Faculty Opinions recommendation of B cell receptor ligation induces display of V-region peptides on MHC class II molecules to T cells.

2019 ◽  
Author(s):  
Jim Drake
Keyword(s):  
T Cells ◽  
B Cell ◽  
Mhc Class Ii ◽  
Cell Receptor ◽  
Class Ii ◽  
B Cell Receptor ◽  
V Region ◽  
Receptor Ligation ◽  
Mhc Class Ii Molecules

scholarly journals B cell receptor ligation induces display of V-region peptides on MHC class II molecules to T cells

2019 ◽  
Vol 116 (51) ◽  
pp. 25850-25859 ◽  
Author(s):  
Peter Csaba Huszthy ◽  
Ramakrishna Prabhu Gopalakrishnan ◽  
Johanne Tracey Jacobsen ◽  
Ole Audun Werner Haabeth ◽  
Geir Åge Løset ◽  
...  
Keyword(s):  
T Cells ◽  
B Cells ◽  
B Cell ◽  
Mhc Class Ii ◽  
Cell Receptor ◽  
B Cell Receptor ◽  
B Cell Receptors ◽  
V Region ◽  
Receptor Ligation

The B cell receptors (BCRs) for antigen express variable (V) regions that are enormously diverse, thus serving as markers on individual B cells. V region-derived idiotypic (Id) peptides can be displayed as pId:MHCII complexes on B cells for recognition by CD4+T cells. It is not known if naive B cells spontaneously display pId:MHCII in vivo or if BCR ligation is required for expression, thereby enabling collaboration between Id+B cells and Id-specific T cells. Here, using a mouse model, we show that naive B cells do not express readily detectable levels of pId:MHCII. However, BCR ligation by Ag dramatically increases physical display of pId:MHCII, leading to activation of Id-specific CD4+T cells, extrafollicular T–B cell collaboration and some germinal center formation, and production of Id+IgG. Besides having implications for immune regulation, the results may explain how persistent activation of self-reactive B cells induces the development of autoimmune diseases and B cell lymphomas.

scholarly journals Dynamics of Major Histocompatibility Complex Class II Compartments during B Cell Receptor–mediated Cell Activation

2002 ◽  
Vol 195 (4) ◽  
pp. 461-472 ◽  
Author(s):  
Danielle Lankar ◽  
Hélène Vincent-Schneider ◽  
Volker Briken ◽  
Takeaki Yokozeki ◽  
Graça Raposo ◽  
...  
Keyword(s):  
B Cells ◽  
B Cell ◽  
Mhc Class Ii ◽  
Cell Receptor ◽  
Class Ii ◽  
B Cell Receptor ◽  
Cathepsin S ◽  
Invariant Chain ◽  
Histocompatibility Complex ◽  
Mhc Class Ii Molecules

Antigen recognition by clonotypic B cell receptor (BcR) is the first step of B lymphocytes differentiation into plasmocytes. This B cell function is dependent on efficient major histocompatibility complex (MHC) class II–restricted presentation of BcR-bound antigens. In this work, we analyzed the subcellular mechanisms underlying antigen presentation after BcR engagement on B cells. In quiescent B cells, we found that MHC class II molecules mostly accumulated at the cell surface and in an intracellular pool of tubulovesicular structures, whereas H2-M molecules were mostly detected in distinct lysosomal compartments devoid of MHC class II. BcR stimulation induced the transient intracellular accumulation of MHC class II molecules in newly formed multivesicular bodies (MVBs), to which H2-M was recruited. The reversible downregulation of cathepsin S activity led to the transient accumulation of invariant chain–MHC class II complexes in MVBs. A few hours after BcR engagement, cathepsin S activity increased, the p10 invariant chain disappeared, and MHC class II–peptide complexes arrived at the plasma membrane. Thus, BcR engagement induced the transient formation of antigen-processing compartments, enabling antigen-specific B cells to become effective antigen-presenting cells.

scholarly journals Binding sites for bacterial and endogenous retroviral superantigens can be dissociated on major histocompatibility complex class II molecules.

1994 ◽  
Vol 179 (3) ◽  
pp. 1029-1034 ◽  
Author(s):  
J Thibodeau ◽  
N Labrecque ◽  
F Denis ◽  
B T Huber ◽  
R P Sékaly
Keyword(s):  
T Cells ◽  
Major Histocompatibility Complex ◽  
Mhc Class Ii ◽  
Binding Sites ◽  
Cell Receptor ◽  
Class Ii ◽  
Bacterial Toxins ◽  
Major Histocompatibility ◽  
Histocompatibility Complex ◽  
Mhc Class Ii Molecules

Bacterial and retroviral superantigens (SAGs) interact with major histocompatibility complex (MHC) class II molecules and stimulate T cells upon binding to the V beta portion of the T cell receptor. Whereas both types of molecules exert similar effects on T cells, they have very different primary structures. Amino acids critical for the binding of bacterial toxins to class II molecules have been identified but little is known of the molecular interactions between class II and retroviral SAGs. To determine whether both types of superantigens interact with the same regions of MHC class II molecules, we have generated mutant HLA-DR molecules which have lost the capacity to bind three bacterial toxins (Staphylococcus aureus enterotoxin A [SEA], S. aureus enterotoxin B [SEB], and toxic shock syndrome toxin 1 [TSST-1]). Cells expressing these mutated class II molecules efficiently presented two retroviral SAGs (Mtv-9 and Mtv-7) to T cells while they were unable to present the bacterial SAGs. These results demonstrate that the binding sites for both types of SAGs can be dissociated.

scholarly journals Role of B cell receptor Igα and Igβ subunits in MHC class II-restricted antigen presentation

Immunity ◽  
1995 ◽  
Vol 3 (3) ◽  
pp. 335-347 ◽  
Author(s):  
Christian Bonnerot ◽  
Danielle Lankar ◽  
Daniel Hanau ◽  
Daniele Spehner ◽  
Jean Davoust ◽  
...  
Keyword(s):  
B Cell ◽  
Antigen Presentation ◽  
Mhc Class Ii ◽  
Cell Receptor ◽  
Class Ii ◽  
B Cell Receptor

scholarly journals Aborted Germinal Center Reactions and B Cell Memory by Follicular T Cells Specific for a B Cell Receptor V Region Peptide

2011 ◽  
Vol 187 (1) ◽  
pp. 212-221 ◽  
Author(s):  
Ryan A. Heiser ◽  
Christopher M. Snyder ◽  
James St. Clair ◽  
Lawrence J. Wysocki
Keyword(s):  
T Cells ◽  
B Cell ◽  
Germinal Center ◽  
Cell Receptor ◽  
B Cell Receptor ◽  
Cell Memory ◽  
B Cell Memory ◽  
V Region

scholarly journals MHC-Restricted Ig V Region-Driven T-B Lymphocyte Collaboration: B Cell Receptor Ligation Facilitates Switch to IgG Production

2004 ◽  
Vol 172 (12) ◽  
pp. 7476-7484 ◽  
Author(s):  
Ludvig A. Munthe ◽  
Audun Os ◽  
Michael Zangani ◽  
Bjarne Bogen
Keyword(s):  
B Cell ◽  
B Lymphocyte ◽  
Cell Receptor ◽  
B Cell Receptor ◽  
V Region ◽  
Receptor Ligation

scholarly journals Generation of PLZF+ CD4+ T cells via MHC class II–dependent thymocyte–thymocyte interaction is a physiological process in humans

2009 ◽  
Vol 207 (1) ◽  
pp. 237-246 ◽  
Author(s):  
You Jeong Lee ◽  
Yoon Kyung Jeon ◽  
Byung Hyun Kang ◽  
Doo Hyun Chung ◽  
Chung-Gyu Park ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Mhc Class Ii ◽  
Cd4 T Cells ◽  
Zinc Finger Protein ◽  
Cell Subset ◽  
Cell Receptor ◽  
Class Ii ◽  
Inkt Cells ◽  
Mhc Class Ii Molecules

Human thymocytes, unlike mouse thymocytes, express major histocompatibility complex (MHC) class II molecules on their surface, especially during the fetal and perinatal stages. Based on this observation, we previously identified a novel developmental pathway for the generation of CD4+ T cells via interactions between MHC class II–expressing thymocytes (thymocyte–thymocyte [T–T] interactions) with a transgenic mouse system. However, the developmental dissection of this T–T interaction in humans has not been possible because of the lack of known cellular molecules specific for T–T CD4+ T cells. We show that promyelocytic leukemia zinc finger protein (PLZF) is a useful marker for the identification of T–T CD4+ T cells. With this analysis, we determined that a substantial number of fetal thymocytes and splenocytes express PLZF and acquire innate characteristics during their development in humans. Although these characteristics are quite similar to invariant NKT (iNKT) cells, they clearly differ from iNKT cells in that they have a diverse T cell receptor repertoire and are restricted by MHC class II molecules. These findings define a novel human CD4+ T cell subset that develops via an MHC class II–dependent T–T interaction.

Sign in / Sign up

Export Citation Format

Share Document