scholarly journals Fc receptor–like 1 intrinsically recruits c-Abl to enhance B cell activation and function

2019 ◽  
Vol 5 (7) ◽  
pp. eaaw0315 ◽  
Author(s):  
Xingwang Zhao ◽  
Hengyi Xie ◽  
Meng Zhao ◽  
Asma Ahsan ◽  
Xinxin Li ◽  
...  
Keyword(s):  
B Cell ◽  
Cell Activation ◽  
Sh2 Domain ◽  
Fc Receptor ◽  
Cross Linking ◽  
B Cell Activation ◽  
Signaling Mechanism ◽  
Immunological Synapses ◽  
And Function ◽  
Deficient Mice

B cell activation is regulated by the stimulatory or inhibitory co-receptors of B cell receptors (BCRs). Here, we investigated the signaling mechanism of Fc receptor-like 1 (FcRL1), a newly identified BCR co-receptor. FcRL1 was passively recruited into B cell immunological synapses upon BCR engagement in the absence of FcRL1 cross-linking, suggesting that FcRL1 may intrinsically regulate B cell activation and function. BCR cross-linking alone led to the phosphorylation of the intracellular Y281ENV motif of FcRL1 to provide a docking site for c-Abl, an SH2 domain-containing kinase. The FcRL1 and c-Abl signaling module, in turn, potently augmented B cell activation and proliferation. FcRL1-deficient mice exhibited markedly impaired formation of extrafollicular plasmablasts and germinal centers, along with decreased antibody production upon antigen stimulation. These findings reveal a critical BCR signal-enhancing function of FcRL1 through its intrinsic recruitment to B cell immunological synapses and subsequent recruitment of c-Abl upon BCR cross-linking.

scholarly journals T Cell Accumulation in B Cell Follicles Is Regulated by Dendritic Cells and Is Independent of B Cell Activation

2003 ◽  
Vol 197 (2) ◽  
pp. 195-206 ◽  
Author(s):  
Simon Fillatreau ◽  
David Gray
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
T Cell ◽  
B Cells ◽  
B Cell ◽  
Cell Activation ◽  
B Cell Activation ◽  
Cell Accumulation ◽  
Antigen Presenting ◽  
Deficient Mice

We investigated the mechanism of CD4 T cell accumulation in B cell follicles after immunization. Follicular T cell numbers were correlated with the number of B cells, indicating B cell control of the niche that T cells occupy. Despite this, we found no role for B cells in the follicular migration of T cells. Instead, T cells are induced to migrate into B cell follicles entirely as a result of interaction with dendritic cells (DCs). Migration relies on CD40-dependent maturation of DCs, as it did not occur in CD40-deficient mice but was reconstituted with CD40+ DCs. Restoration was not achieved by the activation of DCs with bacterial activators (e.g., lipopolysaccharide, CpG), but was by the injection of OX40L–huIgG1 fusion protein. Crucially, the up-regulation of OX40L (on antigen-presenting cells) and CXCR-5 (on T cells) are CD40-dependent events and we show that T cells do not migrate to follicles in immunized OX40-deficient mice.

Critical Role for CD81 in B Cell Activation.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 1342-1342
Author(s):  
Mrinmoy Sanyal ◽  
Rosemary Fernandez ◽  
Shoshana Levy
Keyword(s):  
B Cells ◽  
B Cell ◽  
Cell Activation ◽  
Cell Function ◽  
Calcium Influx ◽  
Critical Role ◽  
B Cell Lymphoma ◽  
Free Calcium ◽  
B Cell Activation ◽  
Deficient Mice

Abstract CD81 is a component of the CD19/CD21 signaling complex in B cells. CD81 was originally discovered as target of an anti-proliferative antibody in a human B cell lymphoma. However, the exact role of CD81 in B cell function is not known. Here we studied B cells from CD81 knockout mice. We demonstrate that upon BCR induction these B cells flux higher intracellular free calcium ion; increase the phosphorylation of BCR-related proximal and distal substrates and increase their proliferation. Similarly, polyclonal activation of CD81-deficient B cells with LPS induced increased proliferation and antibody secretion. Consistent with these intrinsic B cell capabilities, CD81-deficient mice mounted significantly higher immune response upon antigenic stimulation. In addition, bone marrow perisinusoidal B cells (IgM+IgD+) capable of mounting T-independent immune responses against blood-borne pathogens were over represented in CD81-deficient mice. These cells also displayed increased calcium influx kinetics as splenic B cells and produced higher amounts of antibody after polyclonal stimulation. Taken together, these results suggest that CD81 is involved in suppressing B cell activation.

Mouse B Cell Activation is Inhibited by CD44 Cross-Linking

2005 ◽  
Vol 34 (4) ◽  
pp. 399-416 ◽  
Author(s):  
Tiana L. Wyant ◽  
Michael T. Fisher ◽  
Robert J. McKallip ◽  
Prakash S. Nagarkatti ◽  
Mitzi Nagarkatti ◽  
...  
Keyword(s):  
B Cell ◽  
Cell Activation ◽  
Cross Linking ◽  
B Cell Activation

scholarly journals Fc receptor-like 5 inhibits B cell activation via SHP-1 tyrosine phosphatase recruitment

2007 ◽  
Vol 104 (23) ◽  
pp. 9770-9775 ◽  
Author(s):  
C. L. Haga ◽  
G. R. A. Ehrhardt ◽  
R. J. Boohaker ◽  
R. S. Davis ◽  
M. D. Cooper
Keyword(s):  
B Cell ◽  
Cell Activation ◽  
Tyrosine Phosphatase ◽  
Fc Receptor ◽  
B Cell Activation

scholarly journals Wiskott-Aldrich Syndrome Protein-Deficient Mice Reveal a Role for WASP in T but Not B Cell Activation

Immunity ◽  
1998 ◽  
Vol 9 (1) ◽  
pp. 81-91 ◽  
Author(s):  
Scott B. Snapper ◽  
Fred S. Rosen ◽  
Emiko Mizoguchi ◽  
Paul Cohen ◽  
Wasif Khan ◽  
...  
Keyword(s):  
B Cell ◽  
Cell Activation ◽  
B Cell Activation ◽  
Wiskott Aldrich Syndrome ◽  
Syndrome Protein ◽  
Deficient Mice

scholarly journals Distribution of the Src-homology-2-domain-containing inositol 5-phosphatase SHIP-2 in both non-haemopoietic and haemopoietic cells and possible involvement of SHIP-2 in negative signalling of B-cells

1999 ◽  
Vol 342 (3) ◽  
pp. 697-705 ◽  
Author(s):  
Eric MURAILLE ◽  
Xavier PESESSE ◽  
Céline KUNTZ ◽  
Christophe ERNEUX
Keyword(s):  
B Cell ◽  
Cell Activation ◽  
Cell Receptor ◽  
Sh2 Domain ◽  
B Cell Activation ◽  
Mouse Tissues ◽  
Inhibitory Feedback ◽  
Src Homology ◽  
Src Homology 2 Domain ◽  
Haemopoietic Cells

The termination of activation signals is a critical step in the control of the immune response; perturbation of inhibitory feedback pathways results in profound immune defects culminating in autoimmunity and overwhelming inflammation. FcγRIIB receptor is a well described inhibitory receptor. The ligation of B-cell receptor (BCR) and FcγRIIB leads to the inhibition of B-cell activation. Numerous studies have demonstrated that the SH2-domain-containing inositol 5-phosphatase SHIP (referred hereto as SHIP-1) is essential in this process. The cDNA encoding a second SH2-domain-containing inositol 5-phosphatase, SHIP-2, has been cloned [Pesesse, Deleu, De Smedt, Drayer and Erneux (1997) Biochem. Biophys. Res. Commun. 239, 697-700]. Here we report the distribution of SHIP-2 in mouse tissues: a Western blot analysis of mouse tissues reveals that SHIP-2 is expressed in both haemopoietic and non-haemopoietic cells. In addition to T-cell and B-cell lines, spleen, thymus and lung are shown to coexpress SHIP-1 and SHIP-2. Moreover, SHIP-2 is detected in fibroblasts, heart and different brain areas. SHIP-2 shows a maximal tyrosine phosphorylation and association to Shc after ligation of BCR to FcγRIIB but not after stimulation of BCR alone. Our results therefore suggest a possible role for SHIP-2 in the negative regulation of immunocompetent cells.

Fc receptor phosphorylation during receptor-mediated control of B-cell activation

Nature ◽  
1990 ◽  
Vol 345 (6276) ◽  
pp. 628-632 ◽  
Author(s):  
Walter Hunziker ◽  
Terry Koch ◽  
J. Andrew Whitney ◽  
Ira Mellman
Keyword(s):  
B Cell ◽  
Cell Activation ◽  
Fc Receptor ◽  
B Cell Activation ◽  
Receptor Phosphorylation

scholarly journals Perturbation of B cell activation in SLAM-associated protein-deficient mice is associated with changes in gammaherpesvirus latency reservoirs

2007 ◽  
Vol 178 (11) ◽  
pp. 7487.1-7487
Author(s):  
I.-J. Kim ◽  
C. E. Burkum ◽  
T. Cookenham ◽  
P. L. Schwartzberg ◽  
D. L. Woodland ◽  
...  
Keyword(s):  
B Cell ◽  
Cell Activation ◽  
B Cell Activation ◽  
Deficient Mice

scholarly journals Perturbation of B Cell Activation in SLAM-Associated Protein-Deficient Mice Is Associated with Changes in Gammaherpesvirus Latency Reservoirs

2007 ◽  
Vol 178 (3) ◽  
pp. 1692-1701 ◽  
Author(s):  
In-Jeong Kim ◽  
Claire E. Burkum ◽  
Tres Cookenham ◽  
Pamela L. Schwartzberg ◽  
David L. Woodland ◽  
...  
Keyword(s):  
B Cell ◽  
Cell Activation ◽  
B Cell Activation ◽  
Deficient Mice
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