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Chiang, Samuel C. C.
[VerfasserIn];
Wood, Stephanie M.
[VerfasserIn];
Tesi, Bianca
[VerfasserIn];
Akar, Himmet Haluk
[VerfasserIn];
Al–Herz, Waleed
[VerfasserIn];
Ammann, Sandra
[VerfasserIn];
Belen, Fatma Burcu
[VerfasserIn];
Caliskan, Umran
[VerfasserIn];
Kaya, Zühre
[VerfasserIn];
Lehmberg, Kai
[VerfasserIn];
Patiroglu, Turkan
[VerfasserIn];
Tokgoz, Huseyin
[VerfasserIn];
Ünüvar, Ayşegül
[VerfasserIn];
Introne, Wendy J.
[VerfasserIn];
Henter, Jan-Inge
[VerfasserIn];
Nordenskjöld, Magnus
[VerfasserIn];
Ljunggren, Hans-Gustaf
[VerfasserIn];
Meeths, Marie
[VerfasserIn];
Ehl, Stephan
[VerfasserIn];
Krzewski, Konrad
[VerfasserIn];
Bryceson, Yenan T.
[VerfasserIn]
Differences in granule morphology yet equally impaired exocytosis among cytotoxic T cells and NK cells from Chediak–Higashi syndrome patients
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- Medientyp: E-Book; Sonderdruck
- Titel: Differences in granule morphology yet equally impaired exocytosis among cytotoxic T cells and NK cells from Chediak–Higashi syndrome patients
- Beteiligte: Chiang, Samuel C. C. [VerfasserIn]; Wood, Stephanie M. [VerfasserIn]; Tesi, Bianca [VerfasserIn]; Akar, Himmet Haluk [VerfasserIn]; Al–Herz, Waleed [VerfasserIn]; Ammann, Sandra [VerfasserIn]; Belen, Fatma Burcu [VerfasserIn]; Caliskan, Umran [VerfasserIn]; Kaya, Zühre [VerfasserIn]; Lehmberg, Kai [VerfasserIn]; Patiroglu, Turkan [VerfasserIn]; Tokgoz, Huseyin [VerfasserIn]; Ünüvar, Ayşegül [VerfasserIn]; Introne, Wendy J. [VerfasserIn]; Henter, Jan-Inge [VerfasserIn]; Nordenskjöld, Magnus [VerfasserIn]; Ljunggren, Hans-Gustaf [VerfasserIn]; Meeths, Marie [VerfasserIn]; Ehl, Stephan [VerfasserIn]; Krzewski, Konrad [VerfasserIn]; Bryceson, Yenan T. [VerfasserIn]
- Erschienen: Lausanne: Frontiers, 2017
- Erschienen in: Frontiers in immunology ; 8 (2017), 00426
- Umfang: 1 Online-Ressource (15 Seiten); Illustrationen, Diagramme
- Sprache: Englisch
- DOI: 10.3389/fimmu.2017.00426
- ISSN: 1664-3224
- Identifikator:
- Entstehung:
- Anmerkungen:
- Beschreibung: Abstract: Chediak–Higashi syndrome (CHS) is caused by autosomal recessive mutations in LYST, resulting in enlarged lysosomal compartments in multiple cell types. CHS patients display oculocutaneous albinism and may develop life-threatening hemophagocytic lymphohistiocytosis (HLH). While NK cell-mediated cytotoxicity has been reported to be uniformly defective, variable defects in T cell-mediated cytotoxicity has been observed. The latter has been linked to the degree of HLH susceptibility. Since the discrepancies in NK cell- and T cell-mediated cellular cytotoxicity might result from differences in regulation of cytotoxic granule release, we here evaluated perforin-containing secretory lysosome size and number in freshly isolated lymphocytes from CHS patients and furthermore compared their exocytic capacities. Whereas NK cells from CHS patients generally contained a single, gigantic perforin-containing granule, cytotoxic T cells predominantly contained several smaller granules. Nonetheless, in a cohort of 21 CHS patients, cytotoxic T cell and NK cell granule exocytosis were similarly impaired upon activating receptor stimulation. Mechanistically, polarization of cytotoxic granules was defective in cytotoxic lymphocytes from CHS patients, with EEA1, a marker of early endosomes, mislocalizing to lysosomal structures. The results leads to the conclusion that lysosome enlargement corresponds to loss of distinct organelle identity in the endocytic pathway, which on a subcellular level more adversely affects NK cells than T cells. Hence, vesicular size or numbers do not per se dictate the impairment of lysosomal exocytosis in the two cell types studied
- Zugangsstatus: Freier Zugang