B-cell development in young Pax5+/− mice.

Slides:



Advertisements
Similar presentations
C1q g/L C2 g/L C3 g/L C4 g/L A. B. C.D. E. Supplementary Figure 1 - Middleton et al. NR Supplementary Figure 1. Complement concentrations in CLL patient.
Advertisements

Figure 5. FK866 caused apoptosis in MCF-7 cells while nicotinamide adenine dinucleotide (NAD+) reversed FK866-induced apoptosis. (A) Representative quadrant.
Cantharidin Inhibits the Growth of Triple-Negative Breast Cancer Cells by Suppressing Autophagy and Inducing Apoptosis in Vitro and in.
Human Immunodeficiency Virus Type 1 Protease Inhibitor Modulates Activation of Peripheral Blood CD4+ T Cells and Decreases Their Susceptibility to Apoptosis.
by Norman Nausch, Ioanna E
Sunitinib plus rMVA–CEA–TRICOM vaccine decreased tumor burden and increased intratumoral infiltration of T lymphocytes in the MC38-CEA colon carcinoma.
TLR5 signaling in murine bone marrow induces hematopoietic progenitor cell proliferation and aids survival from radiation by Benyue Zhang, Damilola Oyewole-Said,
Effects of AG-221 treatment on survival and cell differentiation in an IDH2R140Q primary human AML xenograft model. Effects of AG-221 treatment on survival.
CD1dhiCD5+ B cells are expanded in pancreatic neoplasia and are functionally important for sustaining growth of KrasG12D-PDEC in vivo. CD1dhiCD5+ B cells.
MP cells are generated from naïve cells in the periphery.
CD7-restricted activation of Fas-mediated apoptosis: a novel therapeutic approach for acute T-cell leukemia by Edwin Bremer, Bram ten Cate, Douwe F. Samplonius,
by Kamira Maharaj, John J
COX-2–PGE2 signaling is required for MSC-induced increase in ALDHhigh CSC-enriched population and tumor initiation. COX-2–PGE2 signaling is required for.
SHIP is required for a functional hematopoietic stem cell niche
Volume 22, Issue 2, Pages (February 2005)
Volume 7, Issue 1, Pages (July 1997)
Effect of expression of constitutively active CAMKK2 on AMPK activation and the cell cycle in G361 cells. Effect of expression of constitutively active.
TDP1 knockdown increases the sensitivity of rhabdomyosarcoma cell lines to CPT treatment. TDP1 knockdown increases the sensitivity of rhabdomyosarcoma.
Genetic FIP200 deletion impairs autophagy induction and causes T cell apoptosis. Genetic FIP200 deletion impairs autophagy induction and causes T cell.
cMΦ develop into 4 subpopulations after birth.
Decreased expression of cell cycle– and apoptosis-related genes in Aml1-excised leukemia cell. Decreased expression of cell cycle– and apoptosis-related.
Volume 50, Issue 2, Pages e4 (February 2019)
MP cells are generated from naïve cells in the periphery.
Fig. 3. Effects of Tec on IL-1β-induced apoptosis in chondrocytes.
B cell development in wild-type and Syk-AQL mice.
NOX1-deficient mice do not respond to GKT771 and exhibit reduced B16-F10 tumor growth associated with decreased production of angiogenic factors and minor.
SW fraction induces S phase arrest and apoptosis.
MK-8628 augments T lymphocyte apoptosis.
CYP1A1 knockdown increases cell death.
Increased pancreatic insulin content and islet size and protection against HFD- and palmitate-induced cell death in PKCδKN-overexpressing mice. Increased.
Spontaneous and strong Tfh cell but not Tfr cell development in IL-2 KO mice. Spontaneous and strong Tfh cell but not Tfr cell development in IL-2 KO mice.
Loss of Tfh and GC B cells in 2KO-Bcl6TC mice.
Overexpression of IL-27 upregulates expression of multiple IR by T cells in vivo. Overexpression of IL-27 upregulates expression of multiple IR by T cells.
DHA induces apoptosis independently from caspase-8 and FADD in Jurkat T-lymphoma cells. DHA induces apoptosis independently from caspase-8 and FADD in.
Reduced tumor growth in CCR5-deficient mice is associated with perturbed killing ability of Treg cells. Reduced tumor growth in CCR5-deficient mice is.
Vaginal CD11c+ DCs from IL-17A−/− mice are impaired in potentiating Th17 responses because of diminished IL-1β production. Vaginal CD11c+ DCs from IL-17A−/−
Effects of knockdown of ANRIL on NSCLC cell cycle and apoptosis in vitro. Effects of knockdown of ANRIL on NSCLC cell cycle and apoptosis in vitro. A,
CD11bhighCD27high conventional NK cells are converted into MDSCs
A, chemical structures of PRIMA-1 and PRIMA-1Met.
TSA-mediated changes in cell cycle inhibitor proteins.
Β-Cryptoxanthin at a concentration of 10 μmol/L decreases proliferation in HCT116 cells after 6 and 8 days of treatment. β-Cryptoxanthin at a concentration.
Mitotic catastrophe symptoms caused by curcumin are followed by apoptosis. Mitotic catastrophe symptoms caused by curcumin are followed by apoptosis. A.
Lamellarin D induces cell death through a Fas-independent pathway.
N-3 PUFAs promote endometrial cancer cell apoptosis in vitro and in vivo. n-3 PUFAs promote endometrial cancer cell apoptosis in vitro and in vivo. HEC-1-A.
In vivo AraC treatment does not induce any consistent changes in CD34+/−CD38+/− phenotypes nor in quiescent leukemic cells but increases apoptotic cell.
Tipifarnib combined with bortezomib induces cell death in diverse multiple myeloma and AML cell lines. Tipifarnib combined with bortezomib induces cell.
Bone marrow stroma partially protects multiple myeloma and AML cell lines from tipifarnib- and bortezomib-induced cell death. 8226/S myeloma cells were.
M-CSFR inhibition decreases tumor-associated macrophages in mesothelioma and improves the DC therapy induced CD8+ T-cell phenotype. M-CSFR inhibition decreases.
A, P causes G2-M arrest with apoptosis in asynchronous population of PC-3 when exposed to 1.5 and 5 μmol/L P for various time points. A, P
SY-1425 induces maturation in RARA-high AML
Apoptotic cell index percentage (a and b) and mitotic cell index percentage (c and d) in small intestinal (a and c) and midcolonic (b and d) crypts of.
Induction of apoptosis by statins in NB4 cells and NB4 variant cell lines. Induction of apoptosis by statins in NB4 cells and NB4 variant cell lines. A,
Combination of R848 and anti-CD200R affects activation of tumor-infiltrating myeloid cells. Combination of R848 and anti-CD200R affects activation of tumor-infiltrating.
Treatment with a Ron inhibitor significantly reduces metastatic outgrowth. Treatment with a Ron inhibitor significantly reduces metastatic outgrowth. A,
W. chinensis extract induces apoptosis in AR-dependent prostate cancer cells. W. chinensis extract induces apoptosis in AR-dependent prostate cancer cells.
Sorafenib inhibits cell proliferation and induces apoptosis in HCC cells. Sorafenib inhibits cell proliferation and induces apoptosis in HCC cells. A,
CREBBP regulates antigen processing and presentation gene enhancers.
IL35 regulation of tumor growth is accompanied by suppression of CD4+ effector T-cell activity and expansion of Tregs. IL35 regulation of tumor growth.
Cabozantinib causes significant tumor cell elimination in vivo, but modest apoptosis induction in vitro. Cabozantinib causes significant tumor cell elimination.
KRAS-addicted lung cancer cells need αvβ3/galectin-3 to maintain low ROS levels. KRAS-addicted lung cancer cells need αvβ3/galectin-3 to maintain low ROS.
THZ1 in combination with targeted therapy enhances cell death and hinders the establishment of drug-resistant colonies in diverse oncogene-addicted cellular.
Quercetin induces autophagy, blocks cell cycle and activation of ERK and JNK signaling pathways participates in the G1 arrest in P39 cells. Quercetin induces.
In vivo efficacy of JAK inhibition in transformed Pax5+/− pro-B cells harboring Jak3V670A. In vivo efficacy of JAK inhibition in transformed Pax5+/− pro-B.
Curcumin decreases viability and proliferation of Bcr-Abl-expressing cells. Curcumin decreases viability and proliferation of Bcr-Abl-expressing cells.
ARQ 531 is cytotoxic to CLL cells, decreases NF-κB function, and inhibits migration. ARQ 531 is cytotoxic to CLL cells, decreases NF-κB function, and inhibits.
E2 induces IL-17–producing γδ+ T cells in the FGT
WEE1 inhibition followed by TRAIL treatment results in apoptotic cell death in MB231 cells. WEE1 inhibition followed by TRAIL treatment results in apoptotic.
Effect of 6-SHO on mouse prostate cancer HMVP2 cells.
DQs have superior anticancer efficacy among dimeric antimalarials.
Inhibition of stromal cell–induced survival of primary B-CLL cells by cyclopamine in vitro. Inhibition of stromal cell–induced survival of primary B-CLL.
Presentation transcript:

B-cell development in young Pax5+/− mice. B-cell development in young Pax5+/− mice. A, percentage of PB B cells (B220+IgM+/−) at different time points in Pax5+/− mice (n = 12) compared with WT mice (n = 22) analyzed by flow cytometry. A significant decrease in PB B cells can be observed in Pax5+/− mice at 3, 6, and 9 months of age. Error bars represent the SD. t test P value is indicated in each case. Four-month-old Pax5+/− mice (n = 8) show increased numbers of pre-B/pro-B cells (B220lowIgM−) and immature B cells (B220lowIgM+) compared with age-matched WT mice (n = 4) but not recirculating B cells (B220++IgM+). Unpaired t test P value is indicated in each case. B, decrease in PB B cells in Pax5+/− mice housed in SPF conditions. Percentage of PB B cells in Pax5+/− mice (n = 10) compared with WT mice (n = 10) analyzed by flow cytometry as B220+IgM+/− cells at 3 and 6 months of age. Error bars represent the mean ± SD. Unpaired t test P value is indicated in each case. A significant decrease in PB B cells can be observed in Pax5+/− mice housed in SPF conditions. C, cell death susceptibility mediated by IL7 removal in Pax5+/− pro-B cells. Sorted B220+ cells from BM of young Pax5+/− and WT mice were cultured under conditions to allow the isolation and expansion of a pure population of pro-B cells. Pro-B cells were cultured with or without IL7 for 24 hours. Induction of apoptosis was assessed by flow cytometry using Annexin V/PI staining. Data represent the mean ± SD of normalized apoptotic cells from six independent experiments. Unpaired t test P value is indicated in each case. D, cell death mediated by JAK inhibitors in WT and Pax5+/− pro-B cells. IL7-dependent pro-B cells were cultured with tofacitinib (JAK1/3 inhibitor; 1 μmol/L), TG101348 (JAK2 inhibitor; 1 μmol/L), and ruxolitinib (JAK1/2 inhibitor; 1 μmol/L) for 24 hours. Induction of apoptosis was assessed by flow cytometry using Annexin V/PI staining. Graphs indicate the fold change of dead cells treated with the inhibitor in each experiment compared with cells treated with the vehicle. Data represent the mean ± SD from three independent experiments. Unpaired t test P value is indicated in each case. Alberto Martín-Lorenzo et al. Cancer Discov 2015;5:1328-1343 ©2015 by American Association for Cancer Research