Abstract

Chediak-Higashi syndrome is characterized by congenital abnormality in exocytosis activity, and accumulation of intracellular lysosome-like structures different types of cells within the body. Accordingly, the lack of appropriate exocytosis and deficiency in lysosomal trafficking accounts for immune-related hypoactivity. Exosomes are other types of cell-derived vesicles that play key role in cell-cell cross talk. However, the possible effect of LYST gene mutation in exosome trafficking and biogenesis remains to be clarified. Herein, we investigated the expression of CD63-Alix-Rab27a exosome axis in Chediak-Higashi syndrome. Real-time PCR analysis showed a marked reduction in the expression of CD63, Alix, and Rab27a genes in mononuclear and polymorphonuclear cells. In addition to accumulated number of intracellular lysosome, it seems that the biogenesis and trafficking of exosomes were also abolished.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.