Follicular dendritic cells in health and disease

Shikh, Mohey Eldin El; Pitzalis, Costantino

doi:10.3389/fimmu.2012.00292

Cited by 68 publications

(70 citation statements)

References 228 publications

(299 reference statements)

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“…This could result from their cognate nature and ability to encounter antigen-laden FDCs. The preferred tumor cell localization in the FDC-rich GC light zone may also be due to the paracrine provision of growth-promoting factors ( 34,35 ). BCR engagement, as evidenced by activated BTK, and the receipt of growth factors could act differentially during tumor ontogeny and in a complementary manner.…”

Section: Research Articlementioning

confidence: 99%

“…4H ). Next, we mimicked cytokine and growth factor conditions that were suggested to support either GC B-cell proliferation or follicular B-cell lymphoma expansion ( 34,35 ). When supplemented, a substantial increase in cell proliferation was obtained for BAFF, CXCL12, Sonic hedgehog (SHH), hepatocyte growth factor (HGF), CXCL13, and IL15 ( Fig.…”

Section: Research Articlementioning

confidence: 99%

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Access to Follicular Dendritic Cells Is a Pivotal Step in Murine Chronic Lymphocytic Leukemia B-cell Activation and Proliferation

et al. 2014

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In human chronic lymphocytic leukemia (CLL) pathogenesis, B-cell antigen receptor signaling seems important for leukemia B-cell ontogeny, whereas the microenvironment infl uences B-cell activation, tumor cell lodging, and provision of antigenic stimuli. Using the murine Eμ-Tcl1 CLL model, we demonstrate that CXCR5-controlled access to follicular dendritic cells confers proliferative stimuli to leukemia B cells. Intravital imaging revealed a marginal zone B cell-like leukemia cell traffi cking route. Murine and human CLL cells reciprocally stimulated resident mesenchymal stromal cells through lymphotoxin-β-receptor activation, resulting in CXCL13 secretion and stromal compartment remodeling. Inhibition of lymphotoxin/lymphotoxin-β-receptor signaling or of CXCR5 signaling retards leukemia progression. Thus, CXCR5 activity links tumor cell homing, shaping a survival niche, and access to localized proliferation stimuli. SIGNIFICANCE: CLL and other indolent lymphoma are not curable and usually relapse after treatment, a process in which the tumor microenvironment plays a pivotal role. We dissect the consecutive steps of CXCR5-dependent tumor cell lodging and LTβR-dependent stroma-leukemia cell interaction; moreover, we provide therapeutic solutions to interfere with this reciprocal tumor-stroma cross-talk. Cancer Discov; 4(12); 1448-65.

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Section: Research Articlementioning

confidence: 99%

Section: Research Articlementioning

confidence: 99%

Access to Follicular Dendritic Cells Is a Pivotal Step in Murine Chronic Lymphocytic Leukemia B-cell Activation and Proliferation

et al. 2014

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“…FDCs are nonphagocytic and do not synthesize MHC class II molecules but instead capture MHC class II + EVs derived from follicular B cells (20). Because FDCs are nonphagocytic, the captured EVs likely remain on the Almost all cell types release extracellular vesicles (EVs), which are derived either from multivesicular bodies or from the plasma membrane.…”

Section: Immune Regulation By Antigen-presenting Cell Evsmentioning

confidence: 99%

“…The binding of EVs to FDCs is likely mediated in part through cell surface adhesion molecules, such as milk fat globule-EGF factor 8 (MFG-E8), ICAM1, and complement receptors 1 and 2 (CR1/2), which bind to EVexpressed phosphatidylserine (PS), CD11a, and C3-derived fragments, respectively (20).…”

Section: Immune Regulation By Antigen-presenting Cell Evsmentioning

confidence: 99%

Regulation of chronic inflammatory and immune processes by extracellular vesicles

Robbins

Dorronsoro

Booker

2016

Journal of Clinical Investigation

236

195

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“…These accessory immune cells are frequently found in autoimmune diseases to retain immune complexes on their surface for years thereby providing a constant antigen depot for memory B-cell stimulation. 27 Since only a limited number of patients (6/28; 21%) tested in remission relapsed, the clinical relevance of circulating ADAMTS13-specific immune complexes in remission remains to be established in prospective studies.Free anti-ADAMTS13 IgG were mainly of subclasses IgG1 and IgG4, in accordance with previous studies, 8,9 and no IgG subclass switch was observed between the acute phase and in remission. For most patients, the distribution of subclasses for free and complexed IgG anti-ADAMTS13 antibodies correlated, suggesting a similar avidity for ADAMTS13 among IgG subclasses.…”

mentioning

confidence: 99%

Persistence of circulating ADAMTS13-specific immune complexes in patients with acquired thrombotic thrombocytopenic purpura

et al. 2013

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© F e r r a t a S t o r t i F o u n d a t i o nTTP. Sixty-eight patients were tested during the acute phase, with 48 patients experiencing their first acute episode and 20 a relapse. For 18 of these patients, corresponding samples in clinical remission were also available. Ten patients were analyzed only during remission, giving a total of 28 patients tested in remission. The patients' demographics and clinical features are summarized in Table 1. The inclusion criteria for patients with acute acquired TTP were: presence of severe ADAMTS13 deficiency (<10%), thrombocytopenia (platelet count <150x10 9 /L), microangiopathic hemolytic anemia (hemoglobin <12 g/dL) with presence of schistocytes on the peripheral blood smear, and elevated lactate dehydrogenase levels (>450 IU/L). Fever, neurological symptoms or renal failure were not mandatory. Remission was defined as a normal platelet count (>150x10 9 /L) and no plasma exchange treatment for ≥30 consecutive days. Relapse was defined as the reappearance of clinical manifestation and/or laboratory data compatible with TTP after remission.Frozen citrated plasma samples were obtained from four international centers. The study was approved by the ethic committees of the University Hospital of Berne, Switzerland; Medical University of Vienna, Austria; Lille University Hospital, France; and Icahn School of Medicine, New York, USA. ADAMTS13 assaysADAMTS13 activity (ADAMTS13:Ac) and ADAMTS13 functional inhibitor titers were measured using fluorometric FRETS-VWF73 assay as described elsewhere. 24,25 The limit of quantification of ADAMTS13:Ac was 0.05 U/mL (5%); values <0.10 U/mL (<10%) were considered severely reduced; levels of 0.10-0.50 U/mL as reduced and levels >0.5 U/mL as normal. An inhibitor titer <0.7 BU/mL was considered negative. Plasma ADAMTS13 antigen (ADAMTS13:Ag) levels were determined by ELISA as described previously. 20 The reference range of the assay was 403 -907 ng/mL; the limit of quantification was 10 ng/mL. Levels of 100 -403 ng/mL were considered reduced, levels <100 ng/mL as severely reduced, and values <10 ng/mL as undetectable. Detection of free anti-ADAMTS13 antibodies by enzyme-linked immunosorbent assayFree antibodies were detected as described elsewhere 25 with modifications (Online Supplementary Methods). Detection of ADAMTS13-specific immune complexesMicrotiter plates were coated with a polyclonal rabbit antihuman ADAMTS13 antibody. After blocking the non-specific sites, diluted patient's plasma samples and controls were added and incubated overnight at 4°C. The next day, the immunoglobulin fraction of the bound immune complexes was detected with horseradish peroxidase-conjugated class-specific secondary antibodies followed by detection with an appropriate chromogenic substrate. For details, see Online Supplementary Methods and Online Supplementary Figure S1.An ELISA to detect total IgG-immune complexes was not established, however, the total amount of IgG-immune complexes was investigated in selected patients by co-immunoprecipitation,...

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Follicular dendritic cells in health and disease

Cited by 68 publications

References 228 publications

Access to Follicular Dendritic Cells Is a Pivotal Step in Murine Chronic Lymphocytic Leukemia B-cell Activation and Proliferation

Access to Follicular Dendritic Cells Is a Pivotal Step in Murine Chronic Lymphocytic Leukemia B-cell Activation and Proliferation

Regulation of chronic inflammatory and immune processes by extracellular vesicles

Persistence of circulating ADAMTS13-specific immune complexes in patients with acquired thrombotic thrombocytopenic purpura

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