scholarly journals Faculty Opinions recommendation of PD-1 regulates germinal center B cell survival and the formation and affinity of long-lived plasma cells.

2010 ◽  
Author(s):  
Ken Smith ◽  
Marion Espeli
Keyword(s):  
B Cell ◽  
Cell Survival ◽  
Germinal Center ◽  
Plasma Cells ◽  
B Cell Survival ◽  
Germinal Center B Cell

scholarly journals PD-1 regulates germinal center B cell survival and the formation and affinity of long-lived plasma cells

2010 ◽  
Vol 11 (6) ◽  
pp. 535-542 ◽  
Author(s):  
Kim L Good-Jacobson ◽  
Courtney G Szumilas ◽  
Lieping Chen ◽  
Arlene H Sharpe ◽  
Mary M Tomayko ◽  
...  
Keyword(s):  
B Cell ◽  
Cell Survival ◽  
Germinal Center ◽  
Plasma Cells ◽  
B Cell Survival ◽  
Germinal Center B Cell

Human follicular dendritic cells promote germinal center B cell survival by providing prostaglandins

2013 ◽  
Vol 55 (3-4) ◽  
pp. 418-423 ◽  
Author(s):  
Jini Kim ◽  
Seungkoo Lee ◽  
Young-Myeong Kim ◽  
Doo-Il Jeoung ◽  
Jongseon Choe
Keyword(s):  
Dendritic Cells ◽  
B Cell ◽  
Cell Survival ◽  
Germinal Center ◽  
Follicular Dendritic Cells ◽  
B Cell Survival ◽  
Germinal Center B Cell ◽  
Follicular Dendritic

scholarly journals CD80 Expression on B Cells Regulates Murine T Follicular Helper Development, Germinal Center B Cell Survival, and Plasma Cell Generation

2012 ◽  
Vol 188 (9) ◽  
pp. 4217-4225 ◽  
Author(s):  
Kim L. Good-Jacobson ◽  
Eunice Song ◽  
Shannon Anderson ◽  
Arlene H. Sharpe ◽  
Mark J. Shlomchik
Keyword(s):  
B Cells ◽  
B Cell ◽  
Cell Survival ◽  
Plasma Cell ◽  
Germinal Center ◽  
Cell Generation ◽  
Follicular Helper ◽  
B Cell Survival ◽  
Germinal Center B Cell

scholarly journals Plasma cells induce apoptosis of pre-B cells by interacting with bone marrow stromal cells

Blood ◽  
1996 ◽  
Vol 87 (8) ◽  
pp. 3375-3383 ◽  
Author(s):  
T Tsujimoto ◽  
IA Lisukov ◽  
N Huang ◽  
MS Mahmoud ◽  
MM Kawano
Keyword(s):  
Bone Marrow ◽  
B Cells ◽  
B Cell ◽  
Cell Survival ◽  
Cell Lines ◽  
Stromal Cells ◽  
Plasma Cells ◽  
Myeloma Cell ◽  
Myeloma Cells ◽  
B Cell Survival

By using two-color phenotypic analysis with fluorescein isothiocyanate- anti-CD38 and phycoerythrin-anti-CD19 antibodies, we found that pre-B cells (CD38+CD19+) signifcantly decreased depending on the number of plasma cells (CD38++CD19+) in the bone marrow (BM) in the cases with BM plasmacytosis, such as myelomas and even polyclonal gammopathy. To clarify how plasma cells suppress survival of pre-B cells, we examined the effect of plasma cells on the survival of pre-B cells with or without BM-derived stromal cells in vitro. Pre-B cells alone rapidly entered apoptosis, but interleukin-7 (IL-7), a BM stromal cell line (KM- 102), or culture supernatants of KM-102 cells could support pre-B cell survival. On the other hand, inhibitory factors such as transforming growth factor-beta1 (TGF-beta1) and macrophage inflammatory protein- 1beta (MIP-1beta) could suppress survival of pre-B cells even in the presence of IL-7. Plasma cells alone could not suppress survival of pre- B cells in the presence of IL-7, but coculture of plasma cells with KM- 102 cells or primary BM stromal cells induced apoptosis of pre-B cells. Supernatants of coculture with KM-102 and myeloma cell lines (KMS-5) also could suppress survival of pre-B cells. Furthermore, we examined the expression of IL-7, TGF-beta1, and MIP-1beta mRNA in KM-102 cells and primary stromal cells cocultured with myeloma cell lines (KMS-5). In these cells, IL-7 mRNA was downregulated, but the expression of TGF- beta1 and MIP-1beta mRNA was augmented. Therefore, these results suggest that BM-derived stromal cells attached to plasma (myeloma) cells were modulated to secrete lesser levels of supporting factor (IL- 7) and higher levels of inhibitory factors (TGF-beta1 and MIP-1beta) for pre-B cell survival, which could explain why the increased number of plasma (myeloma) cells induced suppression of pre-B cells in the BM. This phenomenon may represent a feedback loop between pre-B cells and plasma cells via BM stromal cells in the BM.

scholarly journals CD4+ follicular regulatory T cells optimize the influenza virus–specific B cell response

2020 ◽  
Vol 218 (3) ◽  
Author(s):  
Yisi Lu ◽  
Roy Jiang ◽  
Alec W. Freyn ◽  
Jiawei Wang ◽  
Shirin Strohmeier ◽  
...  
Keyword(s):  
Influenza Virus ◽  
B Cell ◽  
Germinal Center ◽  
Plasma Cells ◽  
Influenza Virus Infection ◽  
Influenza Viruses ◽  
Viral Challenge ◽  
Cell Responses ◽  
Germinal Center B Cell ◽  
B Cell Responses

CD4+ follicular regulatory T (Tfr) cells control B cell responses through the modulation of follicular helper T (Tfh) cells and germinal center development while suppressing autoreactivity; however, their role in the regulation of productive germinal center B cell responses and humoral memory is incompletely defined. We show that Tfr cells promote antigen-specific germinal center B cell responses upon influenza virus infection. Following viral challenge, we found that Tfr cells are necessary for robust generation of virus-specific, long-lived plasma cells, antibody production against both hemagglutinin (HA) and neuraminidase (NA), the two major influenza virus glycoproteins, and appropriate regulation of the BCR repertoire. To further investigate the functional relevance of Tfr cells during viral challenge, we used a sequential immunization model with repeated exposure of antigenically partially conserved strains of influenza viruses, revealing that Tfr cells promote recall antibody responses against the conserved HA stalk region. Thus, Tfr cells promote antigen-specific B cell responses and are essential for the development of long-term humoral memory.

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