Abstract
Mannose-binding lectin (MBL) plays an integral role in innate immunity through complement activation by the lectin pathway facilitating pathogen phagocytosis. Heterozygous or homozygous mutations of the MBL2 gene may result in low levels of MBL.1,2 This predisposes one to a variety of infections with viruses,3 bacteria, protozoa, and fungi as well as malignancies (Table 1).1,4 Homozygous mutations of the MBL2 gene also have been linked to mycobacterial infections. We report a novel association between MBL deficiency and strongyloidiasis, aspergillus mycetoma, and spindle cell tumor.
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