Journal of Clinical and Cellular Immunology
Open Access
ISSN: 2155-9899
ISSN: 2155-9899
Sergio Rivera1, EcheverrÃ?Âa Miriam1, Pedro Salcedo1, Georgina Marquez2, Zuhey Carrillo2, Yennis Parra2, Atilio Farruco1, Ana MarÃ?Âa Cipriani1 and Alvarez Demon M3
1University of Zulia, Venezuela 2Blood Bank of Zulia State, Venezuela 3University of Alcal�¡ de Henares, Spain
Posters-Accepted Abstracts: J Clin Cell Immunol
Chronic myeloid leukemia (CML) in humans is a clonal myeloproliferation caused by a neoplastic transformation of a pluripotential stem cell, characterized by a striking overproduction of granulocytes. Its diagnosis is established by identifying the clonal expansion of hematopoietic stem cell which has a reciprocal translocation between chromosome 9 and 22. The association of leukemia and the major histocompatibility complex (MHC) originates from studies on the Gross virus, inducing murine leukemia, in which it was observed that mice carrying the H-2k haplotype more rapidly succumbed to leukemia than those mice which had the H-2d haplotype. This study confirms the HLA-DRB1*14 positive and DRB1*13 negative association with CML in Venezuelan�s mestizos. The DRB1*14:21 subtype was the most frequent in CML patients, absent in DRB1*14 controls. DRB1*14 patients reacted in 48 hours mixed culture versus DRB1*14 responders mitomycin inactivated, exhibiting increased CD8+ lymphocytes and CD4/CD8 ratio decreased evaluated by cytofluorometry. CML patients were mostly serologically negative to adenovirus unlike controls and patients with Acute Lymphoid Leukemia (ALL), which were mostly IgM positive. CML patients and not controls reacted to the adenovirus peptide sequence LLERRRA, increasing CD4+ and CD8+ T cells. These results let the association link LMC/HLA-DRB1*14 with the generation of autoreactive CD8+ T cell memory, probably specific from peptide sequence of adenovirus in leukemias.
Email: sergio.rivera54@hotmail.es