Antigen receptor triggered upregulation of CD86 and CD80 in human B cells: augmenting role of the CD21/CD19 co-stimulatory complex and IL-4

2002 ◽  
Vol 216 (1-2) ◽  
pp. 50-64 ◽  
Author(s):  
Patricia K.A Mongini ◽  
Sonia Tolani ◽  
Rasem J Fattah ◽  
John K Inman
Keyword(s):  
B Cells ◽  
Antigen Receptor ◽  
Human B Cells

scholarly journals TACI and BAFF-R mediate isotype switching in B cells

2005 ◽  
Vol 201 (1) ◽  
pp. 35-39 ◽  
Author(s):  
Emanuela Castigli ◽  
Stephen A. Wilson ◽  
Sumi Scott ◽  
Fatma Dedeoglu ◽  
Shengli Xu ◽  
...  
Keyword(s):  
B Cells ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Cell Maturation ◽  
Isotype Switching ◽  
B Cell Maturation ◽  
Human B Cells ◽  
Necrosis Factor ◽  
B Cell Maturation Antigen

The tumor necrosis factor family members BAFF and APRIL induce Ig isotype switching in human B cells. We analyzed the ability of BAFF and APRIL to induce isotype switching in murine B cells to IgG1, IgA, and IgE. APRIL and BAFF each engage two receptors, transmembrane activator and calcium-modulator and cytophilin ligand interactor (TACI) and B cell maturation antigen (BCMA), on B cells. In addition, BAFF engages a third receptor on B cells, BAFF-R. To determine the role of these receptors in isotype switching, we examined B cells from mice deficient in TACI, BCMA, and BAFF-R. The results obtained indicate that both TACI and BAFF-R are able to transduce signals that result in isotype switching.

Down-modulation of the antigen receptor by a superantigen for human B cells

2004 ◽  
Vol 92 (1-2) ◽  
pp. 91-96 ◽  
Author(s):  
Muriel Viau ◽  
Béatrice Cholley ◽  
Lars Björck ◽  
Moncef Zouali
Keyword(s):  
B Cells ◽  
Antigen Receptor ◽  
Human B Cells

scholarly journals Grb2 and GRAP connect the B cell antigen receptor to Erk MAP kinase activation in human B cells

2018 ◽  
Vol 8 (1) ◽  
Author(s):  
Kanika Vanshylla ◽  
Caren Bartsch ◽  
Christoffer Hitzing ◽  
Laura Krümpelmann ◽  
Jürgen Wienands ◽  
...  
Keyword(s):  
B Cells ◽  
B Cell ◽  
Map Kinase ◽  
Antigen Receptor ◽  
B Cell Antigen Receptor ◽  
Kinase Activation ◽  
Cell Antigen Receptor ◽  
Cell Antigen ◽  
Human B Cells

scholarly journals The Role of Cell Surface Receptors in the Activation of Human B Cells by Phosphorothioate Oligonucleotides

2000 ◽  
Vol 165 (3) ◽  
pp. 1438-1445 ◽  
Author(s):  
Hua Liang ◽  
Charles F. Reich ◽  
David S. Pisetsky ◽  
Peter E. Lipsky
Keyword(s):  
B Cells ◽  
Cell Surface ◽  
Cell Surface Receptors ◽  
Surface Receptors ◽  
Human B Cells

scholarly journals Absence of surface IgD does not impair naive B cell homeostasis and memory B cell formation in humans

2018 ◽  
Author(s):  
J. Nechvatalova ◽  
S.J.W. Bartol ◽  
Z. Chovancova ◽  
L. Boon ◽  
M. Vlkova ◽  
...  
Keyword(s):  
B Cells ◽  
B Cell ◽  
Cell Activation ◽  
Genetic Defect ◽  
Memory B Cells ◽  
Cell Homeostasis ◽  
Human B Cells ◽  
B Cell Homeostasis

One Sentence SummaryHuman B cells with a genetic defect in IGHD develop normally in vivo, and do not have a competitive disadvantage to IgD-expressing B cells for developing into memory B cells.AbstractSurface immunoglobulin D (IgD) is co-expressed with IgM on naive mature B cells. Still, the role of surface IgD remains enigmatic even 50 years after its initial discovery. We here examined the in vivo role of surface IgD in human B-cell homeostasis and antibody responses in four individuals with heterozygous nonsense mutations in IGHD. All IGHD heterozygous individuals had normal numbers of B cells and serum immunoglobulins, and did not show signs of immunodeficiency or immune dysregulation. IgD+ and IgD– naive mature B cells were present in equal numbers and showed similar immunophenotypes, except for decreased expression of CD79b in the IgD– subset. Furthermore, both IgD+ and IgD– naive mature B cells had normal replication histories, similar capacities to differentiate into plasma cells upon in vitro stimulation, and Ig switched memory B cells showed similar levels of somatic hypermutations. Thus human B cells lacking IgD expression develop normally and generate immunological memory in vivo, suggesting that surface IgD might function more restricted in regulating of B-cell activation to specific antigenic structures.

scholarly journals Lymphocyte Changes in Severe COVID-19: Delayed Over-Activation of STING?

2020 ◽  
Vol 11 ◽  
Author(s):  
Jean-Marie Berthelot ◽  
Frédéric Lioté ◽  
Yves Maugars ◽  
Jean Sibilia
Keyword(s):  
T Cells ◽  
B Cells ◽  
Cd8 T Cells ◽  
Human Lymphocytes ◽  
Dna Damages ◽  
Human B Cells ◽  
Antigen Presenting ◽  
Microbial Dna ◽  
Th2 Differentiation

Upon recognition of microbial DNA or self-DNA, the cyclic-GMP-AMP synthase (cGAS) of the host catalyzes the production of the cyclic dinucleotide cGAMP. cGAMP is the main activator of STING, stimulator of interferon genes, leading to interferon synthesis through the STING-TBK1-IRF3 pathway. STING is also a hub for activation of NF-κB and autophagy. The present review details the striking similarities between T and B cell responses in severe coronavirus disease 2019 (COVID-19) and both animal or human models of STING gain of function (SAVI syndromes: STING-associated vasculopathy with onset in infancy). Those similarities may be further clues for a delayed activation of STING in severe COVID-19 patients, due to DNA damages following severe acute respiratory syndrome coronaviruses (SARS-CoV-2) infection and unusual role of STING in SARS-CoV-2 control. In early stages, Th2 differentiation are noticed in both severe COVID-19 and SAVI syndromes; then, CD4+ and CD8+ T cells functional exhaustion/senescent patterns due to TCR hyper-responsiveness are observed. T cell delayed over-responses can contribute to pneumonitis and delayed cytokine secretion with over-production of IL-6. Last, STING over-activation induces progressive CD4+ and CD8+ T lymphopenia in SAVI syndromes, which parallels what is observed in severe COVID-19. ACE2, the main receptor of SARS-CoV-2, is rarely expressed in immune cells, and it has not been yet proven that some human lymphocytes could be infected by SARS-CoV-2 through CD147 or CD26. However, STING, expressed in humans T cells, might be triggered following excessive transfer of cGAMP from infected antigen presenting cells into activated CD4+ and CD8+ T cells lymphocytes. Indeed, those lymphocytes highly express the cGAMP importer SLC19A1. Whereas STING is not expressed in human B cells, B cells counts are much less affected, either in COVID-19 or SAVI syndromes. The recognition of delayed STING over-activation in severe COVID-19 patients could prompt to target STING with specific small molecules inhibitors already designed and/or aspirin, which inhibits cGAS.

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