Splenic CD19−CD35+B220+ cells function as an inducer of follicular dendritic cell network formation

Murakami, Takaya; Chen, Xin; Hase, Koji; Sakamoto, Ayako; Nishigaki, Chie; Ohno, Hiroshi

doi:10.1182/blood-2007-01-068387

Cited by 23 publications

(20 citation statements)

References 44 publications

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“…33,No. 6 Inflammatory lymph node remodeling During an infection, considerable structural changes occur in the lymph nodes including an increase in size as a consequence of lymphocyte accumulation.…”

Section: Reviewmentioning

confidence: 96%

“…FDCs fail to develop in the absence of tumor necrosis factor (TNF) and lymphotoxin signals provided by B cells [29]. Moreover, lymphotoxin is mandatory for the survival and maintenance of FDCs in fully mature lymph nodes [33][34][35][36]. FDCs, however, produce homeostatic factors for B cells such as the B cell activating factor belonging to the TNF family (BAFF), thereby demonstrating the mutual dependence between B cells and FDCs [36].…”

Section: Fdc Differentiationmentioning

confidence: 99%

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Interdependence of stromal and immune cells for lymph node function

Koning

Mebius

2012

Trends in Immunology

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Section: Reviewmentioning

confidence: 96%

Section: Fdc Differentiationmentioning

confidence: 99%

Interdependence of stromal and immune cells for lymph node function

Koning

Mebius

2012

Trends in Immunology

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“…[2][3][4][5] It has also been found that splenic stromal cell (SSC) monolayers play an essential role by supporting stem cell maintenance, renewal, and the specific differentiation of only DCs and no other hematopoietic cells. 6 Importantly, extensive in vitro studies have provided compelling evidence that suggests that stromal cells can exert profound immunosuppressive effects via the modulation of both cellular and innate immune pathways.…”

Section: Introductionmentioning

confidence: 99%

Indoleamine 2,3-dioxygenase and regulatory dendritic cells contribute to the allograft protection induced by infusion of donor-specific splenic stromal cells

et al. 2010

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It has been reported that splenic stromal cells (SSCs) are capable of directly supporting the development of CD11c lo CD45RB 1 IL-10-producing dendritic cells (DCs) from lineage-negative c-kit 1 progenitor cells in the absence of exogenous cytokines. In vitro, DCs that differentiate on stromal cells suppress mixed leukocyte reaction responses and induce primary alloreactive CD41 T cells to differentiate into IL-10-producing Tr1 cells. However, the precise mechanisms by which these SSCs exert their regulatory functions in vivo remain undefined. Furthermore, their possible contribution to the development of allograft transplantation tolerance has yet to be examined. Here, we have used both murine skin and cardiac allograft transplantation models to explore whether in vivo alloresponses can be regulated by infusion with donor-derived SSCs and to investigate the possible mechanisms by which SSCs exert regulatory effects to prevent allograft rejection. We show that intravenous SSC infusion prolonged murine skin allograft survival. The prolonged graft survival is associated with augmentation of the generation of regulatory DC subsets and CD4 Foxp31 regulatory T cells (Tregs), as well as upregulation of the production of suppressive cytokines IL-10 and transforming growth factor (TGF)-b. Moreover, we found that indoleamine 2,3-dioxygenase and SSC-derived regulatory DCs contribute to allograft protection by infusion of donor-specific SSCs. Our data suggest that donor-derived SSCs could be used as a therapeutic target to promote transplantation tolerance.

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“…Lymphoid tissue inducer cells have been shown to enter embryonic lymphoid tissues and, via interactions with follicular reticular cells and follicular dendritic cells, signal the development of T-cell and B-cell zones. B cells themselves also appear to be required for the proper development of the spleen, via expression of LTα1β2 [4], and for the induction of follicular dendritic cell networks [5]. Such inducer cells may instruct the lymphoid stromal cells to develop and produce the chemokines CCL21 or CXCL13, which help defi ne the organized T-cell and B-cell regions.…”

Section: The Functional Microenvironment Of Lymphoid Organsmentioning

confidence: 98%

The host-tumor interface in B-cell non-Hodgkin lymphoma: A new world to investigate

Rachinel¹,

Salles²

2009

Curr Hematol Malig Rep

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Research on B-cell non-Hodgkin lymphoma focuses mainly on oncogenic events occurring in lymphoma cells, but recently a new component has appeared that may be crucial in lymphomagenesis: the tumor microenvironment. Indeed, compelling evidence demonstrates the key role played by nonmalignant bystander cells in the establishment and proliferation of the tumor. Among these cells, stromal cells, monocytes/macrophages, and T cells in lymphoid organs have all been described as contributing to tumor progression. Interactions linked to cell-cell intimate contacts-but also mediated through soluble mediators such as cytokines and chemokines-do form a specific network. All these interrelations directed by the tumor create a friendly environment for lymphoma cells that permits them to proliferate. Blocking the cross-talk between the tumor microenvironment and lymphoma cells may thus represent a promising new strategy for treating B-cell malignancies.

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Splenic CD19−CD35+B220+ cells function as an inducer of follicular dendritic cell network formation

Cited by 23 publications

References 44 publications

Interdependence of stromal and immune cells for lymph node function

Interdependence of stromal and immune cells for lymph node function

Indoleamine 2,3-dioxygenase and regulatory dendritic cells contribute to the allograft protection induced by infusion of donor-specific splenic stromal cells

The host-tumor interface in B-cell non-Hodgkin lymphoma: A new world to investigate

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