Surface expression of CD69 in chronic lymphocytic leukemia patients

Abstract

-cell chronic lymphocytic leukemia is a lymphoproliferative disorder caused by the clonal expansion of B cells with a distinctive morphological appearance and surface immunophenotype. One of the most striking features of CLL is the extent of its clinical variability as some patients have an aggressive disease requiring early therapy, whereas other patients exhibit a more indolent disease with no benefit from palliative chemotherapy. Several reliable prognostic markers were found to be capable of predicting the progression and outcome of the disease from its early stages including age, sex, lymphocyte morphology and number, lymphocyte doubling time (LDT), serum factors, and, recently immunophenotyping and cytogenetic findings. Recent risk parameters were defined as prognostic markers that appear to be clearly related to the biology of B- CLL including defects detectable on fluorescence in situ hybridization, immunoglobulin heavy-chain variable region (Ig VH) mutational status, surface marker CD38, and intracytoplasmic ZAP-70 levels. The development of more effective treatment strategies requires both a better understanding of the biological factors involved in CLL progression, and the identification of new prognostic factors. CD69 identifies a type II integral membrane protein with a single transmembrane domain belonging to the C-type lectin family of surface receptors and is expressed very quickly (within 4 h) in several hemopoietic cells upon triggering. Indeed, CD69 has been described as a receptor capable of eliciting a broad range of cellular activation responses. However, the nature of the physiologic ligand/s for CD69 remains a mystery. Some authors have recently postulated the involvement of CD69 in the pathogenesis of inflammatory diseases. Such experimental approaches may eventually provide key informations concerning those ligands as well as the