Lex) and sialyl-Lewis x (sLex) exhibited restricted, tissue-dependent expression profiles. Statistical analyses showed that Ley expression varies significantly according to the clinical spectrum of leprosy, while Lewis X and sialyl-Lewis X are primarily dependent on tissue compartment rather than clinical classification. Mechanistically, our findings support a model in which endothelial Ley functions as a central glycan regulator of the inflammatory microenvironment, promoting leukocyte recruitment, endothelial activation, angiogenesis, and immune–vascular interactions. We propose a Ley-driven glyco-immune axis, involving DC-SIGN–mediated interactions with dendritic cells and macrophages, as a unifying mechanism linking glycan remodeling, immune cell trafficking, vascular remodeling, and tissue reorganization in leprosy lesions. Together, these results identify Ley as a tissue-specific glycan signature of inflammatory remodeling and highlight glycan remodeling as a previously underexplored organizing principle in leprosy immunopathology, with translational implications for biomarker discovery, risk stratification, and therapeutic targeting in endemic settings.
Indexed as
Identifiers
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.