(B) Both cska and non-cska-TCRs are degraded in the lysosome following activation. Splenocytes, were non-activated or activated as in (A), in the absence or presence of the lysosomal inhibitor NH 4 Cl, lysed and processed as in (A) for detection of ζ and ZAP-70. (C) Accumulation of cska ζ in activated T-cells following treatment

with NH 4 Cl. Average values and standard deviation were determined from six independent experiments, using ζ expression level of non-activated, NH 4 Cl untreated samples as 100%. Figure S8. FACS gateing strategy. Vemurafenib order In all the FACS results presented in the paper, the first gate distinguished between live and dead/debreas cells (A). The cells were stained using anti-Thy 1.2 antibodies, which enabeled us to focuse on the T cells by gating on the positive population or on the APCs (LK cells in the mixed experiment) by focusing on the negetive population (B). The result was obtained by integreating gate 1 and gate 2 as in the presented sample presented (C). “
“Chronic myelogenous leukemia (CML) is a malignant myeloproliferative disease of hematopoietic stem cells. The disease progresses after several years from an initial chronic phase to a blast phase. Leukemia-specific T cells are regularly detected in CML patients and may be involved in the immunological control of the

disease. Here, we analyzed the role click here of leukemia-specific CD8+ T cells in CML disease control and the mechanism that maintains CD8+ T-cell immunosurveillance in a retroviral-induced murine

CML model. To study antigen-specific immune responses, the glycoprotein of the lymphocytic choriomeningitis virus was used as model leukemia antigen. Leukemia-specific CTL activity was detectable in vivo in CML mice and depletion of CD8+ T cells rapidly led to disease progression. CML-specific CTL were characterized by the expression of the IL-7 receptor PAK5 α-chain. In addition, leukemia cells produced IL-7 that was crucial for the maintenance of leukemia-specific CTL and for disease control. Therefore, CML cells maintain the specific CD8+ T-cell-mediated immune control by IL-7 secretion. This results in prolonged control of disease and probably contributes to the characteristic chronic phase of the disease. Chronic myelogenous leukemia (CML) is a malignant clonal disease originating from a pluripotent hematopoietic stem cell expressing the reciprocal translocation t(9;22), which forms the oncogenic BCR/ABL fusion protein. BCR/ABL is a constitutively activated tyrosine kinase which plays a critical role in the pathogenesis of CML. After several years and acquisition of a second genetic abnormality, the disease progresses from the chronic phase to terminal blast phase in which the patients develop an acute leukemia of either myeloid (AML) or, less frequent, lymphoid (ALL) cell type 1–3. For unknown reasons, CML seems to be the most immunogenic leukemia.