Faculty Opinions recommendation of Myeloid lineage switch of Pax5 mutant but not wild-type B cell progenitors by C/EBPalpha and GATA factors.

2003 ◽  
Author(s):  
Ranjan Sen
Keyword(s):  
B Cell ◽  
Type B ◽  
Wild Type ◽  
Myeloid Lineage ◽  
Gata Factors ◽  
Lineage Switch

scholarly journals Diacylglycerol kinase ζ promotes actin cytoskeleton remodeling and mechanical forces at the B cell immune synapse

2020 ◽  
Vol 13 (627) ◽  
pp. eaaw8214 ◽  
Author(s):  
Sara V. Merino-Cortés ◽  
Sofia R. Gardeta ◽  
Sara Roman-Garcia ◽  
Ana Martínez-Riaño ◽  
Judith Pineau ◽  
...  
Keyword(s):  
B Cells ◽  
B Cell ◽  
Force Generation ◽  
Lymphocyte Function ◽  
Dependent Manner ◽  
Type B ◽  
Wild Type ◽  
Microtubule Organizing Center ◽  
Antigen Uptake ◽  
Immune Synapse

Diacylglycerol kinases (DGKs) limit antigen receptor signaling in immune cells by consuming the second messenger diacylglycerol (DAG) to generate phosphatidic acid (PA). Here, we showed that DGKζ promotes lymphocyte function–associated antigen 1 (LFA-1)–mediated adhesion and F-actin generation at the immune synapse of B cells with antigen-presenting cells (APCs), mostly in a PA-dependent manner. Measurement of single-cell mechanical force generation indicated that DGKζ-deficient B cells exerted lower forces at the immune synapse than did wild-type B cells. Nonmuscle myosin activation and translocation of the microtubule-organizing center (MTOC) to the immune synapse were also impaired in DGKζ-deficient B cells. These functional defects correlated with the decreased ability of B cells to present antigen and activate T cells in vitro. The in vivo germinal center response of DGKζ-deficient B cells was also reduced compared with that of wild-type B cells, indicating that loss of DGKζ in B cells impaired T cell help. Together, our data suggest that DGKζ shapes B cell responses by regulating actin remodeling, force generation, and antigen uptake–related events at the immune synapse. Hence, an appropriate balance in the amounts of DAG and PA is required for optimal B cell function.

scholarly journals Murine B cell proliferation and protection from apoptosis with an antibody against a 105-kD molecule: unresponsiveness of X-linked immunodeficient B cells.

1994 ◽  
Vol 180 (4) ◽  
pp. 1217-1224 ◽  
Author(s):  
K Miyake ◽  
Y Yamashita ◽  
Y Hitoshi ◽  
K Takatsu ◽  
M Kimoto
Keyword(s):  
Monoclonal Antibody ◽  
Cell Proliferation ◽  
B Cells ◽  
B Cell ◽  
Molecular Mass ◽  
Signaling Pathway ◽  
Type B ◽  
Wild Type ◽  
Stimulation Of

We established a novel monoclonal antibody, RP/14, that can protect B cells from apoptosis induced by irradiation or dexamethasone. A molecule recognized by RP/14 (the RP antigen) was expressed on B cells with B220bright, IgMdull, and IgDbright. Immunoprecipitation experiments revealed that RP/14 recognized a monomeric protein with an approximate molecular mass of 105 kD. Stimulation of B cells with RP/14 for 48 h induced B cell proliferation and blastogenesis. In contrast to B cells of wild-type mice, X-linked immunodeficient (XID) B cells did not proliferate upon stimulation with RP/14, although the RP antigen was expressed to the same extent as that of wild-type B cells. These results suggest that the RP antigen-mediated signaling pathway is important for rescuing B cells from apoptosis and is deficient in XID B cells.

scholarly journals Treatment of experimental stroke with IL-10-producing B-cells reduces infarct size and peripheral and CNS inflammation in wild-type B-cell-sufficient mice

2013 ◽  
Vol 29 (1) ◽  
pp. 59-73 ◽  
Author(s):  
Sheetal Bodhankar ◽  
Yingxin Chen ◽  
Arthur A. Vandenbark ◽  
Stephanie J. Murphy ◽  
Halina Offner
Keyword(s):  
B Cells ◽  
Infarct Size ◽  
B Cell ◽  
Experimental Stroke ◽  
Type B ◽  
Wild Type ◽  
Cns Inflammation

scholarly journals Phosphoinositide 3-Kinase P110δ-Signaling Is Critical for Microbiota-Activated IL-10 Production by B Cells that Regulate Intestinal Inflammation

Cells ◽  
2019 ◽  
Vol 8 (10) ◽  
pp. 1121 ◽  
Author(s):  
Akihiko Oka ◽  
Yoshiyuki Mishima ◽  
Bo Liu ◽  
Jeremy W. Herzog ◽  
Erin C. Steinbach ◽  
...  
Keyword(s):  
B Cells ◽  
B Cell ◽  
Intestinal Inflammation ◽  
Mucosal Inflammation ◽  
Regulatory Function ◽  
Type B ◽  
Wild Type ◽  
Phosphoinositide 3 Kinase

The phosphoinositide 3-kinase catalytic subunit p110δ (PI3Kδ) gene maps to a human inflammatory bowel diseases (IBD) susceptibility locus, and genetic deletion of PI3Kδ signaling causes spontaneous colitis in mice. However, little is known regarding the role of PI3Kδ on IL-10-producing B cells that help regulate mucosal inflammation in IBD. We investigated the role of PI3Kδ signaling in B cell production of IL-10, following stimulation by resident bacteria and B cell regulatory function against colitis. In vitro, B cells from PI3KδD910A/D910A mice or wild-type B cells treated with PI3K specific inhibitors secreted significantly less IL-10 with greater IL-12p40 following bacterial stimulation. These B cells failed to suppress inflammatory cytokines by co-cultured microbiota-activated macrophages or CD4+ T cells. In vivo, co-transferred wild-type B cells ameliorated T cell-mediated colitis, while PI3KδD910A/D910A B cells did not confer protection from mucosal inflammation. These results indicate that PI3Kδ-signaling mediates regulatory B cell immune differentiation when stimulated with resident microbiota or their components, and is critical for induction and regulatory function of IL-10-producing B cells in intestinal homeostasis and inflammation.

Intracranial dural based marginal zone MALT-type B-cell lymphoma: a case – Based update and literature review

2021 ◽  
pp. 1-7
Author(s):  
G. La Rocca ◽  
A. M. Auricchio ◽  
E. Mazzucchi ◽  
T. Ius ◽  
G. M. Della Pepa ◽  
...  
Keyword(s):  
Literature Review ◽  
B Cell ◽  
Marginal Zone ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
Type B ◽  
Case Based

scholarly journals A case report of lineage switch from T-cell acute leukemia to B-cell acute leukemia

Medicine ◽  
2020 ◽  
Vol 99 (44) ◽  
pp. e22490
Author(s):  
Yejing Zhu ◽  
Hui Liu ◽  
Shuna Zhang ◽  
Yanyan Liang ◽  
Meng Xiao ◽  
...  
Keyword(s):  
Case Report ◽  
T Cell ◽  
Acute Leukemia ◽  
B Cell ◽  
Lineage Switch

scholarly journals A reassessment of the role of B7-1 expression in tumor rejection.

1995 ◽  
Vol 182 (5) ◽  
pp. 1415-1421 ◽  
Author(s):  
T C Wu ◽  
A Y Huang ◽  
E M Jaffee ◽  
H I Levitsky ◽  
D M Pardoll
Keyword(s):  
T Cells ◽  
Tumor Cells ◽  
Cd8 T Cells ◽  
Tumor Rejection ◽  
Type B ◽  
Wild Type ◽  
Systemic Immunity ◽  
Murine Tumor

Introduction of the B7-1 gene into murine tumor cells can result in rejection of the B7-1 transductants and, in some cases, systemic immunity to subsequent challenge with the nontransduced tumor cells. These effects have been largely attributed to the function of B7-1 as a costimulator in directly activating tumor specific, major histocompatibility class I-restricted CD8+ T cells. We examined the role of B7-1 expression in the direct rejection as well as in the induction of systemic immunity to a nonimmunogenic murine tumor. B-16 melanoma cells with high levels of B7-1 expression did not grow in C57BL/6 recipient mice, while wild-type B-16 cells and cells with low B7-1 expression grew progressively within 21 d. In mixing experiments with B7-1hi and wild-type B-16 cells, tumors grew out in vivo even when a minority of cells were B7-1-. Furthermore, the occasional tumors that grew out after injection of 100% B-16 B7-1hi cells showed markedly decreased B7-1 expression. In vivo antibody depletions showed that NK1.1 and CD8+ T cells, but not CD4+ T cells, were essential for the in vivo rejection of tumors. Animals that rejected B-16 B7-1hi tumors did not develop enhanced systemic immunity against challenge with wild-type B-16 cells. These results suggest that a major role of B7-1 expression by tumors is to mediate direct recognition and killing by natural killer cells. With an intrinsically nonimmunogenic tumor, this direct killing does not lead to enhanced systemic immunity.

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