Presentation is loading. Please wait.

Presentation is loading. Please wait.

Loss of Setdb1 in early B cells leads to impaired B cell development.

Published byΔευκαλίων Τρικούπη Modified over 5 years ago

Similar presentations

Presentation on theme: "Loss of Setdb1 in early B cells leads to impaired B cell development."— Presentation transcript:

1 Loss of Setdb1 in early B cells leads to impaired B cell development.
Loss of Setdb1 in early B cells leads to impaired B cell development. (A) Spleen of control (Mb1-Cre; Setdb1flox/+ or +/+; Setdb1flox/+) and Setdb1Mb1 (Mb1-Cre; Setdb1flox/−) mice. (B) Paraffin sections of control and Setdb1Mb1 spleen stained with Hematoxylin and Eosin. Areas with dark blue staining are follicles with accumulation of lymphocytes. (C) Total cell numbers of bone marrow (BM), spleen (SP) and thymus (TH) in control (con) and Setdb1Mb1 (ko) mice (n=6). (D) Representative FACS plots showing the B cell population (B220+ CD19+) in spleen and bone marrow of control and Setdb1Mb1 mice. (E) The average total numbers of B220+ CD19+ B cells in control and Setdb1Mb1 mice (n=6). (F) Representative FACS plots showing different stages of B cell development in the bone marrow of control and Setdb1Mb1 mice. (G) Average total cell numbers of B cell developmental stages in bone marrow from control and Setdb1Mb1 mice (n=6). (C,E,G) *P<0.05, **P<0.01, ***P<0.001 (unpaired two-tailed Student's t-test); ns, not significant. Alessandra Pasquarella et al. Development 2016;143: © Published by The Company of Biologists Ltd

Download ppt "Loss of Setdb1 in early B cells leads to impaired B cell development."

Similar presentations

by Jad I. Belle, David Langlais, Jessica C

by Jad I. Belle, David Langlais, Jessica C
Ocular defects produced by Daam1 mutation and in combination with diabetes. Ocular defects produced by Daam1 mutation and in combination with diabetes.

Ocular defects produced by Daam1 mutation and in combination with diabetes. Ocular defects produced by Daam1 mutation and in combination with diabetes.
CD1dhiCD5+ B cells are expanded in pancreatic neoplasia and are functionally important for sustaining growth of KrasG12D-PDEC in vivo. CD1dhiCD5+ B cells.

CD1dhiCD5+ B cells are expanded in pancreatic neoplasia and are functionally important for sustaining growth of KrasG12D-PDEC in vivo. CD1dhiCD5+ B cells.
Smaller T cell zone FRC areas in aged spleens.

Smaller T cell zone FRC areas in aged spleens.
Fig. 3. Genetically engineered PD-L1

Fig. 3. Genetically engineered PD-L1
STAT3 regulates IgE class switching in a Th2-type response.

STAT3 regulates IgE class switching in a Th2-type response.
VAY-736 combines effectively with ibrutinib in vivo.

VAY-736 combines effectively with ibrutinib in vivo.
Leukemia involves the accumulation of ISP CD8+T-cells and blockages in B-cell development. Leukemia involves the accumulation of ISP CD8+T-cells and blockages.

Leukemia involves the accumulation of ISP CD8+T-cells and blockages in B-cell development. Leukemia involves the accumulation of ISP CD8+T-cells and blockages.
Osteocytes Regulate Primary Lymphoid Organs and Fat Metabolism

Osteocytes Regulate Primary Lymphoid Organs and Fat Metabolism
STAT3 regulates GC and plasma cell IgE class switching in B cells.

STAT3 regulates GC and plasma cell IgE class switching in B cells.
Depletion of Drosha in the endothelium in mice results in embryonic developmental vascular abnormalities similar to HHT. Depletion of Drosha in the endothelium.

Depletion of Drosha in the endothelium in mice results in embryonic developmental vascular abnormalities similar to HHT. Depletion of Drosha in the endothelium.
Hematological phenotypes of hema6 mice.

Hematological phenotypes of hema6 mice.
Loss of DGKζ and Cbl-b results in a greater percentage of splenic CD8+ T cells with an activated phenotype. Loss of DGKζ and Cbl-b results in a greater.

Loss of DGKζ and Cbl-b results in a greater percentage of splenic CD8+ T cells with an activated phenotype. Loss of DGKζ and Cbl-b results in a greater.
Elysse C. Filipe et al. BTS 2018;3:38-53

Elysse C. Filipe et al. BTS 2018;3:38-53
A rapid, spontaneous, and fully penetrant model of cytogenetically normal AML utilizing Flt3ITD and Dnmt3a haploinsufficiency. A rapid, spontaneous, and.

A rapid, spontaneous, and fully penetrant model of cytogenetically normal AML utilizing Flt3ITD and Dnmt3a haploinsufficiency. A rapid, spontaneous, and.
CXCR5 expression accelerates Eμ-Tcl1 leukemogenesis and is indispensable for tumor cell recruitment to lymphoid B-cell follicles. CXCR5 expression accelerates.

CXCR5 expression accelerates Eμ-Tcl1 leukemogenesis and is indispensable for tumor cell recruitment to lymphoid B-cell follicles. CXCR5 expression accelerates.
Fig. 2 Adoptive transfer of adult Ox40−/− splenocytes into adult HBVEnvRag−/− mice alters hepatic inflammation, HBsAg clearance, HBsAb seroconversion,

Fig. 2 Adoptive transfer of adult Ox40−/− splenocytes into adult HBVEnvRag−/− mice alters hepatic inflammation, HBsAg clearance, HBsAb seroconversion,
Development of human T-cell subsets in NSG hL-7xhIL-15 humanized mice.

Development of human T-cell subsets in NSG hL-7xhIL-15 humanized mice.
(A) Haematoxylin and eosin stained section of multicentric Castleman's disease in a human immunodeficiency virus (HIV) positive patient showing a high.

(A) Haematoxylin and eosin stained section of multicentric Castleman's disease in a human immunodeficiency virus (HIV) positive patient showing a high.
Genetic FIP200 deletion impairs autophagy induction and causes T cell apoptosis. Genetic FIP200 deletion impairs autophagy induction and causes T cell.

Genetic FIP200 deletion impairs autophagy induction and causes T cell apoptosis. Genetic FIP200 deletion impairs autophagy induction and causes T cell.

Similar presentations

Ads by Google