scholarly journals Ibrutinib-Mediated Inhibition of cGVHD Pathogenic Pre-Germinal Center B-Cells and Follicular Helper Cells While Preserving Immune Memory and Th1 T-Cells

2018 ◽  
Vol 24 (3) ◽  
pp. S20-S21 ◽  
Author(s):  
Bita Sahaf ◽  
Dmitry Tebaykin ◽  
Melissa Hopper ◽  
Patricia Cheung ◽  
Fabiola Bittencourt ◽  
...  
Keyword(s):  
T Cells ◽  
B Cells ◽  
Germinal Center ◽  
Immune Memory ◽  
Helper Cells ◽  
Follicular Helper ◽  
Germinal Center B Cells

scholarly journals Normal human lymph node T follicular helper cells and germinal center B cells accessed via fine needle aspirations

2020 ◽  
Vol 479 ◽  
pp. 112746 ◽  
Author(s):  
Colin Havenar-Daughton ◽  
Isabel G. Newton ◽  
Somaye Y. Zare ◽  
Samantha M. Reiss ◽  
Brittany Schwan ◽  
...  
Keyword(s):  
Lymph Node ◽  
B Cells ◽  
Germinal Center ◽  
T Follicular Helper Cells ◽  
Fine Needle ◽  
Helper Cells ◽  
Follicular Helper ◽  
Human Lymph Node ◽  
Normal Human ◽  
Germinal Center B Cells

scholarly journals Increased T follicular helper cells and germinal center B cells are required for cGVHD and bronchiolitis obliterans

Blood ◽  
2014 ◽  
Vol 123 (25) ◽  
pp. 3988-3998 ◽  
Author(s):  
Ryan Flynn ◽  
Jing Du ◽  
Rachelle G. Veenstra ◽  
Dawn K. Reichenbach ◽  
Angela Panoskaltsis-Mortari ◽  
...  
Keyword(s):  
B Cells ◽  
Murine Model ◽  
Germinal Center ◽  
Bronchiolitis Obliterans ◽  
T Follicular Helper Cells ◽  
Novel Therapeutics ◽  
Helper Cells ◽  
Follicular Helper ◽  
Key Points ◽  
Germinal Center B Cells

Key Points T follicular helper cells and germinal center B cells are increased and strongly correlate with the development of cGVHD in a murine model. Blocking mAbs for IL-21, ICOS, and CD40L are potential novel therapeutics for cGVHD.

scholarly journals Distinctive expression pattern of the BCL-6 protein in nodular lymphocyte predominance Hodgkin's disease

Blood ◽  
1996 ◽  
Vol 87 (2) ◽  
pp. 465-471 ◽  
Author(s):  
B Falini ◽  
B Bigerna ◽  
L Pasqualucci ◽  
M Fizzotti ◽  
MF Martelli ◽  
...  
Keyword(s):  
T Cells ◽  
B Cells ◽  
B Cell ◽  
Germinal Center ◽  
Hodgkin's Disease ◽  
Cd4 T Cells ◽  
Zinc Finger Protein ◽  
Hodgkin’S Disease ◽  
Malignant Cell ◽  
Germinal Center B Cells

The BCL-6 gene encoding a nuclear-located Kruppel-type zinc finger protein is rearranged in about 30% diffuse large B-cell lymphomas and is expressed predominantly in normal germinal center B cells and related lymphomas. These findings suggest that BCL-6 may play a role in regulating differentiation of normal germinal center B cells and that its deregulated expression caused by rearrangements may contribute to lymphomagenesis. This prompted us to investigate the expression of the BCL-6 protein in Hodgkin's disease (HD), focusing on the nodular lymphocyte predominance subtype (NLPHD), which differs from classical HD by virtue of the B-cell nature of the malignant cell population (so- called L&H cells) and its relationship with germinal centers. Forty-one HD samples (19 NLPHD, 12 nodular sclerosis, and 10 mixed cellularity) were immunostained with the monoclonal antibodies PG-B6 and PG-B6p that react with a fixative-sensitive and a formalin-resistant epitope on the aminoterminal region of the BCL-6 gene product, respectively. Strong nuclear positivity for the BCL-6 protein was detected in tumor (L&H) cells in all cases of NLPHD. In contrast, BCL-6 was expressed only in a small percentage of Hodgkin and Reed-Sternberg cells in about 30% of classical HD cases. Notably, the nuclei of reactive CD3+/CD4+ T cells nearby to and rosetting around L&H cells in NLPHD were also strongly BCL-6+, but lacked CD40 ligand (CD40L) expression. This staining pattern clearly differed from that of classical HD, whose cellular background was made up of CD3+/CD4+ T cells showing the BCL-6-/CD40L+ phenotype. These results further support the concept that NLPHD is an histogenetically distinct, B-cell-derived subtype of HD and suggest a role for BCL-6 in its development.

scholarly journals Human Germinal Center CD4+CD57+T Cells Act Differently On B Cells Than Do Classical T-Helper Cells

1995 ◽  
Vol 4 (3) ◽  
pp. 189-197 ◽  
Author(s):  
Farida Bouzahzah ◽  
Alain Bosseloir ◽  
Ernst Heinen ◽  
Léon J. Simar
Keyword(s):  
Cell Proliferation ◽  
T Cells ◽  
T Cell ◽  
B Cells ◽  
B Cell ◽  
Germinal Center ◽  
Functional Study ◽  
Target Cells ◽  
Helper Cells ◽  
Ig Synthesis

We have isolated two subtypes of helper T cells from human tonsils: CD4+CD57+cells, mostly located in the germinal center (GC), and CD4+CD57-cells, distributed through the interfollicular areas but also present in the GC. In a functional study, we have compared the capacities of these T-cell subtypes to stimulate B cells in cocultures. In order to block T-cell proliferation while maintaining their activation level, we pretreated isolated T cells with mitomycin C prior to culture in the presence of B cells and added polyclonal activators such as PHA and Con A, combined or not with IL-2. Contrary to CD4+CD57-cells, CD4+CD57+cells did not markedly enhance B-cell proliferation. Even when sIgD-B cells typical of germinal center cells were tested, the CD4 CD57 cells had no significant effect. This is in accordance with the location of these cells: They mainly occupy the light zones of the GC where few B cells divide. Even when added to preactivated, actively proliferating cells, CD4+CD57+cells failed to modulate B-cell multiplication. On the supernatants of B-cell-T-cell cocultures, we examined by the ELISA technique the effect of T cells on Ig synthesis. Contrary to CD57-T cells, whose effect was strong, CD57+T cells weakly stimulated Ig synthesis. More IgM than IgG was generally found. Because CD57 antigen is a typical marker of natural killer cells, we tested the cytolytic activity of tonsillar CD4+CD57+cells on K562 target cells. Unlike NK cells, neither CD4+CD57+nor CD4+CD57-cells exhibit any cytotoxicity. Thus, germinal center CD4+CD57+cells are not cytolytic and do not strongly stimulate either B-cell proliferation or Ig secretion. CD4+CD57-cells, however, enhance B-cell proliferation and differentiation, thus acting like the classical helper cells of the T-dependent areas.

scholarly journals CD10 delineates a subset of human IL-4 producing follicular helper T cells involved in the survival of follicular lymphoma B cells

Blood ◽  
2015 ◽  
Vol 125 (15) ◽  
pp. 2381-2385 ◽  
Author(s):  
Patricia Amé-Thomas ◽  
Sylvia Hoeller ◽  
Catherine Artchounin ◽  
Jan Misiak ◽  
Mounia Sabrina Braza ◽  
...  
Keyword(s):  
T Cells ◽  
B Cells ◽  
Follicular Lymphoma ◽  
B Cell ◽  
Germinal Center ◽  
Helper T Cells ◽  
Follicular Helper T Cells ◽  
Follicular Helper ◽  
Key Points ◽  
Cell Niche

Key Points CD10 identifies a unique subset of fully functional germinal center TFH that are activated and amplified within the FL cell niche. FL CD10pos TFH specifically display an IL-4hiIFN-γlo cytokine profile and encompass the malignant B-cell-supportive TFH subset.

scholarly journals Mucosal T follicular helper cells in SIV-infected rhesus macaques: contributing role of IL-27

2019 ◽  
Vol 12 (4) ◽  
pp. 1038-1054 ◽  
Author(s):  
Félicien Moukambi ◽  
Henintsoa Rabezanahary ◽  
Yasmina Fortier ◽  
Vasco Rodrigues ◽  
Julien Clain ◽  
...  
Keyword(s):  
T Cells ◽  
B Cells ◽  
Cd4 T Cells ◽  
Rhesus Macaques ◽  
T Follicular Helper Cells ◽  
Mesenteric Lymph Nodes ◽  
Tfh Cells ◽  
Helper Cells ◽  
Follicular Helper ◽  
Memory Cd4 T Cells

AbstractMesenteric lymph nodes (MLNs), that drain the large and small intestine, are critical sites for the induction of oral tolerance. Although depletion of CD4 T cells in the intestinal lamina propria is a hallmark of HIV infection, CD4 T cell dynamics in MLNs is less known due to the lack of accessibility to these LNs. We demonstrate the early loss of memory CD4 T cells, including T follicular helper cells (Tfh) and a remodeling of MLN architecture in SIV-infected rhesus macaques (RMs). Along with the loss of Tfh cells, we observe the loss of memory B cells and of germinal center B cells. Tfh cells display a Th1 profile with increased levels of the transcription factors that negatively impact on Tfh differentiation and of Stat5 phosphorylation. MLNs of SIV-infected RMs display lower mRNA transcripts encoding for IL-12, IL-23, and IL-35, whereas those coding for IL-27 are not impaired in MLNs. In vitro, IL-27 negatively impacts on Tfh cells and recapitulates the profile observed in SIV-infected RMs. Therefore, early defects of memory CD4 T cells, as well of Tfh cells in MLNs, which play a central role in regulating the mucosal immune response, may have major implications for Aids.

B-108 Germinal center CD8 T cells can be redirected to eliminate HIV-expressing T follicular helper cells

2014 ◽  
Vol 67 ◽  
pp. 47
Author(s):  
Constantinos Petrovas ◽  
Sara Ferrando-Martinez ◽  
Amarendra Pegu ◽  
Kristin Boswell ◽  
Mangai Asokan ◽  
...  
Keyword(s):  
T Cells ◽  
Cd8 T Cells ◽  
Germinal Center ◽  
T Follicular Helper Cells ◽  
Helper Cells ◽  
Follicular Helper

scholarly journals Co-stimulatory function in primary germinal center responses: CD40 and B7 are required on distinct antigen-presenting cells

2017 ◽  
Vol 214 (9) ◽  
pp. 2795-2810 ◽  
Author(s):  
Masashi Watanabe ◽  
Chiharu Fujihara ◽  
Andrea J. Radtke ◽  
Y. Jeffrey Chiang ◽  
Sumeena Bhatia ◽  
...  
Keyword(s):  
T Cells ◽  
B Cells ◽  
Germinal Center ◽  
Helper T Cells ◽  
Vaccine Responses ◽  
High Affinity ◽  
Prevailing Paradigm ◽  
Follicular Helper ◽  
Cd40 Expression ◽  
Antigen Presenting

T cell–dependent germinal center (GC) responses require coordinated interactions of T cells with two antigen-presenting cell (APC) populations, B cells and dendritic cells (DCs), in the presence of B7- and CD40-dependent co-stimulatory pathways. Contrary to the prevailing paradigm, we found unique cellular requirements for B7 and CD40 expression in primary GC responses to vaccine immunization with protein antigen and adjuvant: B7 was required on DCs but was not required on B cells, whereas CD40 was required on B cells but not on DCs in the generation of antigen-specific follicular helper T cells, antigen-specific GC B cells, and high-affinity class-switched antibody production. There was, in fact, no requirement for coexpression of B7 and CD40 on the same cell in these responses. Our findings support a substantially revised model for co-stimulatory function in the primary GC response, with crucial and distinct contributions of B7- and CD40-dependent pathways expressed by different APC populations and with important implications for understanding how to optimize vaccine responses or limit autoimmunity.

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