scholarly journals Enhanced Gamma Interferon Production through Activation of Vα14+ Natural Killer T Cells by α-Galactosylceramide in Interleukin-18-Deficient Mice with Systemic Cryptococcosis

2001 ◽  
Vol 69 (11) ◽  
pp. 6643-6650 ◽  
Author(s):  
Kazuyoshi Kawakami ◽  
Yuki Kinjo ◽  
Satomi Yara ◽  
Kaori Uezu ◽  
Yoshinobu Koguchi ◽  
...  

ABSTRACT We showed recently that activation of Vα14+ natural killer T cells (NKT cells) by α-galactosylceramide (α-GalCer) resulted in increased gamma interferon (IFN-γ) production and host resistance to intravenous infection with Cryptococcus neoformans. In other studies, interleukin-18 (IL-18) activated NKT cells in collaboration with IL-12, suggesting the possible contribution of this cytokine to α-GalCer-induced IFN-γ synthesis. Here we examined the role of IL-18 in α-GalCer-induced Th1 response by using IL-18KO mice with this infection. In these mice, levels of IFN-γ in serum and its synthesis in vitro by spleen cells stimulated with live organisms were not reduced, but rather enhanced, compared to those in wild-type (WT) mice, while such production was completely absent in IL-12KO mice. The enhanced production of IFN-γ correlated with increased IL-12 synthesis but not with reduced production of IL-4, which was rather increased. IFN-γ synthesis in IL-18KO mice was abolished by neutralizing anti-IL-12 antibody and significantly inhibited by neutralization of endogenous IL-4 with a specific monoclonal antibody. In addition, administration of recombinant IL-4 significantly enhanced the production of IFN-γ in WT mice. Finally, the enhanced production of IFN-γ in IL-18KO mice correlated with increased host defense against cryptococcal infection, as indicated by enhancement in α-GalCer-related clearance of microorganisms. Our results indicated that in IL-18KO mice, IFN-γ synthesis was enhanced through overproduction of IL-12 and IL-4 after intravenous infection with C. neoformans and a ligand-specific activation of Vα14+ NKT cells.

2006 ◽  
Vol 119 ◽  
pp. S62-S63
Author(s):  
Ken Coppieters ◽  
Katrien Van Beneden ◽  
Ann Vervloet ◽  
Pieter Dewint ◽  
Peggy Jacques ◽  
...  

Hepatology ◽  
2014 ◽  
Vol 60 (4) ◽  
pp. 1356-1366 ◽  
Author(s):  
Shi Yin ◽  
Hua Wang ◽  
Adeline Bertola ◽  
Dechun Feng ◽  
Ming-jiang Xu ◽  
...  

2005 ◽  
Vol 53 (6) ◽  
pp. 781-785 ◽  
Author(s):  
Yuri V. Bobryshev ◽  
Reginald S.A. Lord

We previously reported that CD1d, a molecule responsible for the presentation of lipid antigens, is expressed in atherosclerotic lesions and that its expression is restricted to dendritic cells. Recent studies demonstrating that CD1d-restricted natural killer T (NKT) cells are involved in atherogenesis prompted the present study investigating whether NKT cells are present in human atherosclerotic lesions and, if so, whether there is an association between NKT cells and dendritic cells. We found that NKT cells do accumulate in rupture-prone shoulders of atherosclerotic plaques and observed direct contacts of dendritic cells with NKT cells in rupture-prone regions of plaque.


2011 ◽  
Vol 18 (12) ◽  
pp. 1620-1630 ◽  
Author(s):  
Aaron J. Tyznik ◽  
Elisa Farber ◽  
Enrico Girardi ◽  
Alysia Birkholz ◽  
Yali Li ◽  
...  

Blood ◽  
2009 ◽  
Vol 113 (25) ◽  
pp. 6382-6385 ◽  
Author(s):  
Jeremy B. Swann ◽  
Adam P. Uldrich ◽  
Serani van Dommelen ◽  
Janelle Sharkey ◽  
William K. Murray ◽  
...  

Abstract CD1d-restricted T cells are considered to play a host protective effect in tumor immunity, yet the evidence for a role of natural killer T (NKT) cells in tumor immune surveillance has been weak and data from several tumor models has suggested that some (type II) CD1d-restricted T cells may also suppress some types of antitumor immune response. To substantiate an important role for CD1d-restricted T cells in host response to cancer, we have evaluated tumor development in p53+/− mice lacking either type I NKT cells (TCR Jα18−/−) or all CD1d-restricted T cells (CD1d−/−). Our findings support a key role for type I NKT cells in suppressing the onset of sarcomas and hematopoietic cancers caused by p53 loss but do not suggest that other CD1d-restricted T cells are critical in regulating the same tumor development.


2021 ◽  
Vol 320 (5) ◽  
pp. F772-F788
Author(s):  
Jung Nam An ◽  
Seungwon Ryu ◽  
Yong Chul Kim ◽  
Kyung Don Yoo ◽  
Jangwook Lee ◽  
...  

This study makes a significant contribution to the literature because our results indicate that IL-17 is upregulated in lupus nephritis and that natural killer T (NKT) cells are involved in its pathogenesis. Activation of NKT cells regulates IL-17-related immune responses, both systemically and in the kidney, and this mainly involves NK1.1− NKT cells. Furthermore, IL-17-secreting NK1.1− NKT cells could serve as a diagnostic and therapeutic target for lupus nephritis.


2016 ◽  
Author(s):  
Παναγιώτα Καραγιάννη

Τα Natural Killer T cells (ΝΚΤ) αναγνωρίζουν γλυκολιπιδιακά αντιγόνα, εκφράζουν δείκτες επιφανείας φυσικών φονέων και Τ κυτταρικό υποδοχέα, γεφυρώνοντας την φυσική με την ειδική ανοσία. Συμμετέχουν στα πρώιμα στάδια μιας λοίμωξης κατευθύνοντας την ανοσολογική απάντηση. Ο Σακχαρώδης Διαβήτης τύπου 2 (ΣΔ2) θεωρείται κατάσταση ενεργοποιημένης φυσικής ανοσίας. Τα Gram αρνητικά παθογόνα ενεργοποιούν τα NKT κύτταρα, συνδέονται με την αυτοανοσία και είναι συχνά αίτια λοιμώξεων σε ασθενείς με ΣΔ2. Μέθοδος: Η ομάδα ΣΔ2 είχε 22 άτομα , η ομάδα των μαρτύρων είχε 22 άτομα χωρίς ΣΔ2 . Όλοι είχαν λοίμωξη από Gram αρνητικό μικρόβιο. Πραγματοποιήθηκε φυσική εξέταση, λήψη ζωτικών σημείων και περιφερικού αίματος την ημέρα 3 και 6 του εμπύρετου με προσδιορισμό γενικής αίματος, pH, βιοχημικού ελέγχου, ανοσοσφαιρινών, αντιπυρηνικών αντισωμάτων (ANA)/ anti-ds DNA και καλλιέργεια ούρων/αίματος/πύου. Προσδιορίσαμε τα ΝΚΤ με κυτταρομετρία ροής με μονοκλωνικά PE CY 5 anti -CD3, FITC anti- CD4, PE anti-NKT-Cell Receptor , τις ενδοκυττάριες κυταροκίνες με Alexa Fluor anti-IFN-γ/ APC anti- IL-4. Μελετήθηκαν: CD3+IL-4+NKT+ , CD4+IL-4+NKT+, CD3+IFNγ+NKT+, CD4+IFNγ+ΝΚΤ+,CD3+NKT+, CD4+NKT+ ,CD3+IL4+, CD4+IL-4+, CD3+IFNγ+, CD4+IFNγ+ . Η βαρύτητα νόσου ταξινομήθηκε με το σύστημα APACHE IΙ.Αποτελέσματα: Ο αριθμός των ΝΚΤ και οι ενδοκυττάρια παραγόμενες IFNγ/IL4 μειώνονται από την ημέρα 3 στην 6 χωρίς διαφορά ανάμεσα στις δύο ομάδες. Τα CD4+/CD3+ παράγουν μεικτού τύπου απάντηση (Th1/Th2), έχουν στατιστικά σημαντική διαφορά στην ομάδα ΣΔ2 την 3η ημέρα, και παρόμοια αύξηση στατιστικά σημαντική εντός των ομάδων από την ημέρα 3 στην 6. Στις μετρήσεις ANA , anti-ds DNA , ανοσοσφαιρινών δεν διαπιστώνεται διαφορά μεταξύ των ομάδων.


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