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Quantification of specific T and B cells immunological markers in children with chronic and transient ITP
Author(s) -
LevyMendelovich Sarina,
Lev Atar,
Aviner Shraga,
Rosenberg Nurit,
Kaplinsky Caim,
Sharon Nechama,
Miskin Hagit,
Dvir Aviya,
Kenet Gili,
Schushan Irit Eisen,
Somech Raz
Publication year - 2017
Publication title -
pediatric blood and cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.116
H-Index - 105
eISSN - 1545-5017
pISSN - 1545-5009
DOI - 10.1002/pbc.26646
Subject(s) - medicine , transient (computer programming) , immunology , computer science , operating system
Background Immune thrombocytopenic purpura (ITP) is characterized by a transient (nonchronic) or permanent (chronic) decline in the number of platelets. Predicting the course of ITP, at the time of diagnosis, is of importance. Here we studied at diagnosis, clinical and immunological parameters in order to distinguish between different courses. The latter included the measure of new B and T cells using quantification of kappa‐deleting recombination excision circles (KRECs) and T‐cell receptor excision circles (TRECs), respectively. Methods Blood samples were collected from 44 children with a clinical diagnosis of ITP. Real‐time PCR was performed in order to quantify the number of copies of TREC and KREC followed by collection of clinical data from medical files. The children were retrospectively divided into two groups: chronic and nonchronic. Results Twenty‐four patients (54%) were classified as nonchronic ITP and 20 patients (46%) were classified as chronic ITP. We confirmed some clinical parameters (e.g., gender, age) but not others (e.g., preceding infection, level of thrombocytopenia) that distinguish patients with chronic and nonchronic course. While KREC quantification was similar in patients regardless the outcome of their disease, it was significantly higher than the level of controls ( P < 0.05). TREC quantification was not different between patients and controls. Conclusions KREC but not TREC levels are different in patients comparing to controls, pointing to an overreaction of B‐cell development as a role in the pathogenesis of ITP. These results may shed more lights on the immune mechanism of ITP.