Báo cáo hóa học: Quantification of newly produced B and T lymphocytes in untreated chronic lymphocytic leukemia patients

Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành hóa học dành cho các bạn yêu hóa học tham khảo đề tài: Quantification of newly produced B and T lymphocytes in untreated chronic lymphocytic leukemia patients
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Báo cáo hóa học: "Quantification of newly produced B and T lymphocytes in untreated chronic lymphocytic leukemia patients"Motta et al. Journal of Translational Medicine 2010, 8:111http://www.translational-medicine.com/content/8/1/111 RESEARCH Open AccessQuantification of newly produced B andT lymphocytes in untreated chroniclymphocytic leukemia patientsMarina Motta1, Marco Chiarini2, Claudia Ghidini2, Cinzia Zanotti2, Cinzia Lamorgese1, Luigi Caimi2, Giuseppe Rossi1,Luisa Imberti2* Abstract Background: The immune defects occurring in chronic lymphocytic leukemia are responsible for the frequent occurrence of infections and autoimmune phenomena, and may be involved in the initiation and maintenance of the malignant clone. Here, we evaluated the quantitative defects of newly produced B and T lymphocytes. Methods: The output of B and T lymphocytes from the production and maturation sites was analyzed in chronic lymphocytic leukemia patients and healthy controls by quantifying kappa-deleting recombination excision circles (KRECs) and T-cell receptor excision circles (TRECs) by a Real-Time PCR assay that simultaneously detects both targets. T-lymphocyte subsets were analyzed by six-color flow cytometric analysis. Data comparison was performed by two-sided Mann-Whitney test. Results: KRECs level was reduced in untreated chronic lymphocytic leukemia patients studied at the very early stage of the disease, whereas the release of TRECs+ cells was preserved. Furthermore, the observed increase of CD4+ lymphocytes could be ascribed to the accumulation of CD4+ cells with effector memory phenotype. Conclusions: The decreased number of newly produced B lymphocytes in these patients is likely related to a homeostatic mechanism by which the immune system balances the abnormal B-cell expansion. This feature may precede the profound defect of humoral immunity characterizing the later stages of the disease.Background macrophage lineage [2,3]. All these immunologicalProfound defects of both humoral and cell-mediated changes are linked to an increased frequency and sever-immunity have been described in patients with chronic ity of infections [3]. Since CLL represents a heteroge-lymphocytic leukemia (CLL), a disease characterized by neous disease with a very variable outcome, a reliablethe accumulation of mature, malignant, monoclonal B prognosis at the time of initial diagnosis is difficult tolymphocytes in blood, lymph nodes, spleen, liver, and predict; similarly, only few early markers anticipatingbone marrow [1]. The disease is characterized by the the immune defects arising in the later stages of the dis-presence of immune defects, responsible for the fre- ease have been up to now identified. In this context, aquent occurrence of infections and autoimmune phe- small size of the blood T/NK-cell compartment com-nomena, that may be involved in the initiation and pared to that of circulating leukemic clone at the timemaintenance of the malignant clone. The immune of diagnosis was associated with more advanced stages,abnormalities include re duced immunoglobulin (Ig) raising the possibility that CLL patients with efficientlevels, as well as qualitative and quantitative defects of host immunity may experience a more indolent diseaseB, T, NK cells, neutrophils, and the monocyte/ due to a more effective immune response against the disease [2]. However, the maintenance of an immune surveillance needs a continuous source of newly pro-* Correspondence: limberti@yahoo.it duced B and T lymphocytes. While it has been found2 Laboratory of Biotechnology, Diagnostic Department, Spedali Civili, Piazzale that the proliferation of malignant B cells decreases theSpedali Civili 1, 25123, Brescia, ItalyFull list of author information is available at the end of the article © 2010 Motta et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the ...