Spinal cystic echinococcosis - a systematic analysis and review of the literature : part 1. Epidemiology and anatomy

Bone involvement in human cystic echinococcosis (CE) is rare, but affects the spine in approximately 50% of cases. Despite significant advances in diagnostic imaging techniques as well as surgical and medical treatment of spinal CE, our basic understanding of the parasite's predilection for the spine remains incomplete. To fill this gap, we systematically reviewed the published literature of the last five decades to summarize and analyze the currently existing data on epidemiological and anatomical aspects of spinal CE

Inhibition of alpha nascent polypeptide associated complex protein may induce proliferation, differentiation and enhance the cytotoxic activity of human CD8+ T cells

The molecular mechanisms that control CD8+ T cell proliferation and differentiations are poorly understood. Consequently, better understanding of the molecular pathways that regulate these processes may have an impact on the numbers and efficiency of antigen-specific cells that can be generated for cellular immunotherapy applications. Using differential display, we previously determined that alpha nascent polypeptide associated complex (α NAC) was identified as a potential target as its protein expression was found to be down-regulated as differentiation progressed in cultured human CD8+ T cells. Here anti-sense technology was used to further investigate the role which α NAC may play in proliferation and differentiation. Human purified CD8+ T cells were cultured in the presence of sense, non-sense and anti-sense oligonucleotides against the mRNA of α NAC. We reported that in the presence of anti-sense oligonucleotides expanded CD8+ T cells exhibited higher levels of differentiation and activation markers and also increased proliferation response compared to cells cultured with sense-oligonucleotides. Furthermore, the functional cytotoxicity of CD8+ T cells cultured with anti-sense was increased to 66% (±4.7%) compared to 42% (±3.2%) in cells expanded in the presence of oligonucleotides controls. Taken together, our results demonstrated that inhibition of α NAC protein induced not only cell proliferation but also differentiation and cytotoxic activity of CD8+ T cells

Immunocompetent cell functions in Ph+ acute lymphoblastic leukemia patients on prolonged Imatinib maintenance treatment

Imatinib mesylate (Imatinib) is a potent inhibitor of defined tyrosine kinases and is effectively used for the treatment of malignancies characterized by the constitutive activation of these tyrosine kinases, such as Philadelphia chromosome-positive (Ph+) leukemias and gastrointestinal stromal tumors. Suppressive as well as stimulating effects of this drug on T lymphocytes or dendritic cells (DC), which play a major role in immune tumor surveillance, have been reported. For this reason, we questioned whether Imatinib could also affect the phenotypic and functional properties of these subpopulations in Ph+ acute lymphoblastic leukemia (ALL) patients on prolonged Imatinib maintenance treatment. Circulating T lymphocytes and NK cells from Imatinib-treated Ph+ ALL patients showed a subset distribution comparable to that of healthy donors. In addition, T-cell immunomodulant cytokine production (IFN-gamma, TNF-alpha) and proliferative responses were not impaired. A normal monocyte-derived DC differentiation and apoptotic body loading capacity was also observed in the majority of Imatinib-treated patients. In contrast, an impairment in the DC intracellular production of IL-12 was recorded, although this was not observed when normal DC were exposed in vitro to Imatinib. Finally, in vivo Imatinib treatment did not affect the T-lymphocyte proliferation and IFN-gamma production induced by leukemic apoptotic body-loaded DC, underling the potential capability of these cells to generate a specific immune response against tumoral antigens. Taken together, these findings provide evidence that immunotherapeutic approaches aimed at controlling residual disease in Ph+ ALL patients in hematologic remission are not jeopardized by the long-term administration of Imatinib