Different Reticulum Cells of the Lymph Node: Microecological Concept of Lymphoid Tissue Organization

Author(s):  
H. K. Müller-Hermelink ◽  
E. Kaiserling
The Analyst ◽  
2017 ◽  
Vol 142 (4) ◽  
pp. 649-659 ◽  
Author(s):  
Ashley E. Ross ◽  
Maura C. Belanger ◽  
Jacob F. Woodroof ◽  
Rebecca R. Pompano

We present the first microfluidic platform for local stimulation of lymph node tissue slices and demonstrate targeted delivery of a model therapeutic.


1990 ◽  
Vol 51 (2) ◽  
pp. 194-208 ◽  
Author(s):  
Daniel Dziedzic ◽  
Elaine S. Wright ◽  
Nicholas E. Sargent

PEDIATRICS ◽  
1962 ◽  
Vol 30 (4) ◽  
pp. 595-600
Author(s):  
Stanley E. Crawford ◽  
Chester K. Jones

The findings in a fatal case of liver necrosis in a child given diphenylhydantoin sodium are presented. Typical lymph node hyperplasia of the reticulum cells, with mitotic figures and eosinophils, were seen in this instance. These are a well-documented finding in hypersensitivity to this drug.


Blood ◽  
1985 ◽  
Vol 66 (5) ◽  
pp. 1092-1097
Author(s):  
GS Wood ◽  
CF Garcia ◽  
RF Dorfman ◽  
RA Warnke

Follicle lysis is a characteristic alteration of B cell follicles described recently in lymph node biopsies from homosexual men. It consists of disruption of germinal centers by aggregates of small mature lymphocytes variably associated with erythrocyte extravasation. We studied the immunohistology of follicle lysis identified in lymph node biopsies from 11 homosexual men. The results indicate that follicle lysis has two principal immunohistologic features: (1) intrafollicular aggregates of small lymphocytes predominantly of polytypic mantle B cell phenotype (T015+/Leu-8+/mu+/delta+/k+ or lambda+), and (2) disruption of the normal, unified follicular meshwork of R4/23+ dendritic reticulum cells by these B cell aggregates. These structural alterations may affect the functional integrity of the germinal center as it pertains to the abnormal B cell effector function and the increased prevalence of B cell lymphoma recently documented in the acquired immunodeficiency syndrome and related disorders. Because dendritic reticulum cells weakly express the Leu-3 (T4) antigen, which is known to be an essential component of the receptor for human T- lymphotropic virus type III/lymphadenopathy-associated virus (HTLV- III/LAV) retrovirus infection, it is possible that retroviral infection of dendritic reticulum cells may play a role in the pathogenesis of follicle lysis.


2019 ◽  
Vol 23 (2) ◽  
pp. 115-120
Author(s):  
Virginia E Duncan ◽  
Karen M Chisholm ◽  
M Cristina Pacheco

Background Antitumor necrosis alpha (TNFα) therapy is often used in the management of patients with inflammatory bowel disease (IBD) and may have effects on lymphoid tissue architecture and function. The goal of our study was to characterize the effects of TNFα inhibitors on mesenteric lymph node and mucosa-associated lymphoid tissue in patients with IBD. Methods We examined lymphoid tissue morphology in IBD patients treated with TNFα inhibitors compared to untreated controls. Intestinal resections from 19 patients (10 anti-TNFα treated and 9 controls) were reviewed. Immunohistochemistry for CD21, CD20, and CD3 was performed on ileocecal valve lymphoid tissue and mesenteric lymph nodes from the resection specimens to assess follicular architecture. Results Relative to control groups, TNFα-treated groups showed less preserved germinal center architecture, evidenced by lower overall semiquantitative scores for follicular architecture. Likewise, the percentage of secondary follicles to total follicles was decreased in patients treated with TNFα blockade. Conclusions Our results suggest that TNFα inhibitors may play a role in disruption of lymphoid germinal center architecture in patients with IBD. Awareness of this disrupted lymphoid morphology when examining histologic sections from patients with IBD treated with TNFα inhibitors may prevent unnecessary studies to exclude a lymphoproliferative disorder.


Blood ◽  
1999 ◽  
Vol 94 (7) ◽  
pp. 2247-2251 ◽  
Author(s):  
Antonella Aiello ◽  
Ming-Qing Du ◽  
Tim C. Diss ◽  
Huai-Zheng Peng ◽  
Francesco Pezzella ◽  
...  

A 44-year-old woman with a 12-year history of Sjögren’s syndrome (SS) developed a low-grade mucosa-associated lymphoid tissue (MALT) lymphoma in the parotid gland. Two years later, she presented with generalized lymphadenopathy and hepatosplenomegaly and a follicular lymphoma was diagnosed. To investigate the relationship of the two histologically distinct lymphomas, we re-examined their histology and immunophenotype and studied the lymphomatous tissue from the parotid, cervical lymph node, and spleen using molecular genetic methods. Histologic and immunophenotypic studies confirmed the previous diagnoses and also identified a previously unnoticed focus of follicular lymphoma in the second parotid gland biopsy. Polymerase chain reaction (PCR) amplification of the rearranged Ig heavy-chain gene showed the same sized dominant product in the MALT lymphoma and the follicular lymphoma. Similarly, PCR analysis of the t(14:18) translocation yielded an identical sized band from both MALT and follicular lymphoma. Cloning and sequencing of the Ig PCR products showed an identical CDR3 sequence from each lesion, indicating a common clonal lineage. The follicular lymphoma of the parotid gland lymph node and the follicular lymphoma of the spleen showed an identical mutation signature to that of the salivary gland MALT lymphoma. We propose that follicular lymphoma in the parotid gland lymph node may have resulted from colonization of lymphoid follicles by MALT lymphoma cells, following which the tumor cells were induced to express a follicular lymphoma phenotype, due to Bcl-2 overexpression caused by t(14;18), leading to a change in clinical behavior resulting in rapid widespread dissemination of disease. These observations suggest that the distinct phenotypes of low-grade B-cell lymphomas may be the consequence of interplay between genetic and local microenvironmental factors.


2003 ◽  
Vol 47 (1) ◽  
pp. 238-243 ◽  
Author(s):  
Caroline Solas ◽  
Alain Lafeuillade ◽  
Philippe Halfon ◽  
Stéphane Chadapaud ◽  
Gilles Hittinger ◽  
...  

ABSTRACT The variable penetration of antiretroviral drugs into sanctuary sites may contribute to the differential evolution of human immunodeficiency virus (HIV) and the emergence of drug resistance. We evaluated the penetration of indinavir, nelfinavir, and lopinavir-ritonavir (lopinavir/r) in the central nervous system, genital tract, and lymphoid tissue and assessed the correlation with residual viral replication. Plasma, cerebrospinal fluid (CSF), semen, and lymph node biopsy samples were collected from 41 HIV-infected patients on stable highly active antiretroviral therapy regimens to determine drug concentrations and HIV RNA levels. When HIV RNA was detectable, sequencing of the reverse transcriptase and protease genes was performed. Ratios of the concentration in semen/concentration in plasma were 1.9 for indinavir, 0.08 for nelfinavir, and 0.07 for lopinavir. Only indinavir was detectable in CSF, with a concentration in CSF/concentration in plasma ratio of 0.17. Differential penetration into lymphoid tissue was observed, with concentration in lymph node tissue/concentration in plasma ratios of 2.07, 0.58, and 0.21 for indinavir, nelfinavir, and lopinavir, respectively. HIV RNA levels were <50 copies/ml in all CSF samples of patients in whom HIV RNA was not detectable in plasma. HIV RNA was detectable in the semen of three patients (two patients receiving nelfinavir and one patient receiving lopinavir/r), and its detection was associated with multiple resistance mutations, while the viral load in plasma was undetectable. HIV RNA was detectable in all lymph node tissue samples. Differential drug penetration was observed among the three protease inhibitors in the sanctuary sites, but there was no correlation between drug levels and HIV RNA levels, suggesting that multiple factors are involved in the persistence of viral reservoirs. Further studies are required to clarify the role and clinical relevance of drug penetration in sanctuaries in terms of long-term efficacy and drug resistance.


Blood ◽  
2002 ◽  
Vol 99 (7) ◽  
pp. 2483-2489 ◽  
Author(s):  
Rabindra Tirouvanziam ◽  
Ibrahim Khazaal ◽  
Victoire N'Sondé ◽  
Marie-Alix Peyrat ◽  
Annick Lim ◽  
...  

We introduce a novel in vivo model of human mucosal immunity, based on the implantation of human fetal bronchial mucosa and autologous peribronchial lymph node (PLN) in the severe combined immunodeficiency (SCID) mouse. In the SCID host, human fetal bronchi implanted alone retain macrophages and mast cells but lose T cells. In contrast, fetal bronchi co-implanted with PLN contain, in addition to macrophages and mast cells, numerous T cells and B cells, often clustered in intramucosal bronchus-associated lymphoid tissue (BALT). Functionally, bronchus–PLN cografts are able to mount robust αβ and γδ T-cell–mediated immune responses to Pseudomonas aeruginosa and 3,4-epoxy-3-methyl-1-butyl-diphosphate challenges. No other autologous lymphoid organ (bone marrow, thymus, liver) allows for BALT development in co-implanted bronchi, which suggests special ontogenetic and functional relations between extramucosal PLN and intramucosal BALT. Overall, the bronchus–PLN cograft appears as a promising model for human bronchial immune development and function. Our study is the first to document long-term ex vivo maintenance of functional human lymph nodes as native appendices to mucosal tissue. Our results, therefore, suggest a simple strategy for developing similar experimental models of human immune function in other mucosae.


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