bluuebunny/crossref_metadata_2025_split huggingface dataset:
Translational Mini-Review Series on Th17 Cells: Induction of interleukin-17 production by regulatory T cells
Authors: Afzali B , Mitchell P , Lechler R I , John S , Lombardi G 
Published: November 2009

AbstractOTHER ARTICLES PUBLISHED IN THIS MINI-REVIEW SERIES ON Th17 CELLS&#x2028;Function and regulation of human T helper 17 cells in health and disease. Clin Exp Immunol 2009; doi:10.1111/j.1365-2249.2009.04037.x&#x2028;Are T helper 17 cells really pathogenic in autoimmunity? Clin Exp Immunol 2009; doi:10.1111/j.1365-2249.2009.04039.x&#x2028;CD4+ T helper cells: functional plasticity and differential sensitivity to regulatory T cell-mediated regulation. Clin Exp Immunol 2009; doi:10.1111/j.1365-2249.2009.04040.x&#x2028;Development of mouse and human T helper 17 cells. Clin Exp Immunol 2009; doi:10.1111/j.1365-2249.2009.04041.xSummaryUncommitted (naive) CD4+ T helper cells (Thp) can be induced to differentiate to specific lineages according to the local cytokine milieu, towards T helper type 1 (Th1), Th2, Th17 and regulatory T cell (Treg) phenotypes in a mutually exclusive manner. Each phenotype is characterized by unique signalling pathways and expression of specific transcription factors, notably T-bet for Th1, GATA-3 for Th2, forkhead box P3 (FoxP3) for Tregs and receptor-related orphan receptor (ROR)α and RORγt for Th17 cells. Tregs and Th17 cells have been demonstrated to arise from common precursors in a reciprocal manner based on exposure to transforming growth factor (TGF)-β or TGF-β plus interleukin (IL)-6 and carry out diametrically opposing functions, namely suppression or propagation of inflammation, respectively. However, while epigenetic modifications in Th1 and Th2 differentiated cells prevents their conversion to other phenotypes, Th17 cells generated in vitro using TGF-β and IL-6 are unstable and can convert to other phenotypes, especially Th1, both in vitro and in vivo. Tregs are generated from naive precursors both in the thymus (natural, nTregs) and in the periphery (induced, iTregs). The highly suppressive function of Tregs enables them to control many inflammatory diseases in animals and makes them particularly attractive candidates for immunotherapy in humans. The stability of the Treg phenotype is therefore of paramount importance in this context. Recent descriptions of Treg biology have suggested that components of pathogens or inflammatory mediators may subvert the suppressive function of Tregs in order to allow propagation of adequate immune responses. Unexpectedly, however, a number of groups have now described conversion of Tregs to the Th17 phenotype induced by appropriate inflammatory stimuli. These observations are particularly relevant in the context of cell therapy but may also explain some of the dysregulation seen in autoimmune diseases. In this paper, we review Treg to Th17 conversion and propose some potential mechanisms for this phenomenon.
Translational Mini-Review Series on Th17 Cells: Are T helper 17 cells really pathogenic in autoimmunity?
Authors: Koenders M I , Van Den Berg W B 
Published: November 2009

AbstractOTHER ARTICLES PUBLISHED IN THIS MINI-REVIEW SERIES ON Th17 CELLS&#x2028;Function and regulation of human T helper 17 cells in health and disease. Clin Exp Immunol 2009; doi:10.1111/j.1365-2249.2009.04037.x&#x2028;Induction of interleukin-17 production by regulatory T cells. Clin Exp Immunol 2009; doi:10.1111/j.1365-2249.2009.04038.x&#x2028;CD4+ T helper cells: functional plasticity and differential sensitivity to regulatory T cell-mediated regulation. Clin Exp Immunol 2009; doi:10.1111/j.1365-2249.2009.04040.x&#x2028;Development of mouse and human T helper 17 cells. Clin Exp Immunol 2009; doi:10.1111/j.1365-2249.2009.04041.xSummaryIn this review the authors discuss the evidence for T helper type 17 (Th17) cells as pathogenic T cells in autoimmunity. Studies with cytokine-deficient mice or blocking of interleukin (IL)-17, IL-21 and IL-22 have resulted in a conflicting data set. Although in the experimental autoimmune encephalomyelitis model the role of Th17 cells remains a point of debate, this IL-17-producing T cell in experimental arthritis is clearly contributing to inflammation and destruction.
Translational Mini-Review Series on Th17 Cells: CD4+ T helper cells: functional plasticity and differential sensitivity to regulatory T cell-mediated regulation
Authors: O'Connor R A , Taams L S , Anderton S M 
Published: November 2009

AbstractOTHER ARTICLES PUBLISHED IN THIS MINI-REVIEW SERIES ON Th17 CELLS&#x2028;Function and regulation of human T helper 17 cells in health and disease. Clin Exp Immunol 2009; doi:10.1111/j.1365-2249.2009.04037.x&#x2028;Induction of interleukin-17 production by regulatory T cells. Clin Exp Immunol 2009; doi:10.1111/j.1365-2249.2009.04038.x&#x2028;Are T helper 17 cells really pathogenic in autoimmunity? Clin Exp Immunol 2009; doi:10.1111/j.1365-2249.2009.04039.x&#x2028;Development of mouse and human T helper 17 cells. Clin Exp Immunol 2009; doi:10.1111/j.1365-2249.2009.04041.xSummaryCD4+ T cells display considerable flexibility in their effector functions, allowing them to tackle most effectively the range of pathogenic infections with which we are challenged. The classical T helper (Th) 1 and Th2 subsets have been joined recently by the Th17 lineage. If not controlled, the potent effector functions (chiefly cytokine production) of which these different cells are capable can lead to (sometimes fatal) autoimmune and allergic inflammation. The primary cell population tasked with providing this control appears to be CD4+ regulatory T (Treg) cells expressing the forkhead box P3 (FoxP3) transcription factor. Here we consider the comparative capacity of FoxP3+ Tregs to influence the polarization, expansion and effector function of Th1, Th2 and Th17 cells in vitro and in vivo as well as in relation to human disease. This remains a particularly challenging series of interactions to understand, especially given our evolving understanding of Treg and T effector interrelationships, as well as recent insights into functional plasticity that cast doubt upon the wisdom of a strict categorization of T effector cells based on cytokine production.
Translational Mini-Review Series on Th17 Cells: Development of mouse and human T helper 17 cells
Authors: De Jong E , Suddason T , Lord G M 
Published: November 2009

AbstractOTHER ARTICLES PUBLISHED IN THIS MINI-REVIEW SERIES ON Th17 CELLS&#x2028;Function and regulation of human T helper 17 cells in health and disease. Clin Exp Immunol 2009; doi:10.1111/j.1365-2249.2009.04037.x&#x2028;Induction of interleukin-17 production by regulatory T cells. Clin Exp Immunol 2009; doi:10.1111/j.1365-2249.2009.04038.x&#x2028;Are T helper 17 cells really pathogenic in autoimmunity? Clin Exp Immunol 2009; doi:10.1111/j.1365-2249.2009.04039.x&#x2028;CD4+ T helper cells: functional plasticity and differential sensitivity to regulatory T cell-mediated regulation. Clin Exp Immunol 2009; doi:10.1111/j.1365-2249.2009.04040.xSummaryThere has been a considerable amount of interest in the immunological community about new phenotypic subsets of CD4+ T cells, particularly cells that produce the cytokine interleukin (IL)-17 [named T helper type 17 (Th17) cells]. While the initial discovery of Th17 cells and the pathways that controlled their development was in the mouse, recent attention has shifted to the existence of these cells and the relevant upstream cytokine signals in humans. While it is clear that CD4+ T cells producing IL-17 exist in vivo, their relevance to disease pathogenesis is only just being understood. In this paper, we review the data regarding the generation of human Th17 cells in vitro and the evidence that this effector population is important in human disease states.
Recipient NOD2/CARD15 status affects cellular infiltrates in human intestinal graft-versus-host disease
Authors: Landfried K , Bataille F , Rogler G , Brenmoehl J , Kosovac K , Wolff D , Hilgendorf I , Hahn J , Edinger M , Hoffmann P , Obermeier F , Schoelmerich J , Andreesen R , Holler E 
Published: November 2009

Summary
Nucleotide-binding oligomerization domain 2/caspase recruitment domain 15 (NOD2/CARD15) polymorphisms have been identified as risk factors of both Crohn's disease and graft-versus-host disease (GVHD) following allogeneic stem cell transplantation. However, the role of these receptors of innate immunity in the pathophysiology of gastrointestinal GVHD is still poorly defined. Immunohistological features of intestinal GVHD were analysed in gastrointestinal biopsies from 58 patients obtained at the time of first onset of intestinal symptoms. The observed changes were correlated with concomitant risk factors and the presence of polymorphisms within the pathogen recognition receptor gene NOD2/CARD15. Intestinal GVHD was associated with a stage-dependent decrease in CD4 T cell infiltrates and an increase in CD8 T cells in the lamina propria; CD8 infiltrates correlated with extent of apoptosis and consecutive epithelial proliferation. The presence of NOD2/CARD15 variants in the recipient was associated with a significant loss of CD4 T cells: in a semiquantitative analysis, the median CD4 score for patients with wild-type NOD2/CARD15 was 1·1 (range 3), but only 0·4 (range 2) for patients with variants (P = 0·002). This observation was independent from severity of GVHD in multivariate analyses and could not be explained by the loss of forkhead box P3+ T cells. Our results suggest a loss of protective CD4 T cells in intestinal GVHD which is enhanced further by the presence of NOD2/CARD15 variants. Our study might help to identify more selective therapeutic strategies in the future.
Gene expression profiles for the human pancreas and purified islets in Type 1 diabetes: new findings at clinical onset and in long-standing diabetes
Authors: Planas R , Carrillo J , Sanchez A , Ruiz de Villa M C , Nuñez F , Verdaguer J , James R F L , Pujol-Borrell R , Vives-Pi M 
Published: November 2009

SummaryType 1 diabetes (T1D) is caused by the selective destruction of the insulin-producing β cells of the pancreas by an autoimmune response. Due to ethical and practical difficulties, the features of the destructive process are known from a small number of observations, and transcriptomic data are remarkably missing. Here we report whole genome transcript analysis validated by quantitative reverse transcription–polymerase chain reaction (qRT–PCR) and correlated with immunohistological observations for four T1D pancreases (collected 5 days, 9 months, 8 and 10 years after diagnosis) and for purified islets from two of them. Collectively, the expression profile of immune response and inflammatory genes confirmed the current views on the immunopathogenesis of diabetes and showed similarities with other autoimmune diseases; for example, an interferon signature was detected. The data also supported the concept that the autoimmune process is maintained and balanced partially by regeneration and regulatory pathway activation, e.g. non-classical class I human leucocyte antigen and leucocyte immunoglobulin-like receptor, subfamily B1 (LILRB1). Changes in gene expression in islets were confined mainly to endocrine and neural genes, some of which are T1D autoantigens. By contrast, these islets showed only a few overexpressed immune system genes, among which bioinformatic analysis pointed to chemokine (C-C motif) receptor 5 (CCR5) and chemokine (CXC motif) receptor 4) (CXCR4) chemokine pathway activation. Remarkably, the expression of genes of innate immunity, complement, chemokines, immunoglobulin and regeneration genes was maintained or even increased in the long-standing cases. Transcriptomic data favour the view that T1D is caused by a chronic inflammatory process with a strong participation of innate immunity that progresses in spite of the regulatory and regenerative mechanisms.
Serum insulin‐like growth factor‐I and body composition in community dwelling older people
Authors: Jakobsdóttir Sigridur , Caroline van Nieuwpoort I. , Schaap Laura A. , Van Schoor Natasja M. , Lips Paul , Drent Madeleine L. 
Published: November 2009

SummaryObjectives The decline in the growth hormone/insulin‐like growth factor‐I (GH/IGF‐I) axis during normal aging might be involved in the changes in body composition associated with increasing age. We conducted a study to investigate serum IGF‐I levels across different age categories and a possible association between serum IGF‐I and measurements of body composition in older people.Design A cross‐sectional analysis of community dwelling older people, which participated in a large longitudinal cohort study (Longitudinal Aging Study Amsterdam).Subjects 1319 subjects, 644 men, mean age 75·6 ± 6·6 years and 675 women, mean age 75·4 ± 6·6 years.Main Outcome Measurements IGF‐I, body mass index (BMI), waist, waist‐hip ratio (WHR), fat mass, lean body mass and total bone mineral density.Results IGF‐I levels were significantly lower in the highest age categories. BMI and biceps skinfold measurements were lower in the lowest IGF‐I quartile in men aged ≥75·5 years. In men with a low total physical activity score (<131 min/day), BMI, WHR and skinfolds were significantly lower in the lowest IGF‐I quartile. In women with a high total physical activity score (>174 min/day), WHR was lower in the lowest IGF‐I quartiles.Conclusion In this large cohort of community dwelling older people, we observed lower serum IGF‐I levels in the higher age categories. A low serum IGF‐I was associated with significantly lower measurements of body composition, such as BMI, skinfolds and WHR. These results do not support previous findings that high IGF‐I levels are favourable for a healthy body composition in community dwelling older people.
Characterization of thyroglobulin epitopes in Sardinian adults and juveniles with Hashimoto’s thyroiditis: evidence against a major effect of age and genetic background on B‐cell epitopes
Authors: Latrofa Francesco , Ricci Debora , Vitti Paolo , Prinzis Alessia , Cambuli Valentina Maria , Ghiani Mariangela , Pilia Sabrina , Carta Daniela , Loche Sandro , Pinchera Aldo , Mariotti Stefano 
Published: November 2009

SummaryBackground  Using recombinant human monoclonal thyroglobulin antibodies expressed as Fab molecules (TgAb‐Fab), we have recently confirmed the restriction of Tg epitopes in Hashimoto’s thyroiditis (HT).Objective  To investigate Tg epitopes of serum TgAb in HT adults and HT juveniles from a geographically isolated area (Sardinia).Design and Patients  Serum TgAb of 39 Sardinian HT adults, 53 Sardinian HT juveniles and 45 non‐Sardinian HT adults were evaluated. The binding of serum TgAb to Tg in ELISA was inhibited by four recombinant human TgAb‐Fab, identifying Tg epitopic regions A–D. The percentage of Tg binding inhibition was calculated comparing the binding of serum TgAb in presence of each TgAb‐Fab with that in its absence.Results  In the whole cohort of 137 patients, A region TgAb‐Fab induced the highest levels of inhibition (55·3 ± 17·8%) (mean ± SD). Lower levels of inhibition were induced by TgAb‐Fab of regions B (27·8 ± 25·8%), C (26·8 ± 24·6%) and D (17·5 ± 18·4%). In Sardinian HT adults inhibition by TgAb‐Fab of regions A, B and C were comparable to Sardinian HT juveniles; the marginal D region TgAb‐Fab induced a slightly higher inhibition (22·1 vs. 13·8%; P = 0·034) in the former than in the latter group. In Sardinian and non‐Sardinian HT adults inhibitions by the four TgAb‐Fab were similar.Conclusions  In HT, the Tg epitope pattern of serum TgAb was similar in juveniles and adults from a geographically restricted area and in two adult populations from different geographical areas. Thus, in HT, neither age nor genetic background appear to influence B‐cell epitopes.
Urinary L‐FABP and anaemia: distinct roles of urinary markers in type 2 diabetes
Authors: Von Eynatten M. , Baumann M. , Heemann U. , Zdunek D. , Hess G. , Nawroth P. P. , Bierhaus A. , Humpert P. M. 
Published: November 2009

Eur J Clin Invest 2010; 40 (2): 95–102AbstractBackground  Urinary liver‐type fatty acid binding protein (L‐FABP) and kidney injury molecule (KIM)‐1, novel urinary biomarkers of renal tubulointerstitial function, have previously been associated with acute ischaemic kidney injury. We studied the clinical significance of urinary L‐FABP, KIM‐1 and N‐acetyl‐β‐glucosaminidase (NAG) as potential markers of renal function and chronic ischaemic injury in patients with diabetic nephropathy.Material and methods  A total of 130 type 2 diabetes patients with early diabetic nephropathy and 40 healthy controls were studied. Urinary L‐FABP, KIM‐1, NAG, albumin excretion rate (AER) and creatinine clearance were obtained from 24‐h urine samples, and correlated with measures of red blood cell count, renal function and metabolic control.Results  Urinary L‐FABP was significantly increased in diabetes patients compared with healthy controls [8·1 (interquartile 0·6–11·6) vs. 2·4 (0·5–3·6) μg/g creatinine, P < 0·001] and correlated with AER (r = 0·276, P = 0·002), creatinine clearance (r = −0·189, P = 0·033) and haemoglobin levels (r = −0·190, P = 0·030). In multivariable linear regression analysis, haemoglobin (β = −0·247, P = 0·015) and AER (β = 0·198, P = 0·046) were significant predictors of urinary L‐FABP. Prevalent anaemia was independently associated with a 6‐fold risk for increased tubulointerstitial kidney damage (upper vs. lower two L‐FABP tertiles: OR, 6·06; 95% CI: 1·65–22·23; P = 0·007). Urinary KIM‐1 was not significantly associated with kidney function, AER, or measures of red blood cell count while urinary NAG was associated with parameters of glucose control and renal function.Conclusions  Different urinary biomarkers may reflect distinct pathophysiological mechanisms of tubulointerstitial damage in early diabetic nephropathy: Urinary L‐FABP could be a novel biomarker for chronic intrarenal ischaemia.
A micro‐computed tomographic evaluation of apical root canal preparation using three instrumentation techniques
Authors: Moore J. , Fitz‐Walter P. , Parashos P. 
Published: November 2009

AbstractAim  To investigate the morphological changes in the apical third of the root canal after preparation with three techniques.Methodology  Forty molar teeth were scanned using micro‐computed tomography before and after instrumentation with: Group 1 – stainless steel K‐files using the balanced force technique; Group 2 – stainless steel K‐files (balanced force) and then refining the apical preparation with the equivalent size 0.04 taper FlexMaster instrument; Group 3 – a hybrid ProTaper/FlexMaster (ProFile for sizes 45 and 60) sequence. Eight canals were excluded because of artefacts in the images or unnegotiable blockages leaving 110 canals that could be analysed. Apical root canal preparation was evaluated with respect to the amount of dentine removed, canal roundness, transportation and how the dimensions of the prepared apical root canal correlated with those of the final instrument used.Results  The median apical preparation sizes for the three groups respectively were: 30, 30 and 40. Despite the larger size and less experienced operator, the volumetric change (the amount of dentine removed) in canals prepared with a hybrid rotary nickel–titanium instrumentation technique remained small and, a more rounded preparation (P < 0.001) that closely matched the final instrument dimensions (P < 0.001) was produced. There was a trend for less canal transportation using rotary nickel–titanium instruments.Conclusions  Stainless steel hand preparation was not conservative of apical dentine. When used correctly, even by less experienced operators, rotary nickel–titanium instruments were able to precisely ‘machine’ a canal to larger apical sizes with minimal risk of iatrogenic damage.
Distance from file tip to the major apical foramen in relation to the numeric meter reading on the display of three different electronic apex locators
Authors: Higa R. A. , Adorno C. G. , Ebrahim A. K. , Suda H. 
Published: November 2009

AbstractAim  To establish and compare the relationship between the distance from the file tip to the apical foramen and the numeric meter reading on the display of three different electronic apex locators (EALs).Methodology  A total of 12 extracted intact, straight, single‐rooted human teeth with complete roots were used. The actual root canal length (AL) was determined after access preparation. For the electronic measurements with each EAL, silicon stops were fixed with auto‐polymerizing resin to size 15 K‐files at AL and 0.5, 1, 2, 3, 4 mm short of AL. The data was analysed by two‐way anova and Tukey’s honestly significant difference (HSD) test for multiple comparisons amongst EALs. Additionally, one‐way anova and Tukey’s HSD test were carried out for multiple comparisons amongst the measurements of each EAL.Results  There was a statistically significant difference amongst all EALs in indicating the position of file tips in relation to the major foramen (P < 0.05). The correlation between the meter reading and the position of the file tip from the apical foramen was statistically significant in the three EALs. There were significant differences amongst the measurements at distances from 0 to 2 mm in Justy III. In Dentaport, significant differences were found from 0 to 1 mm. However, the E‐Magic Finder showed significant differences from 0 to 0.5 mm.Conclusions  Justy III was more capable of displaying the intracanal position of the file tip from the major foramen in mm whilst advancing through the root canal during electronic measurements than the Dentaport and E‐Magic Finder Deluxe.
Micro‐computed tomography of tooth tissue volume changes following endodontic procedures and post space preparation
Authors: Ikram O. H. , Patel S. , Sauro S. , Mannocci F. 
Published: November 2009

AbstractAim  To compare the volume of hard tooth tissue lost after caries removal, access cavity preparation, root canal preparation, fibre post space and cast post preparation in carious premolar teeth. The null hypothesis tested was that there is no difference between the volumes of hard tooth tissue lost expressed as a percentage of the preoperative hard tooth tissue volume, after each operative procedure.Methodology  Twelve extracted human premolars with mesial or distal carious cavities penetrating into the pulp chamber were selected. Teeth were scanned using a microCT scanner. After each operative procedure the loss of hard tooth tissue volume was measured. The data were statistically analysed using one‐way analysis of variance and Fisher’s PLSD test with statistical significance set at α = 0.01.Results  The percentage of preoperative hard tooth tissue volume lost after caries removal was 8.3 ± 5.83, after access cavity preparation the loss of volume reached 12.7 ± 6.7% (increase of 4.4%). After root canal preparation, fibre post space and cast post preparation the hard tissue volume lost reached, 13.7 ± 6.7 (increase of 1%), 15.1 ± 6.3 (increase of 1.4%) and 19.2 ± 7.4 (increase of 4.1%) respectively. Each procedure performed after caries removal significantly increased (P < 0.01) the amount of hard tissue volume lost with the exception of the root canal preparation.Conclusions  Access cavity and post space preparation are the procedures during root canal treatment which result in the largest loss of hard tooth tissue structure. Cast post space preparation causes a larger loss of tooth structure than fibre post space preparation. This should be taken into account when planning root canal treatment and restoration of root filled teeth that are to be restored with cuspal coverage restorations.