Aims: The effects of mannose-binding lectin (MBL) deficiency are well known in children and in those with a compromised immune system. However, its effects in adults are debateable, with little research having been carried out in the UK regarding infection risk in otherwise healthy adults with an MBL deficiency.
Methods: Using an ELISA, we investigated the prevalence of MBL deficiency in both healthy adults and those with recurrent infection. The aim was to determine first if there was a disparity in MBL levels between the two groups and second to investigate the effect of severe deficiency.
Results: Overall, the difference between the two groups for MBL level was found not to be statistically significant (p=0.203); however, there was a higher prevalence of severe deficiency (MBL<75 ng/mL) in the patients with recurrent infection (p=0.03).
Conclusions: It was concluded that there is justified reason for continuing to perform the MBL test in adult patients suffering recurrent infection.
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http://dx.doi.org/10.1136/jclinpath-2015-203065 | DOI Listing |
Front Immunol
January 2025
Department of Biomedicine, Aarhus University, Aarhus, Denmark.
The innate immune system plays a critical role in the rapid recognition and elimination of pathogens through pattern recognition receptors (PRRs). Among these PRRs are the C-type lectins (CTLs) langerin, mannan-binding lectin (MBL), and surfactant protein D (SP-D), which recognize carbohydrate patterns on pathogens. Each represents proteins from different compartments of the body and employs separate effector mechanisms.
View Article and Find Full Text PDFHematol Rep
January 2025
Laboratory of Immunobiology and Immunogenetics, Post Graduation Program in Genetics and Molecular Biology (PPGBM), Universidade Federal do Rio Grande do Sul (UFRGS), Porto Alegre 91501-970, Brazil.
A quarter of a century ago, sickle cell disease (SCD) was mainly viewed as a typical genetic disease inherited as a classical Mendelian trait. Therefore, the main focus concerning SCD was on diagnosis, meaning, genotyping, and identification of homozygous and heterozygous individuals carrying the relevant HbS mutant allele. Nowadays, it is well established that sickle cell disease is indeed the result of homozygosis for the HbS variant, although this single feature is not capable of explaining the highly diverse clinical presentation of SCD.
View Article and Find Full Text PDFInt J Biol Macromol
January 2025
Departmento de Biofísica e Radiobiologia, Universidade Federal de Pernambuco, Recife, Pernambuco 50670-901, Brazil. Electronic address:
Mannose-binding lectin (MBL) is an important glycoprotein of the human innate immune system. Furthermore, individuals with sickle cell anemia (SCA) and MBL deficiency seem more susceptible to vaso-occlusive crises, suggesting an MBL role on HbSS red blood cells (RBCs). This study investigated the interaction of MBL with HbA (healthy) and HbSS RBCs using optical tweezers (OT) and atomic force microscopy (AFM).
View Article and Find Full Text PDFToxicology
January 2025
Department of Pharmacology, Shantou University Medical College, Shantou 515041, China. Electronic address:
Aflatoxin B1 (AFB1) has been reported to synergize with hepatitis B virus (HBV) to induce development of hepatocellular carcinoma (HCC). Precise daily exposure to AFB1 and its contribution to liver injury have not been quantified and have even been disregarded due to lack of convenient detection, and the strong species specificity of HBV infection has restricted research on their synergistic harm. Hence, our objective was to investigate the molecular mechanisms by which AFB1 exacerbates HBV-related injury.
View Article and Find Full Text PDFSci Transl Med
January 2025
College of Pharmaceutical Sciences, State Key Laboratory of Advanced Drug Delivery and Release Systems, Zhejiang University, Hangzhou 310058, China.
Macrophages play a central role in antitumor immunity, making them an attractive target for gene therapy strategies. However, macrophages are difficult to transfect because of nucleic acid sensors that can trigger the degradation of foreign plasmid DNA. Here, we developed a macrophage-specific editing (MAGE) system by which compact plasmid DNA encoding a CasRx editor can be delivered to macrophages by a poly(β-amino ester) (PBAE) carrier to bypass the DNA sensor and enable RNA editing in vitro and in vivo.
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