ArticleFrontiers in immunology2026
The protective role of MDL-1 in sepsis-induced lung injury: insights from a murine CLP model.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: The Myeloid DAP12-associating lectin-1 (MDL-1) serves as a pivotal pattern recognition receptor crucial for recognizing various pathogenic microorganisms and orchestrating immune responses during infections. This study aimed to elucidate the role of MDL-1 in the pathogenesis of sepsis-associated acute lung injury (ALI). Methods: Experiments were conducted using wild-type (WT) and MDL-1-deficient (MDL-1 Results: Survival analysis revealed that MDL-1 deficiency significantly exacerbated mortality in septic mice. In the CLP-induced sepsis model, the 7-day survival rate was 78.6% in the WT-CLP group, whereas it was markedly reduced to 42.9% in the MDL-1 Discussion: Our findings demonstrate that MDL-1 deficiency exacerbates lung inflammation in a CLP-induced murine sepsis model. These results underscore the essential immunomodulatory role of MDL-1 in mitigating excessive pulmonary inflammatory responses during sepsis.The Myeloid DAP12-associating lectin-1 (MDL-1) serves as a pivotal pattern recognition receptor crucial for recognizing various pathogenic microorganisms and orchestrating immune responses during infections. In this study, we elucidate that MDL-1 exhibits predominant expression within the mononuclear phagocyte system and plays a significant role in modulating the severity of lung injury in sepsis. Notably, MDL-1-deficient (MDL-1
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