Repertoire and functionality of innate and adaptive immune receptors in Chronic Lyphocytic Leukemia.

Doctoral Dissertation uoadl:1309323 525 Read counter

Unit:
Τομέας Γενετικής και Βιοτεχνολογίας
Library of the School of Science
Deposit date:
2013-02-13
Year:
2013
Author:
Ντούφα Σταυρούλα
Dissertation committee:
Βασιλική Αλεπόρου-Μαρίνου Αναπλ. Καθηγ. (Επιβλέπουσα), Ελένη Παπαδάκη Καθηγ. Ιατρική Σχολή Πανεπιστήμιο Κρήτης, Παναγούλα Κόλλια Επικ. Καθηγ.
Original Title:
Ρεπερτόριο και λειτουργικότητα Υποδοχέων έμφυτης και προσαρμοστική ανοσίας στη Χρόνια Λεμφοκυτταρική Λευχαιμία
Languages:
Greek
Translated title:
Repertoire and functionality of innate and adaptive immune receptors in Chronic Lyphocytic Leukemia.
Summary:
It is nowadays obvious that antigenic stimulation plays an important role in
Chronic Lympocytic Leukemia (CLL). B cell receptor (BcR) signaling plays an
important role in CLL development and evolution. Besides BcR that B cells
recognize pathogens also through innate immunity receptors, such as Toll Like
Receptors, TLRs. This study aims in investigating the repertoire and
functionality of adaptive immunity receptors (BcR) and innate immunity
receptors (TLR and NOD) in a large group of well characterized CLL patients.
The analysis of TLR pathway expression levels revealed significant differences
between subgroups of CLL cases, based ony specific molecular features of the
clonotypic BcRs. Moreover, functional studies revealed that there are
differential functional profiles between CLL subgroups. All together these
results indicate that the biological behavior of the malignant clone, which is
reflected to the clinical course of the patients, is the result of the
collaboration between the clonotypic BcRs and specific TLRs, which differ among
different CLL subgroups. These results could e very useful for the
implementation of targeted therapies.
Keywords:
Immunity, Leukemia, Energy, Apoptosis, Signaling
Index:
No
Number of index pages:
0
Contains images:
Yes
Number of references:
171
Number of pages:
210
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