The Experts below are selected from a list of 243 Experts worldwide ranked by ideXlab platform
Johan Rönnelid - One of the best experts on this subject based on the ideXlab platform.
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Immune complexes from rheumatoid arthritis synovial fluid induce FcγRIIa dependent and rheumatoid factor correlated production of tumour necrosis factor-α by peripheral blood mononuclear cells
Arthritis Research & Therapy, 2006Co-Authors: Linda Mathsson, Jon Lampa, Mohammed Mullazehi, Johan RönnelidAbstract:Immune complexes (ICs) can induce production of cytokines by peripheral blood mononuclear cells via Fc receptors. Rheumatoid factor (RF) develop in response to ICs in many clinical and experimental settings. We investigated whether and how polyethylene glycol (PEG) Precipitated ICs from rheumatoid arthritis (RA) sera and synovial fluid (SF) can influence cytokine production by peripheral blood mononuclear cells. We also examined the relationship between RF and IC induced cytokine production. Parallel sera and SF from 47 RA patients and sera from 15 healthy control individuals were PEG Precipitated. The Precipitates were added to serum-free peripheral blood mononuclear cell cultures and tumour necrosis factor (TNF)-α levels were measured after 20 hours. In separate cell culture experiments FcγRIIa and FcγRIII were blocked and monocytes were depleted or enriched. RF in serum was determined by nephelometry, and IgG levels in Precipitates and anti-cyclic citrullinated peptide antibodies in serum were measured using ELISA. Clinical data were collected from the patients' charts. In two separate investigations, we demonstrated a correlation between RF, PEG-Precipitated IgG levels and induction of the proinflammatory cytokine TNF-α by PEG-Precipitated SF ICs. No such correlation was found for serum ICs. TNF-α levels induced by SF Precipitates, but not serum Precipitates, correlated with the number of swollen and tender joints. Monocytes/macrophages were shown to be the main responder cells, and blockade of FcγRIIa, but not blockade of FcγRIII, inhibited TNF-α production in cultures stimulated with Precipitated ICs. Anti-cyclic citrullinated peptide correlated with RF but exhibited no association with IgG content in PEG Precipitates or with Precipitate-induced TNF-α levels. These findings support the hypothesis that SF ICs and correlated RF production are directly linked to cytokine-dependent inflammation in RA. Suppression of monocytes/macrophages in RA joints or blockade of the primate-specific activating FcγRIIa receptor might be ways to reduce IC-induced TNF-α production in the joints of seropositive RA patients.
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immune complexes from rheumatoid arthritis synovial fluid induce fcγriia dependent and rheumatoid factor correlated production of tumour necrosis factor α by peripheral blood mononuclear cells
Arthritis Research & Therapy, 2006Co-Authors: Linda Mathsson, Jon Lampa, Mohammed Mullazehi, Johan RönnelidAbstract:Immune complexes (ICs) can induce production of cytokines by peripheral blood mononuclear cells via Fc receptors. Rheumatoid factor (RF) develop in response to ICs in many clinical and experimental settings. We investigated whether and how polyethylene glycol (PEG) Precipitated ICs from rheumatoid arthritis (RA) sera and synovial fluid (SF) can influence cytokine production by peripheral blood mononuclear cells. We also examined the relationship between RF and IC induced cytokine production. Parallel sera and SF from 47 RA patients and sera from 15 healthy control individuals were PEG Precipitated. The Precipitates were added to serum-free peripheral blood mononuclear cell cultures and tumour necrosis factor (TNF)-α levels were measured after 20 hours. In separate cell culture experiments FcγRIIa and FcγRIII were blocked and monocytes were depleted or enriched. RF in serum was determined by nephelometry, and IgG levels in Precipitates and anti-cyclic citrullinated peptide antibodies in serum were measured using ELISA. Clinical data were collected from the patients' charts. In two separate investigations, we demonstrated a correlation between RF, PEG-Precipitated IgG levels and induction of the proinflammatory cytokine TNF-α by PEG-Precipitated SF ICs. No such correlation was found for serum ICs. TNF-α levels induced by SF Precipitates, but not serum Precipitates, correlated with the number of swollen and tender joints. Monocytes/macrophages were shown to be the main responder cells, and blockade of FcγRIIa, but not blockade of FcγRIII, inhibited TNF-α production in cultures stimulated with Precipitated ICs. Anti-cyclic citrullinated peptide correlated with RF but exhibited no association with IgG content in PEG Precipitates or with Precipitate-induced TNF-α levels. These findings support the hypothesis that SF ICs and correlated RF production are directly linked to cytokine-dependent inflammation in RA. Suppression of monocytes/macrophages in RA joints or blockade of the primate-specific activating FcγRIIa receptor might be ways to reduce IC-induced TNF-α production in the joints of seropositive RA patients.
Linda Mathsson - One of the best experts on this subject based on the ideXlab platform.
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Immune complexes from rheumatoid arthritis synovial fluid induce FcγRIIa dependent and rheumatoid factor correlated production of tumour necrosis factor-α by peripheral blood mononuclear cells
Arthritis Research & Therapy, 2006Co-Authors: Linda Mathsson, Jon Lampa, Mohammed Mullazehi, Johan RönnelidAbstract:Immune complexes (ICs) can induce production of cytokines by peripheral blood mononuclear cells via Fc receptors. Rheumatoid factor (RF) develop in response to ICs in many clinical and experimental settings. We investigated whether and how polyethylene glycol (PEG) Precipitated ICs from rheumatoid arthritis (RA) sera and synovial fluid (SF) can influence cytokine production by peripheral blood mononuclear cells. We also examined the relationship between RF and IC induced cytokine production. Parallel sera and SF from 47 RA patients and sera from 15 healthy control individuals were PEG Precipitated. The Precipitates were added to serum-free peripheral blood mononuclear cell cultures and tumour necrosis factor (TNF)-α levels were measured after 20 hours. In separate cell culture experiments FcγRIIa and FcγRIII were blocked and monocytes were depleted or enriched. RF in serum was determined by nephelometry, and IgG levels in Precipitates and anti-cyclic citrullinated peptide antibodies in serum were measured using ELISA. Clinical data were collected from the patients' charts. In two separate investigations, we demonstrated a correlation between RF, PEG-Precipitated IgG levels and induction of the proinflammatory cytokine TNF-α by PEG-Precipitated SF ICs. No such correlation was found for serum ICs. TNF-α levels induced by SF Precipitates, but not serum Precipitates, correlated with the number of swollen and tender joints. Monocytes/macrophages were shown to be the main responder cells, and blockade of FcγRIIa, but not blockade of FcγRIII, inhibited TNF-α production in cultures stimulated with Precipitated ICs. Anti-cyclic citrullinated peptide correlated with RF but exhibited no association with IgG content in PEG Precipitates or with Precipitate-induced TNF-α levels. These findings support the hypothesis that SF ICs and correlated RF production are directly linked to cytokine-dependent inflammation in RA. Suppression of monocytes/macrophages in RA joints or blockade of the primate-specific activating FcγRIIa receptor might be ways to reduce IC-induced TNF-α production in the joints of seropositive RA patients.
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immune complexes from rheumatoid arthritis synovial fluid induce fcγriia dependent and rheumatoid factor correlated production of tumour necrosis factor α by peripheral blood mononuclear cells
Arthritis Research & Therapy, 2006Co-Authors: Linda Mathsson, Jon Lampa, Mohammed Mullazehi, Johan RönnelidAbstract:Immune complexes (ICs) can induce production of cytokines by peripheral blood mononuclear cells via Fc receptors. Rheumatoid factor (RF) develop in response to ICs in many clinical and experimental settings. We investigated whether and how polyethylene glycol (PEG) Precipitated ICs from rheumatoid arthritis (RA) sera and synovial fluid (SF) can influence cytokine production by peripheral blood mononuclear cells. We also examined the relationship between RF and IC induced cytokine production. Parallel sera and SF from 47 RA patients and sera from 15 healthy control individuals were PEG Precipitated. The Precipitates were added to serum-free peripheral blood mononuclear cell cultures and tumour necrosis factor (TNF)-α levels were measured after 20 hours. In separate cell culture experiments FcγRIIa and FcγRIII were blocked and monocytes were depleted or enriched. RF in serum was determined by nephelometry, and IgG levels in Precipitates and anti-cyclic citrullinated peptide antibodies in serum were measured using ELISA. Clinical data were collected from the patients' charts. In two separate investigations, we demonstrated a correlation between RF, PEG-Precipitated IgG levels and induction of the proinflammatory cytokine TNF-α by PEG-Precipitated SF ICs. No such correlation was found for serum ICs. TNF-α levels induced by SF Precipitates, but not serum Precipitates, correlated with the number of swollen and tender joints. Monocytes/macrophages were shown to be the main responder cells, and blockade of FcγRIIa, but not blockade of FcγRIII, inhibited TNF-α production in cultures stimulated with Precipitated ICs. Anti-cyclic citrullinated peptide correlated with RF but exhibited no association with IgG content in PEG Precipitates or with Precipitate-induced TNF-α levels. These findings support the hypothesis that SF ICs and correlated RF production are directly linked to cytokine-dependent inflammation in RA. Suppression of monocytes/macrophages in RA joints or blockade of the primate-specific activating FcγRIIa receptor might be ways to reduce IC-induced TNF-α production in the joints of seropositive RA patients.
Jon Lampa - One of the best experts on this subject based on the ideXlab platform.
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Immune complexes from rheumatoid arthritis synovial fluid induce FcγRIIa dependent and rheumatoid factor correlated production of tumour necrosis factor-α by peripheral blood mononuclear cells
Arthritis Research & Therapy, 2006Co-Authors: Linda Mathsson, Jon Lampa, Mohammed Mullazehi, Johan RönnelidAbstract:Immune complexes (ICs) can induce production of cytokines by peripheral blood mononuclear cells via Fc receptors. Rheumatoid factor (RF) develop in response to ICs in many clinical and experimental settings. We investigated whether and how polyethylene glycol (PEG) Precipitated ICs from rheumatoid arthritis (RA) sera and synovial fluid (SF) can influence cytokine production by peripheral blood mononuclear cells. We also examined the relationship between RF and IC induced cytokine production. Parallel sera and SF from 47 RA patients and sera from 15 healthy control individuals were PEG Precipitated. The Precipitates were added to serum-free peripheral blood mononuclear cell cultures and tumour necrosis factor (TNF)-α levels were measured after 20 hours. In separate cell culture experiments FcγRIIa and FcγRIII were blocked and monocytes were depleted or enriched. RF in serum was determined by nephelometry, and IgG levels in Precipitates and anti-cyclic citrullinated peptide antibodies in serum were measured using ELISA. Clinical data were collected from the patients' charts. In two separate investigations, we demonstrated a correlation between RF, PEG-Precipitated IgG levels and induction of the proinflammatory cytokine TNF-α by PEG-Precipitated SF ICs. No such correlation was found for serum ICs. TNF-α levels induced by SF Precipitates, but not serum Precipitates, correlated with the number of swollen and tender joints. Monocytes/macrophages were shown to be the main responder cells, and blockade of FcγRIIa, but not blockade of FcγRIII, inhibited TNF-α production in cultures stimulated with Precipitated ICs. Anti-cyclic citrullinated peptide correlated with RF but exhibited no association with IgG content in PEG Precipitates or with Precipitate-induced TNF-α levels. These findings support the hypothesis that SF ICs and correlated RF production are directly linked to cytokine-dependent inflammation in RA. Suppression of monocytes/macrophages in RA joints or blockade of the primate-specific activating FcγRIIa receptor might be ways to reduce IC-induced TNF-α production in the joints of seropositive RA patients.
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immune complexes from rheumatoid arthritis synovial fluid induce fcγriia dependent and rheumatoid factor correlated production of tumour necrosis factor α by peripheral blood mononuclear cells
Arthritis Research & Therapy, 2006Co-Authors: Linda Mathsson, Jon Lampa, Mohammed Mullazehi, Johan RönnelidAbstract:Immune complexes (ICs) can induce production of cytokines by peripheral blood mononuclear cells via Fc receptors. Rheumatoid factor (RF) develop in response to ICs in many clinical and experimental settings. We investigated whether and how polyethylene glycol (PEG) Precipitated ICs from rheumatoid arthritis (RA) sera and synovial fluid (SF) can influence cytokine production by peripheral blood mononuclear cells. We also examined the relationship between RF and IC induced cytokine production. Parallel sera and SF from 47 RA patients and sera from 15 healthy control individuals were PEG Precipitated. The Precipitates were added to serum-free peripheral blood mononuclear cell cultures and tumour necrosis factor (TNF)-α levels were measured after 20 hours. In separate cell culture experiments FcγRIIa and FcγRIII were blocked and monocytes were depleted or enriched. RF in serum was determined by nephelometry, and IgG levels in Precipitates and anti-cyclic citrullinated peptide antibodies in serum were measured using ELISA. Clinical data were collected from the patients' charts. In two separate investigations, we demonstrated a correlation between RF, PEG-Precipitated IgG levels and induction of the proinflammatory cytokine TNF-α by PEG-Precipitated SF ICs. No such correlation was found for serum ICs. TNF-α levels induced by SF Precipitates, but not serum Precipitates, correlated with the number of swollen and tender joints. Monocytes/macrophages were shown to be the main responder cells, and blockade of FcγRIIa, but not blockade of FcγRIII, inhibited TNF-α production in cultures stimulated with Precipitated ICs. Anti-cyclic citrullinated peptide correlated with RF but exhibited no association with IgG content in PEG Precipitates or with Precipitate-induced TNF-α levels. These findings support the hypothesis that SF ICs and correlated RF production are directly linked to cytokine-dependent inflammation in RA. Suppression of monocytes/macrophages in RA joints or blockade of the primate-specific activating FcγRIIa receptor might be ways to reduce IC-induced TNF-α production in the joints of seropositive RA patients.
Mohammed Mullazehi - One of the best experts on this subject based on the ideXlab platform.
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Immune complexes from rheumatoid arthritis synovial fluid induce FcγRIIa dependent and rheumatoid factor correlated production of tumour necrosis factor-α by peripheral blood mononuclear cells
Arthritis Research & Therapy, 2006Co-Authors: Linda Mathsson, Jon Lampa, Mohammed Mullazehi, Johan RönnelidAbstract:Immune complexes (ICs) can induce production of cytokines by peripheral blood mononuclear cells via Fc receptors. Rheumatoid factor (RF) develop in response to ICs in many clinical and experimental settings. We investigated whether and how polyethylene glycol (PEG) Precipitated ICs from rheumatoid arthritis (RA) sera and synovial fluid (SF) can influence cytokine production by peripheral blood mononuclear cells. We also examined the relationship between RF and IC induced cytokine production. Parallel sera and SF from 47 RA patients and sera from 15 healthy control individuals were PEG Precipitated. The Precipitates were added to serum-free peripheral blood mononuclear cell cultures and tumour necrosis factor (TNF)-α levels were measured after 20 hours. In separate cell culture experiments FcγRIIa and FcγRIII were blocked and monocytes were depleted or enriched. RF in serum was determined by nephelometry, and IgG levels in Precipitates and anti-cyclic citrullinated peptide antibodies in serum were measured using ELISA. Clinical data were collected from the patients' charts. In two separate investigations, we demonstrated a correlation between RF, PEG-Precipitated IgG levels and induction of the proinflammatory cytokine TNF-α by PEG-Precipitated SF ICs. No such correlation was found for serum ICs. TNF-α levels induced by SF Precipitates, but not serum Precipitates, correlated with the number of swollen and tender joints. Monocytes/macrophages were shown to be the main responder cells, and blockade of FcγRIIa, but not blockade of FcγRIII, inhibited TNF-α production in cultures stimulated with Precipitated ICs. Anti-cyclic citrullinated peptide correlated with RF but exhibited no association with IgG content in PEG Precipitates or with Precipitate-induced TNF-α levels. These findings support the hypothesis that SF ICs and correlated RF production are directly linked to cytokine-dependent inflammation in RA. Suppression of monocytes/macrophages in RA joints or blockade of the primate-specific activating FcγRIIa receptor might be ways to reduce IC-induced TNF-α production in the joints of seropositive RA patients.
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immune complexes from rheumatoid arthritis synovial fluid induce fcγriia dependent and rheumatoid factor correlated production of tumour necrosis factor α by peripheral blood mononuclear cells
Arthritis Research & Therapy, 2006Co-Authors: Linda Mathsson, Jon Lampa, Mohammed Mullazehi, Johan RönnelidAbstract:Immune complexes (ICs) can induce production of cytokines by peripheral blood mononuclear cells via Fc receptors. Rheumatoid factor (RF) develop in response to ICs in many clinical and experimental settings. We investigated whether and how polyethylene glycol (PEG) Precipitated ICs from rheumatoid arthritis (RA) sera and synovial fluid (SF) can influence cytokine production by peripheral blood mononuclear cells. We also examined the relationship between RF and IC induced cytokine production. Parallel sera and SF from 47 RA patients and sera from 15 healthy control individuals were PEG Precipitated. The Precipitates were added to serum-free peripheral blood mononuclear cell cultures and tumour necrosis factor (TNF)-α levels were measured after 20 hours. In separate cell culture experiments FcγRIIa and FcγRIII were blocked and monocytes were depleted or enriched. RF in serum was determined by nephelometry, and IgG levels in Precipitates and anti-cyclic citrullinated peptide antibodies in serum were measured using ELISA. Clinical data were collected from the patients' charts. In two separate investigations, we demonstrated a correlation between RF, PEG-Precipitated IgG levels and induction of the proinflammatory cytokine TNF-α by PEG-Precipitated SF ICs. No such correlation was found for serum ICs. TNF-α levels induced by SF Precipitates, but not serum Precipitates, correlated with the number of swollen and tender joints. Monocytes/macrophages were shown to be the main responder cells, and blockade of FcγRIIa, but not blockade of FcγRIII, inhibited TNF-α production in cultures stimulated with Precipitated ICs. Anti-cyclic citrullinated peptide correlated with RF but exhibited no association with IgG content in PEG Precipitates or with Precipitate-induced TNF-α levels. These findings support the hypothesis that SF ICs and correlated RF production are directly linked to cytokine-dependent inflammation in RA. Suppression of monocytes/macrophages in RA joints or blockade of the primate-specific activating FcγRIIa receptor might be ways to reduce IC-induced TNF-α production in the joints of seropositive RA patients.
Tonio Buonassisi - One of the best experts on this subject based on the ideXlab platform.
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analyses of the evolution of iron silicide Precipitates in multicrystalline silicon during solar cell processing
IEEE Journal of Photovoltaics, 2013Co-Authors: Jonas Schon, Antti Haarahiltunen, Hele Savin, David P Fenning, Tonio Buonassisi, Wilhelm Warta, Martin C SchubertAbstract:We simulate the precipitation of iron during the multicrystalline ingot crystallization process and the redistribution of iron during subsequent phosphorus diffusion gettering with a 2-D model. We compare the simulated size distribution of the Precipitates with the X-ray fluorescence microscopy measurements of iron Precipitates along a grain boundary. We find that the simulated and measured densities of Precipitates larger than the experimental detection limit are in good agreement after the crystallization process. Additionally, we demonstrate that the measured decrease of the line density and the increase of the mean size of the iron Precipitates after phosphorus diffusion gettering can be reproduced with the simulations. The size and spatial distribution of iron Precipitates affect the kinetics of iron redistribution during the solar cell process and, ultimately, the recombination activity of the Precipitated iron. Variations of the cooling rate after solidification and short temperature peaks before phosphorus diffusion strongly influence the Precipitate size distribution. The lowest overall density of iron Precipitates after phosphorus diffusion is obtained in the simulations with a temperature peak before phosphorus diffusion, followed by moderate cooling rates.
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Engineering metal Precipitate size distributions to enhance gettering in multicrystalline silicon
physica status solidi (a), 2012Co-Authors: Jasmin Hofstetter, David P Fenning, Jean-françois Lelièvre, Carlos Del Cañizo, Tonio BuonassisiAbstract:The extraction of metal impurities during phosphorus diffusion gettering (PDG) is one of the crucial process steps when fabricating high-efficiency solar cells using low-cost, lower-purity silicon wafers. In this work, we show that for a given metal concentration, the size and density of metal silicide Precipitates strongly influences the gettering efficacy. Different Precipitate size distributions can be already found in silicon wafers grown by different techniques. In our experiment, however, the as-grown distribution of Precipitated metals in multicrystalline Si sister wafers is engineered through different annealing treatments in order to control for the concentration and distribution of other defects. A high density of small Precipitates is formed during a homogenization step, and a lower density of larger Precipitates is formed during extended annealing at 740o C. After PDG, homogenized samples show a decreased interstitial iron concentration compared to as-grown and ripened samples, in agreement with simulations.
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iron distribution in silicon after solar cell processing synchrotron analysis and predictive modeling
Applied Physics Letters, 2011Co-Authors: David P Fenning, Jasmin Hofstetter, Jean-françois Lelièvre, Carlos Del Cañizo, Mariana I Bertoni, Steve Hudelson, Markus Rinio, Barry Lai, Tonio BuonassisiAbstract:The evolution during silicon solar cell processing of performance-limiting iron impurities is investigated with synchrotron-based x-ray fluorescence microscopy. We find that during industrial phosphorus diffusion, bulk Precipitate dissolution is incomplete in wafers with high metal content, specifically ingot border material. Postdiffusion low-temperature annealing is not found to alter appreciably the size or spatial distribution of FeSi2 Precipitates, although cell efficiency improves due to a decrease in iron interstitial concentration. Gettering simulations successfully model experiment results and suggest the efficacy of high- and low-temperature processing to reduce both Precipitated and interstitial iron concentrations, respectively.
