The role of non-hematopoietic stromal cells in the persistence of inflammation

Barone, Francesca; Nayar, Saba; Buckley, Chris

doi:10.3389/fimmu.2012.00416

Cited by 22 publications

(25 citation statements)

References 113 publications

(118 reference statements)

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“…Moreover, the level of chemokine expression influences the degree of organization among aggregates of a similar size (100). Critically, treatments aimed at depleting lymphocytes in human conditions have partially failed where established chronic TLOs were present, thus suggesting that both stromal and leukocyte components should be targeted in TLO-associated pathologies (202).…”

Section: What Are the Role And Origin Of Stromal Cells In Secondary Amentioning

confidence: 99%

“…Pathogenic tissue fibroblasts therefore play a key role not only in immune cell recruitment but also in aggregate organization (202). This phenomenon, which leads to the generation of TLOs, potentially represents the attempt of targeted stromal cells to respond locally and efficiently to the increased request of survival factors for the incoming lymphocytes.…”

Section: What Are the Role And Origin Of Stromal Cells In Secondary Amentioning

confidence: 99%

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Stromal Cells in Chronic Inflammation and Tertiary Lymphoid Organ Formation

Buckley

Barone

Nayar

et al. 2015

Annu. Rev. Immunol.

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196

193

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Inflammation is an unstable state. It either resolves or persists. Why inflammation persists and the factors that define tissue tropism remain obscure. Increasing evidence suggests that tissue-resident stromal cells not only provide positional memory but also actively regulate the differential accumulation of inflammatory cells within inflamed tissues. Furthermore, at many sites of chronic inflammation, structures that mimic secondary lymphoid tissues are observed, suggesting that chronic inflammation and lymphoid tissue formation share common activation programs. Similarly, blood and lymphatic endothelial cells contribute to tissue homeostasis and disease persistence in chronic inflammation. This review highlights our increasing understanding of the role of stromal cells in inflammation and summarizes the novel immunological role that stromal cells exert in the persistence of inflammatory diseases.

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Section: What Are the Role And Origin Of Stromal Cells In Secondary Amentioning

confidence: 99%

Section: What Are the Role And Origin Of Stromal Cells In Secondary Amentioning

confidence: 99%

Stromal Cells in Chronic Inflammation and Tertiary Lymphoid Organ Formation

Buckley

Barone

Nayar

et al. 2015

Annu. Rev. Immunol.

Self Cite

196

193

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“…85 However, it is now recognized that FLSs also have an active role in the pathogenesis of RA, releasing inflammatory cytokines, leukocyteattracting chemokines and leukocyte survival factors. 86 FLSs also directly mediate joint destruction by secretion of cartilage-degrading matrix metalloproteinases (MMPs), cathepsins and RANKL (promoting osteoclastogenesis) and Dickkopf-related protein 1 (DKK-1, which inhibits osteoblast function).…”

Section: Fibroblastsmentioning

confidence: 99%

Vitamin D in rheumatoid arthritis—towards clinical application

2015

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In addition to its well-documented involvement in mineral homeostasis, vitamin D seems to have broad effects on human health that go beyond the skeletal system. Prominent among these so-called nonclassical effects of vitamin D are its immunomodulatory properties. In vitro studies have shown anti-inflammatory effects of 1,25-dihydroxyvitamin D (1,25(OH)2D), the active form of vitamin D. In addition, epidemiological analysis of patients with established inflammatory disease identified associations between vitamin D deficiency (low serum concentrations of inactive 25-hydroxyvitamin D, abbreviated to 25(OH)D) and inflammatory conditions, including rheumatoid arthritis (RA). The association of vitamin D deficiency with RA severity supports the hypothesis of a role for vitamin D in the initiation or progression of the disease, or possibly both. However, whether 25(OH)D status is a cause or consequence of RA is still incompletely understood and requires further analysis in prospective vitamin D supplementation trials. The characterization of factors that promote the transition from preclinical to clinical phases of RA has become a major focus of research, with the aim to facilitate earlier diagnosis and treatment, and improve therapeutic outcomes. In this Review, we aim to describe the current knowledge of vitamin D and the immune system specifically in RA, and discuss the potential benefits that vitamin D might have on slowing RA progression.

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“…RA is characterised by a massive influx of immune and inflammatory cells into joints 5. This process is governed by activation of resident fibroblasts secreting pro-inflammatory cytokines that sustain activation of inflammatory cells,6 matrix metalloproteinases (MMPs) that degrade the cartilaginous matrix and mediators of bone destruction, such as the receptor activator of NF-kB ligand (RANKL), that locally support differentiation and activity of bone resorbing osteoclasts 1 2 7–10. Importantly, fibroblast hyperplasia is a determinant factor contributing to severity and chronicity of RA 4 7 11.…”

Section: Introductionmentioning

confidence: 99%