All animals were housed under specific pathogen–free conditions on a 12-h light/dark cycle. Single-agent lenalidomide induces complete remission of acute myeloid leukemia in patients with isolated trisomy 13. 4, D and F), which might be responsible for the observed increase of CD4+ T cells in the secondary lymphoid organs of GSDMD−/− mice. 4′6-Diamidino-2-phenylindole was added at a concentration of 0.2 μL/mL. This was directly addressed by performing in vitro T cell proliferation and differentiation assays that revealed GSDMD−/− DCs to be greatly impaired in driving EAE MOG-induced T cell activation and differentiation relative to WT DCs (Fig. In contrast, there are examples in which modulation of the microglia response toward Aβ did have a major impact on disease progression (vom Berg et al., 2012; Heneka et al., 2013; Chakrabarty et al., 2015; Guillot-Sestier et al., 2015). RNA was extracted from T-cell fractions using Trizol (Invitrogen). R.L.D., D.C.T., and A.G.R. 3 A). 0000021957 00000 n
6, E and F). 6, C and D). The lysates were centrifuged for 10 min at 14,000 g for removal of cell debris and nuclei. injected with rIL-1β and rIL-18 combination or PBS at day 4, 8, 12, and 16 after EAE induction, respectively (n = 5 mice per group). GAPDH was used as an endogenous control. To directly test the hypothesis that peripheral myeloid cells are better Aβ-combatting cells than resident microglia, we used an experimental mouse model that allows for the exchange of resident microglia by peripherally derived myeloid cells upon conditional depletion of these CNS-resident cells (Varvel et al., 2012). Peripheral Blood Flow-Cytometry Chronic Myeloid Leukemia Stem Cells Detection and Quantification during Tyrosine Kinase Inhibitors Therapy Monica Bocchia, Monica Bocchia * 1 Chair of Hematology, University of Siena, Siena, Italy . CD25 and CD69 expression is significantly higher in CD3+56+ cells compared with CD3+56− cells in healthy controls (■) and AML patients (□) and significantly higher in the CD3+56+ cells of AML patients (□) compared with healthy controls. From this, we conclude that the gene expression changes observed in T cells in AML are different from those seen in CLL. Miller, and F.L. GSDMD deficiency attenuates the expression of genes required for T cell response in CD11b+ cell and CD4+ T cell of peripheral lymphoid organs during EAE. To induce EAE, MOG35-55 peptide (200 μg per mouse) was emulsified with CFA (50 μl per mouse, including 4 mg/ml M. tuberculosis H37Ra) and 50 μl incomplete Freund’s adjuvant. (B) and CD4 T cell transfer by i.c.v. For CD4+ T cell from EAE mice, KEGG pathway analysis showed that the biological terms down-regulated in GSDMD−/− cells majorly include Th1 and Th17 cell differentiation, T cell signaling pathway, cell adhesion molecules, and cytokine–chemokine signaling. Fresh PB or bone marrow (BM) was obtained from 36 AML patients and from 17 age-matched healthy volunteers. Because of this, granulocytes are often referred to as polymorphonuclear leukocytes (PMNs). (E) Representative plot from flow-cytometric analysis of immune cells infiltrated to the CNS (spinal cord and brain) of the mice in D. (F) H&E staining and LFB staining of spinal cord sections harvested from WT mice adoptively transferred with WT or GSDMD−/− bone marrow cells showing inflammatory cell infiltration and demyelination, respectively (arrows).