These include a reduction in
B cell differentiation to plasma cells and a reduced proliferation of T cells.
«Mechanism for inducing memory
B cell differentiation elucidated: Efficient induction of immune cells that remember antigens will lead to the development of new vaccines.»
Not exact matches
Their results demonstrated shared mechanisms by which miR -17-92 mediates cGVHD progression — namely by regulating T helper -
cell differentiation,
B -
cell activation, germinal center responses, and autoantibody production.
Based on this work, they decided to investigate whether miR -17-92 regulates T - and
B -
cell differentiation and function in the development of cGVHD.
A group of researchers at Immunology Frontier Research Center (IFReC), Osaka University and RIKEN Center for Integrative Medical Sciences jointly clarified the mechanism for inducing germinal - center
B cells»
differentiation into memory
B cells, immune
cells that remember antigens, at the molecular level.
For the proliferation and
differentiation to occur,
B cells must cycle between the two zones.
Using mice deficient in Del - 1, they found that the protein promotes proliferation and
differentiation of hematopoetic stem
cells, sending more of these progenitor
cells down a path toward becoming myeloid
cells, such as macrophages and neutrophils, rather than lymphocytes, such as T
cells and
B cells.
Dendritic
cells directly modulate
B cell growth and
differentiation.
Differential regulation of the a (2)
b (1) and a (IIb)
b (3) integrin genes during megakaryocytic
differentiation of pluripotent K562 leukemia
cells.
Analogous to bacterial infection, CpG -
B triggers the
differentiation of both plasmacytoid and conventional DCs, as well as the proliferation and activation of
B cells.
We notably follow the time course of structural changes in response to cues that affect gene expression either transiently or permanently: changes in genome structure during transient hormonal response of differentiated
cells and stable trans -
differentiation of
B cells to macrophages.
Nuclear Factor Kappa
B Signaling Initiates Early
Differentiation of Neural Stem
Cells.
Anaplastic, plasmablastic, and plasmacytic plasmacytomas of mice: relationships to human plasma
cell neoplasms and late - stage
differentiation of normal
B cells.
CD20 is a
B - lymphocyte surface molecule that is widely expressed during
B -
cell ontogeny, from early pre-
B-
cell developmental stages until final
differentiation into plasma
cells.
Ari Melnick, M.D. Weill Medical College of Cornell University
Differentiation therapy for
B -
cell lymphomas
Deletion of genes encoding PU.1 and Spi -
B in
B cells impairs
differentiation and induces pre-
B cell acute lymphoblastic leukemia
This is in accordance with previous reports that decitabine and 5 - azacytidine produce a marked synergistic effect in combination with suberoylanilide hydroxamic acid and romidepsin in T - lymphoma
cell lines by modulating
cell cycle arrest and apoptosis.26, 27 As a mechanism of action, KMT2D mutations of
B - lymphoma
cells promote malignant outgrowth by perturbing methylation of H3K4 that affect the JAK - STAT, Toll - like receptor, or
B -
cell receptor pathway.28, 29 Here our study indicated that dual treatment with chidamide and decitabine enhanced the interaction of KMT2D with the transcription factor PU.1, thereby inactivating the H3K4me - associated signaling pathway MAPK, which is constitutively activated in T -
cell lymphoma.13, 30,31 The transcription factor PU.1 is involved in the development of all hematopoietic lineages32 and regulates lymphoid
cell growth and transformation.33 Aberrant PU.1 expression promotes acute myeloid leukemia and is related to the pathogenesis of multiple myeloma via the MAPK pathway.34, 35 On the other hand, PU.1 is also shown to interact with chromatin remodeler and DNA methyltransferease to control hematopoiesis and suppress leukemia.36 Our data thus suggested that the combined action of chidamide and decitabine may interfere with the
differentiation and / or viability of PTCL - NOS through a PU.1 - dependent gene expression program.
Carayon et al. «Modulation and Functional Involvement of CB2 Peripheral Cannabinoid Receptors During
B -
Cell Differentiation», Blood, 92 (10): 3605 - 3615, 1998.
Repression of the transcription factor Bach2 contributes to predisposition of IgG1 memory
B cells toward plasma
cell differentiation.
Upon transfer of aged donor CD4 T
cells to young hosts, there was significantly reduced expansion and germinal center (GC)
differentiation of the antigen - specific
B cell population after immunization.
Her current research focuses on the
differentiation of the early
B cells.
Furthermore, we found that there was no difference in
B cell expansion and
differentiation or in IgG production when young CD4 T
cells were transferred to young or aged hosts.
<b> Results b>: The application of specific optimised conditions induce multiple rounds of memory
B cell proliferation equally across Ig isotypes,
differentiation of memory
B cells to antibody secreting
cells, and importantly do not alter the Ig genotype of the stimulated
cells.
DIC images of endothelial progenitor
cells (EPCs) during in vitro expansion (A) and
differentiation (
B).
These include: a) Global Clusters that consist of a small, tight subset of genes that are co-expressed under the entire spectrum of experimental conditions;
b) Time Series of gene expression profiles during successive days of standard ES
cell differentiation; c) Specific Gene Classes based on hierarchical clustering of transcriptional factors and ESTs; d) Expression Waves of genes with characteristic expression profiles during ES
cell differentiation, juxtaposed to waves of genes that behave in the exact opposite way; e) Pathway Animations that illustrate dynamic changes in the components of individual KEGG signaling and metabolic pathways viewed in time - related manner; and, f) Search Engines to display the expression pattern of any transcript, or groups of transcripts, during the course of ES
cell differentiation, or to query the association of candidate genes with various FunGenES database clusters.
We subsequently used a novel Design of Experiments approach to finely tune the optimal memory
B cell expansion and
differentiation conditions for human memory
B cell subsets.
(A) shows
cell morphology when passage 1 EPCs were differentiated while (
B, C) show
cell morphology of
cells at high passage number (10th and 20th passage), at 8 days after induction of
differentiation, respectively.
Power frequency fields promote
cell differentiation coincident with an increase in transforming growth factor -
b 1 expression.
A chemical called
B - catenin is required for
differentiation of skin
cells into hair follicles.