Restoration of lymphoid organ integrity through the interaction of lymphoid tissue–inducer cells with stroma of the T cell zone

Scandella, Elke; Bolinger, Beatrice; Lattmann, Evelyn; Miller, Simone; Favre, Stéphanie; Littman, Dan R.; Finke, Daniela; Luther, Sanjiv A.; Junt, Tobias; Ludewig, Burkhard

doi:10.1038/ni.1605

Cited by 308 publications

(325 citation statements)

References 57 publications

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“…Within the splenic white pulp, there is also disruption to both the follicular DC (FDC) network in B cell follicles (21) and the gp38 + fibroblastic reticular cell (FRC) network that guides T cell and DC migration in the T cell zone (22). Similar alterations to splenic architecture are also observed in other infectious causes of splenomegaly, including experimental malaria (23,24), trypanosomiasis (25), and following infection with LCMV (26)(27)(28); furthermore, although less well characterized, they are also a feature of human VL (29).…”

Section: Introductionmentioning

confidence: 58%

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Inhibition of receptor tyrosine kinases restores immunocompetence and improves immune-dependent chemotherapy against experimental leishmaniasis in mice

Dalton¹,

Maroof²,

Owens³

et al. 2010

J. Clin. Invest.

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Receptor tyrosine kinases are involved in multiple cellular processes, and drugs that inhibit their action are used in the clinic to treat several types of cancer. However, the value of receptor tyrosine kinase inhibitors (RTKIs) for treating infectious disease has yet to be explored. Here, we have shown in mice that administration of the broad-spectrum RTKI sunitinib maleate (Sm) blocked the vascular remodeling and progressive splenomegaly associated with experimental visceral leishmaniasis. Furthermore, Sm treatment restored the integrity of the splenic microarchitecture. Although restoration of splenic architecture was accompanied by an increase in the frequency of IFN-γ + CD4 + T cells, Sm treatment alone was insufficient to cause a reduction in tissue parasite burden. However, preconditioning by short-term Sm treatment proved to be successful as an adjunct therapy, increasing the frequency of IFN-γ + and IFN-γ + TNF + CD4 + T cells, enhancing NO production by splenic macrophages, and providing dose-sparing effects when combined with a first-line immune-dependent anti-leishmanial drug. We propose, therefore, that RTKIs may prove clinically useful as agents to restore immune competence before the administration of chemo-or immunotherapeutic drugs in the treatment of visceral leishmaniasis or other diseases involving lymphoid tissue remodeling, including cancer.

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Section: Introductionmentioning

confidence: 58%

“…Thus, we and others have proposed that lymphoid tissue remodeling may be a common mechanism that underpins disease-associated immunosuppression (18,22,26,28). Direct evidence in support of this concept has recently been obtained in mice infected with LCMV.…”

Section: Introductionmentioning

confidence: 76%

Inhibition of receptor tyrosine kinases restores immunocompetence and improves immune-dependent chemotherapy against experimental leishmaniasis in mice

Dalton¹,

Maroof²,

Owens³

et al. 2010

J. Clin. Invest.

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“…IL‐22 production by ILC3s is critical in containing commensal bacteria,25 and IL‐23‐responsive ILC3s also mediate colitis26 and accumulate in the inflamed intestine of CD patients 27. ILC3s also include the LTi cells involved in organizing tertiary lymphoid structures and tissue repair 28, 29…”

Section: The Ilc Familymentioning

confidence: 99%

Innate‐like CD8+ T‐cells and NK cells: converging functions and phenotypes

2018

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SummaryNew data in the worlds of both innate‐like CD8+ T‐cells and natural killer (NK) cells have, in parallel, clarified some of the phenotypes of these cells and also their associated functions. While these cells are typically viewed entirely separately, the emerging innate functions of T‐cells and, similarly, the adaptive functions of NK cells suggest that many behaviours can be considered in parallel. In this review we compare the innate functions of CD8+ T‐cells (especially mucosal‐associated invariant T‐cells) and those of NK cells, and how these relate to expression of phenotypic markers, especially CD161 and CD56.

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“…However, recent studies indicated that plasticity in LN structural organization continues to exist throughout life, particularly during inflammation and infection (8,9). Reorganization of LN microanatomy during inflammation is characterized by the remodeling and expansion of key LN stromal cells, including lymphatic endothelial cells (LECs) (10), blood endothelial cells (BECs) (11,12), and fibroblastic reticular cells (FRCs) (13,14). Importantly, increasing evidence reveal the immunological significance of the remodeling of these stromal elements.…”

mentioning

confidence: 99%

Expansion of Cortical and Medullary Sinuses Restrains Lymph Node Hypertrophy during Prolonged Inflammation

Tan

Yeo

Wong

et al. 2012

The Journal of Immunology

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During inflammation, accumulation of immune cells in activated lymph nodes (LNs), coupled with a transient shutdown in lymphocyte exit, results in dramatic cellular expansion. Counter-regulatory measures to restrain LN expansion must exist and may include re-establishment of lymphocyte egress to steady-state levels. Indeed, we show in a murine model that egress of lymphocytes from LNs was returned to steady-state levels during prolonged inflammation following initial retention. This restoration in lymphocyte egress was supported by a preferential expansion of cortical and medullary sinuses during late inflammation. Cortical and medullary sinus remodeling during late inflammation was dependent on temporal and spatial changes in vascular endothelial growth factor-A distribution. Specifically, its expression was restricted to the subcapsular space of the LN during early inflammation, whereas its expression was concentrated in the paracortical and medullary regions of the LN at later stages. We next showed that this process was mostly driven by the synergistic cross-talk between fibroblastic reticular cells and interstitial flow. Our data shed new light on the biological significance of LN lymphangiogenesis during prolonged inflammation and further underscore the collaborative roles of stromal cells, immune cells, and interstitial flow in modulating LN plasticity and function.

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Restoration of lymphoid organ integrity through the interaction of lymphoid tissue–inducer cells with stroma of the T cell zone

Cited by 308 publications

References 57 publications

Inhibition of receptor tyrosine kinases restores immunocompetence and improves immune-dependent chemotherapy against experimental leishmaniasis in mice

Inhibition of receptor tyrosine kinases restores immunocompetence and improves immune-dependent chemotherapy against experimental leishmaniasis in mice

Innate‐like CD8+ T‐cells and NK cells: converging functions and phenotypes

Expansion of Cortical and Medullary Sinuses Restrains Lymph Node Hypertrophy during Prolonged Inflammation

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