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Lenart, Marzena
2012
Praca doktorska
The loss of the B73.1/Leu11c epitope of CD16a (FcγRIIIa) receptor, detected by a monoclonal antibody commonly used in routine immunophenotyping of NK cells and CD14+CD16++ monocytes subpopulation, has been previously observed in several children suffering from severe recurrent infections with Herpesviridae and was associated with L48R/H polymorphism. Presented studies revealed statistically significant correlation between the B73.1/Leu11c epitope loss and primary immunodeficiencies, while it was not detected in patients with gastrointestinal malignancies or healthy controls. Also, no linkage between the defect and herpesviral infections was observed. Patients with the epitope loss did not suffer from any herpesviral infections, apart from one child with mild herpes simplex virus infection, while none of the children suffering from severe herpesviral infections had the epitope loss detected. Thus, the B73.1/Leu11c epitope loss seems not to be an isolated NK cells deficiency and its analysis is of limited use in predicting severity of clinical course of herpesviral infections. The genetic analysis of FcγRIIIa gene suggests that the epitope loss is not connected with L48R/H polymorphism, as all of analyzed individuals had FcγRIIIa-L/L coding genotype. This indicate that the change of amino acid 48 is rather a naturally occurring polymorphism that a disease-causing mutation.
Kraków
2 - studia doktoranckie
immunologia
Wydział Lekarski
Siedlar, Maciej
2011
oai:dl.cm-uj.krakow.pl:3443
ZB-116994
pol
nieograniczony
Jun 26, 2023
Mar 7, 2013
485
104
http://dl.cm-uj.krakow.pl:8080/publication/3443
RDF
OAI-PMH
Rutkowska-Zapała, Magdalena
Strach, Magdalena
Citation style: chicago-author-date iso690-author-date
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