scholarly journals Lymph Node Germinal Centers Form in the Absence of Follicular Dendritic Cell Networks

1999 ◽  
Vol 189 (5) ◽  
pp. 855-864 ◽  
Author(s):  
Pandelakis A. Koni ◽  
Richard A. Flavell
Keyword(s):  
Dendritic Cell ◽  
B Cell ◽  
Follicular Dendritic Cell ◽  
Germinal Centers ◽  
Affinity Maturation ◽  
Antibody Affinity ◽  
B Cell Memory ◽  
Follicular Dendritic ◽  
Cell Networks ◽  
Deficient Mice

Follicular dendritic cell networks are said to be pivotal to both the formation of germinal centers (GCs) and their functions in generating antigen-specific antibody affinity maturation and B cell memory. We report that lymphotoxin β–deficient mice form GC cell clusters in the gross anatomical location expected of GCs, despite the complete absence of follicular dendritic cell networks. Furthermore, antigen-specific GC generation was at first relatively normal, but these GCs then rapidly regressed and GC-phase antibody affinity maturation was reduced. Lymphotoxin β–deficient mice also showed substantial B cell memory in their mesenteric lymph nodes. This memory antibody response was of relatively low affinity for antigen at week 4 after challenge, but by week 10 after challenge was comparable to wild-type, indicating that affinity maturation had failed in the GC phase but developed later.

scholarly journals Antiviral B Cell Memory in the Absence of Mature Follicular Dendritic Cell Networks and Classical Germinal Centers in TNFR1−/−Mice

2000 ◽  
Vol 164 (2) ◽  
pp. 768-778 ◽  
Author(s):  
U. Karrer ◽  
C. López-Macías ◽  
A. Oxenius ◽  
B. Odermatt ◽  
M. F. Bachmann ◽  
...  
Keyword(s):  
Dendritic Cell ◽  
B Cell ◽  
Follicular Dendritic Cell ◽  
Germinal Centers ◽  
Cell Memory ◽  
B Cell Memory ◽  
Follicular Dendritic ◽  
Cell Networks

scholarly journals Immune and inflammatory responses in TNF alpha-deficient mice: a critical requirement for TNF alpha in the formation of primary B cell follicles, follicular dendritic cell networks and germinal centers, and in the maturation of the humoral immune response.

1996 ◽  
Vol 184 (4) ◽  
pp. 1397-1411 ◽  
Author(s):  
M Pasparakis ◽  
L Alexopoulou ◽  
V Episkopou ◽  
G Kollias
Keyword(s):  
Immune Response ◽  
Dendritic Cell ◽  
B Cell ◽  
Knockout Mice ◽  
Humoral Immune Response ◽  
Follicular Dendritic Cell ◽  
Germinal Centers ◽  
Tnf Alpha ◽  
Humoral Immune ◽  
Deficient Mice

To investigate the role of TNF alpha in the development of in vivo immune response we have generated TNF alpha-deficient mice by gene targeting. Homozygous mutant mice are viable and fertile, develop lymph nodes and Peyer's patches and show no apparent phenotypic abnormalities, indicating that TNF alpha is not required for normal mouse development. In the absence of TNF alpha mice readily succumb to L. monocytogenes infections and show reduced contact hypersensitivity responses. Furthermore, TNF alpha knockout mice are resistant to the systemic toxicity of LPS upon D-galactosamine sensitization, yet they remain sensitive to high doses of LPS alone. Most interestingly, TNF alpha knockout mice completely lack splenic primary B cell follicles and cannot form organized follicular dendritic cell (FDC) networks and germinal centers. However, despite the absence of B cell follicles, Ig class-switching can still occur, yet deregulated humoral immune responses against either thymus-dependent (TD) or thymus-independent (TI) antigens are observed. Complementation of TNF alpha functioning by the expression of either human or murine TNF alpha transgenes is sufficient to reconstitute these defects, establishing a physiological role for TNF alpha in regulating the development and organization of splenic follicular architecture and in the maturation of the humoral immune response.

scholarly journals Enhanced Follicular Dendritic Cell-B Cell Interaction in HIV and SIV Infections and its Potential Role in Polyclonal B Cell Activation

1998 ◽  
Vol 6 (1-2) ◽  
pp. 61-70 ◽  
Author(s):  
Yvonne J. Rosenberg ◽  
Mark. G. Lewis ◽  
Marie H. Kosco-Vilbois
Keyword(s):  
Lymph Node ◽  
Dendritic Cell ◽  
B Cell ◽  
Cell Activation ◽  
Follicular Dendritic Cell ◽  
Cell Interaction ◽  
Germinal Centers ◽  
B Cell Activation ◽  
Immunodeficiency Virus ◽  
Follicular Dendritic

Human immunodeficiency virus (HIV) infections have been characterized by both polyclonal Bcell activation and enhanced responsiveness to B-cell growth factors on one hand and the loss of specific antibody (Ab) responses and refractoriness to the normal signals for B-cell activation on the other. Histopathological studies of lymph node from HIV- and simian immunodeficiency virus (SIV)-infected individuals have indicated initial follicular hyperplasia and the appearance of large irregular germinal centers that undergo progressive involution concomitant with follicular dendritic-cell (FDC) disruption. During this process, follicular dendritic-cell -enriched lymph-node-cell cultures exhibit increased ability to induce cluster formation (“in vitrogerminal centers”), lymphocyte proliferation and antibody production compared to uninfected controls. This paper discusses how enhanced FDC-B-cell interaction within SIV-infected germinal centers may result in a reduced ability to select high-affinity B cells and alter the dynamics of antibodyproducing- cell and memory-cell generation resulting in the observed hyperactivity.

scholarly journals Large B-Cell Lymphoma with T-Cell–Rich Background and Nodules Lacking Follicular Dendritic Cell Meshworks: A Case Report with Complete Response to Chemotherapy and a Review of the Literature

2020 ◽  
Vol 5 (11) ◽  
pp. 561-565
Author(s):  
Walid Shalata ◽  
Ismaell Massalha ◽  
Kayed Al-Athamen
Keyword(s):  
T Cell ◽  
Dendritic Cell ◽  
B Cell ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
Complete Response ◽  
Follicular Dendritic Cell ◽  
Large B Cell Lymphoma ◽  
Follicular Dendritic ◽  
Large B Cell

In this report, we describe a 38-year-old male with a very rare type of lymphoma, large B cell lymphoma with T cell-rich background and nodules lacking follicular dendritic cell meshworks (THRLBCL). In 2016 the patient presented hot flashes and night sweats (B-symptoms) and peripheral edema. He was treated with R-CHOP (doxorubicin, vincristine, cyclophosphamide, rituximab and Prednisone) chemotherapy, a Positron emission tomography–computed tomography (PET-CT) scan was performed after four cycles of treatment which showed radiologic complete response and blood test (complete blood count (CBC)) results showed normal ranges. As of September, 2020 he patient remains in complete remission. We searched the literature for descriptions of cases spanning the diagnostic spectrum of THRLBCL and we identified only five cases worldwide. The last reported case was in 2014 with distinctive features that were difficult to classify according to the World Health Organization criteria or previously described variants. Our patient is the sixth case of THRLBCL to be reported. He is the youngest of the reported cases and the first from Israel and the Middle East.

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