-
[show abstract]
[hide abstract]
ABSTRACT: A histopathological classification system for ANCA-associated vasculitis was recently published, but whether this system predicts renal outcome requires validation. Here, we analyzed data from 164 consecutive patients with biopsy-proven renal involvement of ANCA-associated vasculitis. The ANCA-associated GN (AGN) classification categorizes patients as having focal, mixed, crescentic, or sclerotic GN. Five-year renal survival rates by categories of the AGN classification scheme were 91% for focal, 69% for mixed, and 64% for crescentic (log-rank P<0.0001). Only one patient was classified as sclerotic. Furthermore, the percentage of normal glomeruli found on biopsy estimated renal survival with the same precision as did the AGN classification scheme. Patients classified as crescentic or mixed, however, had worse survival when the percentage of normal glomeruli was <25%. In conclusion, the AGN classification for renal biopsy specimens is a practical and informative scheme with which to categorize patients
Journal of the American Society of Nephrology. 06/2013;
-
[show abstract]
[hide abstract]
ABSTRACT: OBJECTIVES: To investigate the nature of the relationship between proteinase 3 anti-neutrophil cytoplasm autoantibody (PR3-ANCA) and relapse in patients with early systemic granulomatosis with polyangiitis (Wegener's) (GPA).METHODS: Clinical data from 16 relapsing and 12 non-relapsing patients with early systemic GPA from a randomised clinical trial were correlated to monthly PR3-ANCA values over 18 months. Each sample was examined using 9 different enzyme-linked immunosorbent assays (ELISAs) to ensure reliability of ANCA results. PR3-ANCA peaks were identified by the highest sum of logarithmic transformation values from all assays in samples after remission. RESULTS: A PR3-ANCA peak was identified in all relapsing and non-relapsing patients and coincided with relapse in all 14 evaluable relapsing patients. The monthly increment before the peak, however, was similar in relapsing and non-relapsing patients in all assays. Increments from remission to peak were higher in relapsing patients in 2/9 assays. PR3-ANCA values at entry and peak PR3-ANCA values were higher in relapsing patients in 3/9 and 2/9 assays, respectively. However, large overlaps of PR3-ANCA values prevented a distinction between relapsing and non-relapsing patients. The median time to reach peak values was 14 months in relapsing and 12 months in non-relapsing patients with scheduled termination of treatment at 12 months. CONCLUSIONS: The predictive value for relapses of PR3-ANCA determinations confirm and extend previous reports. Although all relapses were related to PR3-ANCA increases, reduction or withdrawal of immunosuppression without relapse was also related to increases and may explain the lack of predictive value of sequential PR3-ANCA determinations.
Clinical and experimental rheumatology 02/2013; · 2.15 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Background
Anti-neutrophil cytoplasmic antibody (ANCA)-associated glomerulonephritis has a poor prognosis. In the current study, we assessed whether prognosis in these patients improved over the last three decades.Methods
In a large inception cohort, all consecutive patients with ANCA-associated glomerulonephritis were included between January 1979 and December 2009. Inclusion criteria were the presence of ANCA and the availability of a kidney biopsy. To assess renal and patient survival, patients were divided in three groups through time: 1979-89, 1990-2000 and 2001-09.ResultsA total of 181 patients were included. One-, 5- and 10-year survival was 77, 66 and 49%, respectively. Survival within the time groups was significantly different, yielding a hazard ratio for death of 2.9 for 1990-2000 and 3.9 for 1979-89 compared with 2001-09 (P < 0.001). Serum creatinine and active lesions as found in the kidney biopsy significantly decreased through the three decades.Conclusions
Both patient and renal survival in patients with ANCA-associated renal vasculitis have improved over the last three decades. We postulate that both earlier diagnosis and better therapeutic management of patients are responsible for this effect.
Nephrology Dialysis Transplantation 12/2012; · 3.40 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Objective. The metabolic syndrome (MetS) is a cluster of cardiovascular risk factors and a major cause of morbidity and mortality in the western world. Despite the fact that cardiovascular diseases are a major cause of mortality in patients with ANCA-associated vasculitis (AAV), the relationship between MetS and AAV has not yet been explored. Thus it is the aim of this study to investigate the prevalence of MetS within a cohort of patients with AAV and to assess whether MetS in AAV is associated with a pro-inflammatory state.Methods. Ninety-one patients with AAV were compared with 89 healthy controls (HCs) in a cross-sectional study. Both groups underwent anthropometric measures and laboratory tests to determine the prevalence of MetS in accordance with the National Cholesterol Education Program Adults Treatment Panel III (NCEP-ATP-III) definitions. Furthermore, the clinical course of AAV was related to the occurrence of MetS.Results. Within the AAV patient group, 39 (43%) fulfilled the NCEP-ATP-III criteria for MetS compared with 22 (25%) of the controls (P = 0.012). This difference in prevalence could not be explained by current or cumulative prednisone use in patients with AAV. Among patients with AAV, the presence of MetS was significantly associated with increased levels of CRP and neopterin. Finally, the relapse rate was higher in patients with MetS as compared with those without MetS.Conclusion. The prevalence of MetS is significantly increased in AAV. MetS is associated with a more pro-inflammatory state in AAV and might increase the risk of developing a relapse of AAV.
Rheumatology (Oxford, England) 11/2012; · 4.24 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: INTRODUCTION: In autoimmune diseases, IL-17 producing T-cells (Th17), a pro-inflammatory subset of T-cells, are pathophysiologically involved. There is little knowledge on the role of Th17 cells in granulomatosis with polyangiitis (GPA). In the present study, we investigated Th17 cells, Tregs and subsets of circulating Th17 cells in GPA and related results to disease activity. METHODS: 42 GPA patients in remission, 18 with active disease and 14 healthy controls (HC) were enrolled. Th17 cells, their subsets and regulatory T-cells were determined by intracellular fluorescence activated cell sorter (FACS). Data is given as mean percentage +/-SD of total T-helper-cells . RESULTS: Th17 cells are expanded in active and quiescent GPA as compared to HC (1.7+/-1.4% vs. 0.7 +/-0.3%, P=0.006 and 1.9 +/-1.5% vs. 0.7 +/-0.3%, P<0.0001). Th17 expansion is stable over time and does not decline when remission is achieved. However, a negative association of Th17 cells and steroid dosage is observed (r=-0.46, P=0.002). The Th17 expansion was not balanced by Tregs as indicated by skewed Th17/Treg ratios in active and quiescent GPA. Th17 subsets co-producing IFNgamma or IL-10 are significantly increased in GPA. GPA patients in remission not receiving maintenance therapy have significantly more IL-10/IL-17A double positive T-cells than HC (0.0501 +/-0.031% vs. 0.0282 +/-0.016%, P=0.007). CONCLUSIONS: We provide evidence for a persistent, unbalanced expansion of Th17 cells and Th17 subsets which seems to be independent of disease activity. Maintenance therapy reduces -but does not normalize- Th17 expansion.
Arthritis research & therapy 10/2012; 14(5):R227. · 4.27 Impact Factor
-
Paul A Lyons,
Tim F Rayner,
Sapna Trivedi,
Julia U Holle,
Richard A Watts,
David R W Jayne,
Bo Baslund,
Paul Brenchley,
Annette Bruchfeld,
Afzal N Chaudhry, [......],
Mårten Segelmark,
Coen A Stegeman,
Vladimir Tesař,
Augusto Vaglio,
Stefan Wieczorek,
Benjamin Wilde,
Jochen Zwerina,
Andrew J Rees,
David G Clayton,
Kenneth G C Smith
[show abstract]
[hide abstract]
ABSTRACT: Antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis is a severe condition encompassing two major syndromes: granulomatosis with polyangiitis (formerly known as Wegener's granulomatosis) and microscopic polyangiitis. Its cause is unknown, and there is debate about whether it is a single disease entity and what role ANCA plays in its pathogenesis. We investigated its genetic basis.
A genomewide association study was performed in a discovery cohort of 1233 U.K. patients with ANCA-associated vasculitis and 5884 controls and was replicated in 1454 Northern European case patients and 1666 controls. Quality control, population stratification, and statistical analyses were performed according to standard criteria.
We found both major-histocompatibility-complex (MHC) and non-MHC associations with ANCA-associated vasculitis and also that granulomatosis with polyangiitis and microscopic polyangiitis were genetically distinct. The strongest genetic associations were with the antigenic specificity of ANCA, not with the clinical syndrome. Anti-proteinase 3 ANCA was associated with HLA-DP and the genes encoding α(1)-antitrypsin (SERPINA1) and proteinase 3 (PRTN3) (P=6.2×10(-89), P=5.6×10(-12,) and P=2.6×10(-7), respectively). Anti-myeloperoxidase ANCA was associated with HLA-DQ (P=2.1×10(-8)).
This study confirms that the pathogenesis of ANCA-associated vasculitis has a genetic component, shows genetic distinctions between granulomatosis with polyangiitis and microscopic polyangiitis that are associated with ANCA specificity, and suggests that the response against the autoantigen proteinase 3 is a central pathogenic feature of proteinase 3 ANCA-associated vasculitis. These data provide preliminary support for the concept that proteinase 3 ANCA-associated vasculitis and myeloperoxidase ANCA-associated vasculitis are distinct autoimmune syndromes. (Funded by the British Heart Foundation and others.).
New England Journal of Medicine 07/2012; 367(3):214-23. · 53.30 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Infections with cardiotrophic viruses and immune-mediated responses against the heart have been suggested to play a dominant role in the pathogenesis of idiopathic dilated cardiomyopathy (DCM). Furthermore, immune-mediated inflammatory diseases (IMIDs) may result in DCM. It has not previously been assessed whether DCM patients with and without an IMID have different prevalences and quantities of cardiotrophic viruses in the heart. Therefore, we compared the profiles of cardiotrophic viruses in heart tissue of DCM patients with and without an IMID. Serum and myocardial tissue samples were obtained from 159 consecutive patients with DCM and 20 controls. Patients were subdivided into three groups, the first two based on the presence (n = 34) or absence (n = 125) of an IMID and the third being a control group. The parvovirus B19 virus genome was detected in equal quantities in the non-IMID DCM patients (100/125) and the control group (15/20) but in lower quantities in the IMID patients (21/34, P = 0.02). Both the non-IMID and IMID DCM patients demonstrated increased myocardial inflammation compared to controls: 12.5 ± 1.8 and 14.0 ± 3.2 CD45-positive inflammatory cells, respectively, versus 5.1 ± 0.7 for the controls (P < 0.05 for both). Importantly, significantly higher parvovirus B19 copy numbers could be amplified in non-IMID than in IMID patients (561 ± 97 versus 191 ± 92 copies/μg DNA, P < 0.001) and control subjects (103 ± 47 copies/μg DNA, P < 0.001). The present study shows decreased parvovirus B19 prevalence and copy numbers in hearts of DCM patients with an IMID compared to those without an IMID. These findings may suggest that DCM patients with an IMID have a different pathophysiologic mechanism from that which is present in the virus-induced form of DCM.
Clinical and vaccine immunology: CVI 06/2012; 19(8):1182-7. · 2.37 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Antineutrophil cytoplasmic antibodies (ANCA) are traditionally detected by an indirect immunofluorescence technique. According to the international consensus on ANCA testing, ANCA should also be tested by antigen-specific tests for myeloperoxidase-ANCA and proteinase 3-ANCA. The direct noncompetitive enzyme-linked immunosorbent assay (ELISA) used to be the method of choice. Nowadays, these assays are called "first-generation" assays. Second-generation tests (capture ELISA) or third-generation tests (anchor ELISA) are more sensitive and specific for ANCA testing. We postulate that ANCA as detected by these newer ANCA tests may replace the need to perform indirect immunofluorescence-based assays. For classification of patients, ANCA serotype seems more important than classifying patients according to their clinical subtype, since genetics, clinical manifestations and response to therapy are more related to ANCA serotype than to clinical subtype. Detection of ANCA to monitor disease activity is still a controversial issue. Treatment based on ANCA levels is at present only experimentally performed in those patients who are treated with B-cell depletion therapy with rituximab. Future studies are needed to establish whether this way of monitoring patients is warranted.
Clinical Reviews in Allergy & Immunology 06/2012; · 3.68 Impact Factor
-
Arie Altman,
Martine Szyper-Kravitz,
Nancy Agmon-Levin,
Boris Gilburd,
Juan-Manuel Anaja,
Ori Barzilai,
Maya Ram,
Nicola Bizzaro,
Ljudmila Stojanovich,
Jan Damoiseaux, Jan Willem Cohen Tervaert,
Stefano Bombardieri,
Howard Amital,
Ari Shamis,
Yehuda Shoenfeld
[show abstract]
[hide abstract]
ABSTRACT: The association between infections and autoimmune diseases (AID) has been well described in the medical literature. Several infectious agents have been implicated as inducers of autoimmune responses, such as Parvovirus B19, Epstein-Barr virus, cytomegalovirus, and hepatitis viruses.
We examined 1,173 sera from patients with 14 different AID and 238 sera from geographically matched healthy controls, for evidence of prior infection with rubella. All samples were tested for the presence of serum antibodies against rubella using the Bio-Rad BioPlex 2200 system.
As a group, patients with AID had a higher prevalence of IgM anti-rubella antibodies as compared to healthy controls (11.7% versus 5.4%; P = 0.001). The prevalence of IgM anti-rubella antibodies was significantly higher in 5/14 AID, namely in patients with giant cell arteritis (33.3%), primary biliary cirrhosis (24%), antiphospholipid syndrome (20.6%), polymyositis (16%), and inflammatory bowel disease (16%). A similar prevalence of IgM anti-rubella antibodies was detected among controls from different countries. A high prevalence of IgG anti-rubella antibodies was detected among patients with AID (89.9%) and controls.
The increased prevalence of IgM anti-rubella antibodies in AID suggests a possible role for rubella in the etiopathogenesis of several AID.
Revista Brasileira de Reumatologia 06/2012; 52(3):307-18.
-
[show abstract]
[hide abstract]
ABSTRACT: Bullous pemphigoid (BP) is an autoimmune blistering skin disease. Autoantibodies to BP180 and BP230 can be detected by indirect immunofluorescence (IIF) on different substrates (oesophagus, salt-split-skin, BP180-antigen dots, BP230-transfected cells) and ELISA. Here, we compared test characteristics of these test systems. We analysed sera from BP patients (n=60) in whom the clinical diagnosis had been confirmed histopathologically. The control cohort comprised sera from patients with other autoimmune-associated (n=22) or inflammatory (n=35) skin diseases. All samples were tested by IIF (EUROIMMUN™ Dermatology Mosaic) and ELISA (EUROIMMUN and MBL). Anti-BP180 is best detected with BP180-antigen dots by IIF (sensitivity: 88%; specificity: 97%). As compared to IIF, the differences with both BP180 ELISA techniques are small though. Likelihood ratios (LRs) for positive and negative test results are >10 and between 0.1 and 0.2, respectively, for all test systems. Detection of anti-BP230 is highly variable (sensitivity range 38-60%; specificity range 83-98%). Only the IIF test reveals a LR for positive test results >10. Since the LRs for a negative test are all ~0.5, negative test results for anti-BP230 antibodies do not help to exclude BP. In conclusion, the multi-parameter IIF test reveals a good diagnostic performance in BP. Since this test simultaneously allows for the detection of anti-Dsg1 and anti-Dsg3 antibodies, involved in pemphigus foliaceus and vulgaris, a single test-incubation may be sufficient to differentiate between the most frequent autoimmune blistering diseases.
Journal of immunological methods 05/2012; 382(1-2):76-80. · 2.35 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: In the past two decades, interleukin-10 (IL-10) has gained much attention as an important regulatory cytokine involved in self-tolerance. Functional assessment of IL-10 producing immune cells is traditionally done by stimulation and measurement of cytokine production by flowcytometry. Thereby a protein transport inhibitor like monensin is used to accumulate the cytokine of interest intracellularly. In this study we elaborated on the monensin effect on cytokine detection and focused on IL-10 detection in human T cells. Peripheral blood mononuclear cells (PBMC) of 32 study subjects were isolated and stimulated with PMA/ionomycin, in the absence and presence of monensin, and stained intracellularly for IFN-γ, IL-4, IL-10 and IL-17A. Our results re-established that detection of IFN-γ+ and IL-4+ T cells benefited from the presence of monensin during stimulation. However, stimulation in the presence of monensin yielded lower proportions of IL-10+ T cells (0.45% (0.28-0.80) versus 0.80% (0.50-1.50) of CD4+ T cells, p<0.01), although monensin addition did result in an increased MFI (2431 (1273-4959) versus 1928 (1147-3760), p<0.01). Detectable fractions of IL-17A+ CD4+ T cells were not affected by monensin. A shorter incubation time, but not lower monensin concentrations, was effective in improving the detection of IL-10+ T cells. We found a strong correlation between the fraction of IL-10+ CD4+ T cells in the presence and absence of monensin (R=0.80 p<0.01). Next to this, also the detection of IL-10+ NK-T cells and IL-10+ monocytes, but not IL-10+ B cells, is impaired in the presence of monensin. This study shows that the effect of monensin on cytokine accumulation is time and cytokine dependent. Due to the use of monensin, previous research may have underestimated the number of IL-10+ leukocytes or may even have not been able to detect them at all. It is important to consider this for future research or when interpreting historical IL-10 data.
Journal of immunological methods 04/2012; 381(1-2):59-65. · 2.35 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Persistent T-cell activation is frequently observed in granulomatosis with polyangiitis (GPA, formerly known as Wegener's granulomatosis). T-cell activation is usually balanced by negative costimulatory molecules. The negative costimulator programmed death receptor-1 (PD-1) and its relevance to T-cell immunity have not been studied so far in GPA. Thus it is the aim of the study to characterize the role of PD-1 in GPA.
Thirty-two patients suffering from GPA and 19 age-matched healthy controls (HCs) were enrolled. T-lymphocyte subsets from peripheral blood were analysed by flow cytometry for the expression of PD-1. The frequency of memory T cells and T cells producing pro-inflammatory cytokines was determined. Renal biopsies from GPA patients were stained for CD3 and PD-1.
PD-1 expression was increased on T-helper cells (Th cells) from GPA patients as compared with HCs. In addition, parameters of persistent T-cell activation and production of pro-inflammatory cytokines were positively associated with numbers of PD-1(+) Th cells in patients but not in HCs. Latent infection with CMV seemed to enhance PD-1 expression on CD4(+) and CD4(+)CD25(-) T cells. Interestingly, expression of PD-1 on CD4(+)CD25(+)T cells was inversely correlated with relapse rate. Importantly, lesional T cells were mostly lacking PD-1.
The expression of the negative costimulator PD-1 is altered in GPA and might counterbalance persistent T-cell activation.
Rheumatology (Oxford, England) 03/2012; 51(7):1188-97. · 4.24 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: The ANCA consensus prescribes screening by indirect immunofluorescence on neutrophils. We evaluated the first automated ANCA-pattern recognition system. C-ANCA (n = 39) and P-ANCA (n = 40) samples were selected from patients with ANCA-associated vasculitis (AAV). Non-AAV controls included sera from healthy controls (n = 40), sera with possible interfering antibodies (n = 46), or miscellaneous ANCA reactivity (n = 31). ANCA slides were analysed by AKLIDES and routine fluorescence microscopy. The C-ANCA pattern was recognized by routine microscopy in 92% and 97% on ethanol- and formalin-fixed slides, respectively. AKLIDES reported C-ANCA in 74% and 95%, respectively. P-ANCA was recognized by routine microscopy on ethanol-fixed neutrophils in 90%, while AKLIDES reported P-ANCA in 80%. Typically, only 65% and 33% of these samples showed the expected C-ANCA on formalin-fixed neutrophils by routine microscopy and AKLIDES, respectively. A C- or P-ANCA pattern was observed on ethanol-fixed neutrophils in 28% and 23% of the controls by routine microscopy and AKLIDES, respectively. Only 5% of the controls revealed C-ANCA on formalin-fixed neutrophils by routine microscopy and AKLIDES. Altogether, automated ANCA-pattern recognition by AKLIDES is promising. Distinction of C- and P-ANCA is good, but sensitivity on ethanol-fixed neutrophils needs improvement. When optimized, pattern recognition software may play an important role in AAV diagnostics.
Clinical and Developmental Immunology 01/2012; 2012:762874. · 1.84 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Cerebral small vessel disease (CSVD) may be caused by endothelial dysfunction, whereas endothelial progenitor cells (EPC) may attenuate endothelial dysfunction. Their vitality is lower in CSVD. A subset of lymphocytes, angiogenic T-cells, is capable to stimulate EPC function. The purpose of our study was to explore the relation between CSVD manifestations, angiogenic T-cells, and EPC in hypertensive patients with CSVD.
We compared 32 essential hypertensive patients with CSVD (white matter lesions, asymptomatic lacunar infarcts, or microbleeds on 1.5-Tesla MRI) to 29 age-matched and sex-matched hypertensive controls. We counted angiogenic T-cells (CD3(+)/CD31(+)/CD184(+)) and putative EPC (CD31(+)/CD34(+)/CD45(-)/KDR(+)) by flow cytometry and determined EPC vitality by in vitro cluster formation.
Putative EPC numbers were lower in hypertensive individuals with CSVD than in those without (10±7(.)10(3)/mL versus 13±6(.)10(3)/mL [median±interquartile range]; P=0.011). Angiogenic T-cell numbers were also lower in hypertensive individuals with CSVD than in those without (0.56±0.25(.)10(9)/mL versus 0.78±0.50(.)10(9)/mL; P=0.008). Higher angiogenic T-cell numbers independently related to absence of CSVD (odds ratio, 0.088; 95% confidence interval, 0.012-0.627).
Our data suggest that angiogenic T-cells and putative EPC independently relate to radiological CSVD manifestations in hypertensive patients.
Stroke 01/2012; 43(1):256-8. · 5.73 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: In this study, percentages of CD39(+) Treg and Th17 cells were compared between relapsing-remitting MS patients and controls and were related to the vitamin D status. The Th17 cell population was expanded in about 40% of the MS patients. In MS patients in remission, but not during relapse, a positive association was found between Th17 cell and CD39(+) Treg percentages (r=0.468, p=0.007). Since CD39(+) Tregs have been shown to have Th17 suppressive capacities, we propose that a dysregulated Th17/CD39(+) Treg balance might contribute to disease exacerbation. A clear role for vitamin D in this regulation could not be established.
Journal of neuroimmunology 12/2011; 240-241:97-103. · 2.84 Impact Factor
-
11/2011; , ISBN: 978-953-307-786-4
-
[show abstract]
[hide abstract]
ABSTRACT: In this study, we assessed B cell subsets, including Bregs, during stable and active disease in relapsing remitting multiple sclerosis (RRMS) patients and related B cell subsets to vitamin D status. We report that RRMS patients have a decreased percentage of both memory B cells and Bregs compared to healthy controls. During a relapse, the reduction in Bregs involved in particular naïve Bregs. We found no correlation between vitamin D status and B cell subsets. An effect of vitamin D on Bregs cannot be ruled out, since it might be the function that is interfered with instead of relative numbers.
Journal of neuroimmunology 09/2011; 239(1-2):80-6. · 2.84 Impact Factor
-
Jan Willem Cohen Tervaert
Nephrology Dialysis Transplantation 09/2011; 26(10):3077-9. · 3.40 Impact Factor
-
The Lancet 08/2011; 378(9790):540. · 38.28 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Polymorphonuclear cells (PMN) are widely recognized as sophisticated killers during microbial infections. In recent years, PMN have been shown to interact and functionally interfere with other cells of the immune system. In this study, we investigated PMN-T cell interactions in an in vitro co-culture system. A relative increase in T cells in the co-culture was associated with the upregulation of CD66b expression on PMN. In addition, PMN were found to dose-dependently impair anti-CD3 induced CD4(+) T cell activation, proliferation and viability. In a transwell co-culture system, proliferation of T cells was, however, enhanced which illustrates that suppression was contact-dependent. The addition of an arginase-inhibitor or blocking antibodies against calprotectin, but not myeloperoxidase (MPO), partially restored T cell proliferation. Furthermore, the presence of PMN in the co-culture dose-dependently increased the fraction of IFN-γ and IL-17 producing T cells and decreased the percentage of IL-10 producing CD4(+) T cells. Altogether, these data show that there is cross-talk between PMN and T cells which, in non-inflammatory conditions, results in the effects described above. Further studies should investigate PMN-T cell functional interference in inflammatory situations and clarify the importance of this PMN-T cell cross-talk in the regulation of the immune response.
Molecular Immunology 08/2011; 48(15-16):2094-101. · 2.90 Impact Factor
