bluuebunny/crossref_metadata_2025_split huggingface dataset:
iNKT Cell Frequency in Peripheral Blood of Caucasian Children and Adolescent: The Absolute iNKT Cell Count is Stable from Birth to Adulthood
Authors: Bienemann K. , Iouannidou K. , Schoenberg K. , Krux F. , Reuther S. , Feyen O. , Bienemann K. , Schuster F. , Uhrberg M. , Laws H.‐J. , Borkhardt A. 
Published: June 2011

AbstractHuman invariant natural killer T cells (iNKT cells) are a unique population of T cells that express a semi‐invariantly rearranged T cell receptor (TCR) and are involved in a variety of immunoregulatory processes. We assessed the frequency of peripheral blood iNKT cells in 64 healthy Caucasian children from 7 months to 18 years of age and five cord blood samples by flow cytometry. iNKT cells were measured as CD3+cells co‐expressing TCRVα24 and TCRVβ11 and using the monoclonal antibody 6B11, which recognizes specifically their invariant TCR rearrangement. The absolute number of iNKT cells ranged from 86 to 10,499 (CD3+/TCRVα24+/ TCRVβ11+) and 233 to 11,167 (CD3+/6B11+) iNKT cells per millilitre of blood. This range is stable from birth to adulthood. The relative iNKT cell count was found to be 0.003–0.71% (CD3+/TCRVα24/TCRVβ11) and 0.019–0.776% (CD3/6B11) of peripheral blood T cells and shows only a slight increase with age.
Resistin is Associated with Breach of Tolerance and Anti‐nuclear Antibodies in Patients with Hepatobiliary Inflammation
Authors: Boström E. A. , Ekstedt M. , Kechagias S. , Sjöwall C. , Bokarewa M. I. , Almer S. 
Published: June 2011

AbstractResistin is a cysteine‐rich protein, which is abundantly expressed at the site of inflammation, and acts as a regulator of the NF‐kB‐dependent cytokine cascade. The aim of this study was to evaluate resistin levels in relation to inflammatory mediators, disease phenotype and autoantibody status in a spectrum of pathological conditions of the gastrointestinal tract. Resistin levels were measured with an ELISA in sera originated from 227 patients and 40 healthy controls (HC). Fifty patients diagnosed with non‐alcoholic fatty liver disease (NAFLD), 53 ulcerative colitis (UC), 51 Crohn’s disease (CD), 46 autoimmune hepatitis (AIH) and 27 primary sclerosing cholangitis (PSC) were included. The sera were analysed with respect to biochemical parameters of systemic inflammation and liver function and to the presence of antibodies to nuclear antigens (ANA), mitochondria (AMA) and smooth muscle (SMA). Compared with HC, resistin levels were raised in AIH (P = 0.017) and PSC (P = 0.03); compared with NAFLD, levels were elevated in CD (P = 0.041), AIH (P < 0.001) and PSC (P < 0.001). Patients with elevated levels of resistin were more often treated with corticosteroids, but no difference was found between active disease and clinical remission. Resistin levels were significantly higher in ANA‐positive individuals compared with ANA‐negative (P = 0.025). Resistin levels were directly correlated with IL‐6 (r = 0.30, P = 0.02) and IL‐8 (r = 0.51, P < 0.001). Elevated levels of resistin were prominent in patients with hepatobiliary inflammation and were associated with breach of self‐tolerance, i.e. ANA positivity. Thus, we propose that resistin may be an important marker of disease severity in autoantibody‐mediated gastrointestinal inflammatory diseases.
Somatic Mosaicism Caused by Monoallelic Reversion of a Mutation in T Cells of a Patient with ADA‐SCID and the Effects of Enzyme Replacement Therapy on the Revertant Phenotype
Authors: Moncada‐Vélez M. , Vélez‐Ortega A. , Orrego J. , Santisteban I. , Jagadeesh J. , Olivares M. , Olaya N. , Hershfield M. , Candotti F. , Franco J. 
Published: June 2011

AbstractPatients with adenosine deaminase (ADA) deficiency exhibit spontaneous and partial clinical remission associated with somatic reversion of inherited mutations. We report a child with severe combined immunodeficiency (T‐B‐ SCID) due to ADA deficiency diagnosed at the age of 1 month, whose lymphocyte counts including CD4+ and CD8+ T and NK cells began to improve after several months with normalization of ADA activity in Peripheral blood lymphocytes (PBL), as a result of somatic mosaicism caused by monoallelic reversion of the causative mutation in the ADA gene. He was not eligible for haematopoietic stem cell transplantation (HSCT) or gene therapy (GT); therefore he was placed on enzyme replacement therapy (ERT) with bovine PEG‐ADA. The follow‐up of metabolic and immunologic responses to ERT included gradual improvement in ADA activity in erythrocytes and transient expansion of most lymphocyte subsets, followed by gradual stabilization of CD4+ and CD8+ T (with naïve phenotype) and NK cells, and sustained expansion of TCRγδ+ T cells. This was accompanied by the disappearance of the revertant T cells as shown by DNA sequencing from PBL. Although the patient’s clinical condition improved marginally, he later developed a germinal cell tumour and eventually died at the age of 67 months from sepsis. This case adds to our current knowledge of spontaneous reversion of mutations in ADA deficiency and shows that the effects of the ERT may vary among these patients, suggesting that it could depend on the cell and type in which the somatic mosaicism is established upon reversion.
Drug use and HIV in West Africa: a neglected epidemic
Authors: Raguin Gilles , Lepretre Annie , Ba Idrissa , Ndoye Ibrahim , Toufik Abdalla , Brucker Gilles , Girard Pierre‐Marie 
Published: June 2011

SummaryInjecting drug use is poorly documented in West Africa. HIV prevalence studies are still rare. Recent studies show that drug injection is on the rise. There is an urgent need to take this component of the HIV epidemic into account and to establish adapted intervention strategies.
The increase in allergy and extended challenges
Authors: Linneberg A. 
Published: June 2011

To cite this article: Linneberg A. The increase in allergy and extended challenges. Allergy 2011; 66 (Suppl. 95):1–3.AbstractThe prevalence of allergic diseases shows a well‐documented increase in developed countries over several decades. Currently, 20–25% of European adults are affected. Westernisation, urbanisation, and affluence contribute to allergy development, so allergy is expected to increase in developing countries in the future. Identifying primary causes, developing new therapies, and increasing treatment access may interrupt the allergic epidemic.
Effect of parasite infection on allergic disease
Authors: Capron M. 
Published: June 2011

To cite this article: Capron M. The effect of parasite infection on allergic disease. Allergy 2011; 66 (Suppl. 95): 16–18.AbstractVertebrates and helminths have co‐evolved for 500 million years, developing mutual adaptation mechanisms between parasites and hosts. Today, however, helminth diseases are among the most neglected communicable diseases. Epidemiological evidence shows that exposure to helminth parasites is inversely correlated with allergy incidence, and helminths induce immune hyporeactivity in both the innate and adaptive systems. The mechanisms include parasite‐derived regulatory molecules, the study of which opens new avenues for the control of allergic and autoimmune diseases.
Mechanisms of immunotherapy and surrogate markers
Authors: Till S. 
Published: June 2011

To cite this article: Till S. Mechanisms of immunotherapy and surrogate markers. Allergy 2011; 66 (Suppl. 95): 25–27.AbstractUnderstanding mechanisms of inducible antigen‐specific tolerance will improve immunotherapy and reveal the most relevant biomarkers for objectively measuring response to immunotherapy in clinical trials and routine practice. Various physiological and laboratory parameters are proposed as biomarkers of an immunological response to vaccines, although their surrogacy for clinical end points is unproven. Examples of physiological biomarkers include suppression of allergen‐induced early‐ and late‐phase responses. Laboratory biomarkers include increases in bioactive allergen‐specific IgG and IgA levels and T‐cell interleukin (IL)‐10 production. There is a continuing unmet need for biomarkers that will allow prediction of treatment efficacy and assist in monitoring the response after starting therapy or postwithdrawal.
The role of IgG antibodies in allergy and immunotherapy
Authors: Aalberse R. 
Published: June 2011

To cite this article: Aalberse R. The role of IgG antibodies in allergy and immunotherapy. Allergy 2011; 66 (Suppl. 95): 28–30.AbstractIn specific immunotherapy (SIT), a beneficial response is associated with an increase in allergen‐specific IgG4. This does not indicate that IgE‐producing B cells have switched to IgG4 production, because in human DNA, IgE is downstream from IgG4. Thus, by conventional switching, B cells should produce IgG4 before IgE. This presentation discusses three possible hypotheses explaining the favourable association between IgG4 and SIT, including that SIT causes B cells to become regulatory. Regulatory B cells may produce cytokines like IL‐10 that promote IgG4 production. IgG4 can undergo in vitro switching to create bispecific antibodies that recognize more than one antigen, which has important consequences for reducing IgE–allergen complexes in immunotherapy.
Provocation tests as measure of efficacy and dosage
Authors: de Blay F. 
Published: June 2011

To cite this article: de Blay F. Provocation tests as measure of efficacy and dosage. Allergy 2011; 66 (Suppl. 95): 47–49.AbstractProvocation and challenge tests have been used to understand the pathobiology of asthma, to facilitate diagnosis and to assess therapeutic efficacy and dosage. Current challenge tests expose the patient to ‘natural conditions’, for example, in an allergen chamber. For determining drug efficacy in asthma, allergen challenge has a moderate positive predictive value and an excellent negative predictive value. The best challenge tests are standardized, and the best bronchial challenge tests use a large allergen particle size. Allergen provocation tests are safe when performed by experienced investigators.
Sustained effects of grass pollen AIT
Authors: Durham S. R. ,   on behalf of the GT‐08 investigators
Published: June 2011

To cite this article: Durham SR, on behalf of the GT‐08 investigators. Sustained effects of grass pollen AIT. Allergy 2011; 66 (Suppl. 95): 50–52.AbstractWe report the sustained efficacy of the SQ‐standardized grass allergy immunotherapy tablet Grazax® (Phleum pratense 75 000 SQ‐T/2,800 BAU, ALK, Denmark) from a 5‐year randomized, double‐blind, placebo‐controlled phase III trial. Adults with moderate‐to‐severe grass pollen allergy inadequately controlled by symptomatic medications were followed for 2 years after the completion of 3 years of treatment. The active group demonstrated a 31% reduction in median rhinoconjunctivitis symptom score over the season compared with placebo. Individual symptom scores favoured active treatment. Combined symptom and medication scores demonstrated a 33% reduction in medians with active treatment. Persistent clinical efficacy was accompanied by prolonged increases in allergen‐specific IgG4 antibodies and IgE‐blocking factor, confirming clinical and immunological tolerance for at least 2 years after the treatment completion. No safety issues were identified during follow‐up.
Tolerability and efficacy of house dust mite AIT
Authors: Mosbech H. 
Published: June 2011

To cite this article: Mosbech H. Tolerability and efficacy of house dust mite AIT. Allergy 2011; 66 (Suppl. 95): 55–56.AbstractSublingual immunotherapy based on grass pollen allergy immunotherapy tablets is an efficacious and well‐tolerated treatment for rhinoconjunctivitis, and subcutaneous house dust mite (HDM) immunotherapy is effective against allergic asthma. Three studies have investigated a new ALK tablet for HDM allergy: two studies on tolerability in adults and children, and one on efficacy and safety in adults and adolescents with asthma. Treatment was well tolerated, mainly with mild‐to‐moderate local reactions pertaining to the administration site, such as temporary oral pruritus. The primary efficacy endpoint was a significant reduction in inhaled corticosteroid dose compared to baseline after 1 year of daily treatment. A positive therapeutic effect on asthma was demonstrated by a reduction of more than 80 μg/day inhaled budesonide for a group receiving six developmental units daily compared to the placebo group.
Focal segmental glomerulosclerosis after renal transplantation
Authors: Shimizu Akira , Higo Seiichiro , Fujita Emiko , Mii Akiko , Kaneko Tomohiro 
Published: June 2011

Shimizu A, Higo S, Fujita E, Mii A, Kaneko T. Focal segmental glomerulosclerosis after renal transplantation. Clin Transplant 2011: 25 (Suppl. 23): 6–14. © 2011 John Wiley & Sons A/S.Abstract:  Focal segmental glomerulosclerosis (FSGS) is a clinicopathologic syndrome of proteinuria, usually of nephrotic range, associated with focal and segmental sclerotic glomerular lesions. Therefore, FSGS is diagnosed by clinical features and histopathological examination of renal biopsy. The natural history of the condition varies, and although it may respond to treatment, FSGS is an important disease in the etiology of end‐stage renal disease (ESRD). Furthermore, after kidney transplantation, approximately 30% of patients with FSGS develop recurrent FSGS. The risk factors for recurrence of FSGS include childhood onset and age <15 yr, rapid progression of the primary FSGS to ESRD, recurrence of FSGS in a previous allograft, diffuse mesangial hypercellularity in the native kidney, collapsing FSGS, and podocin gene mutation. In addition, after kidney transplantation, de novo FSGS also develops in approximately 10–20% of allografts, associated with a complication of hyperfiltration injury, chronic transplant glomerulopathy, and calcineurin inhibitor toxicity. FSGS is considered a podocyte disease, and the pathology is characterized by segmental FSGS lesion with glomerular epithelial hypercellularity. The pathological diagnosis of FSGS is based on the 2004 Columbia classification system. In the present minireview, we discuss the pathology of recurrence and de novo FSGS after kidney transplantation.
A case of tacrolimus‐associated thrombotic microangiopathy after ABO‐blood‐type‐incompatible renal transplantation
Authors: Takeda Asami , Ohtsuka Yasuhiro , Horike Keij , Inaguma Daizyo , Goto Norihiko , Watarai Yoshihiko , Uchida Kazuharu , Morozumi Kunio 
Published: June 2011

Takeda A, Ohtsuka Y, Horike K, Inaguma D, Goto N, Watarai Y, Uchida K, Morozumi K. A case of tacrolimus‐associated thrombotic microangiopathy after ABO‐blood‐type‐incompatible renal transplantation. Clin Transplant 2011: 25 (Suppl. 23): 15–18. © 2011 John Wiley & Sons A/S.Abstract:  De novo thrombotic microangiopathy(TMA) is most commonly triggered by calcineurin inhibitors (CNI) and the prognosis is less severe than with recurrent TMA. However, it is difficult to distinguish de novo TMA from CNI toxicity and acute antibody‐mediated rejection(AMR) soon after renal transplantation. We present a case of tacrolimus‐associated TMA soon after ABO blood type incompatible renal transplantation that was difficult to differentiate from acute AMR. On day 9 his urine output decreased dramatically and the Scr level increased. His anti‐blood type A antibody titer increased to ×16 postopratively and the tacrolimus trough level was higher than in our immunosuppressive regimen. Although we gave priority to anti‐AMR treatment, adequate dose adjustment of tacrolimus after tacrolimus nephrotoxicity was diagnosed from graft biopsy could correct allograft dysfunction.
Successful treatment of nephrotic syndrome caused by recurrent IgA nephropathy with chronic active antibody‐mediated rejection three years after kidney transplantation
Authors: Yaginuma Tatsuhiro , Yamamoto Hiroyasu , Mitome Jun , Kobayashi Akimitsu , Yamamoto Izumi , Tanno Yudo , Hayakawa Hiroshi , Miyazaki Youichi , Yokoyama Keitaro , Utsunomiya Yasunori , Miki Jun , Yamada Hiroki , Furuta Nozomu , Yamaguchi Yutaka , Hosoya Tatsuo 
Published: June 2011

Yaginuma T, Yamamoto H, Mitome J, Kobayashi A, Yamamoto I, Tanno Y, Hayakawa H, Miyazaki Y, Yokoyama K, Utsunomiya Y, Miki J, Yamada H, Furuta N, Yamaguchi Y, Hosoya T. Successful treatment of nephrotic syndrome caused by recurrent IgA nephropathy with chronic active antibody‐mediated rejection three years after kidney transplantation. Clin Transplant 2011: 25 (Suppl. 23): 28–33. © 2011 John Wiley & Sons A/S.Abstract:  Here, we report the successful treatment of a 38‐yr‐old Japanese man diagnosed with recurrent immunoglobulin A nephropathy (IgAN) with chronic active antibody‐mediated rejection (CAAMR), three yr after undergoing living‐related donor kidney transplantation. Immediately after transplantation, the allograft function was well maintained with a serum creatinine (S‐Cr) level of <1.8 mg/dL. About three yr after transplantation, urine protein excretion had reached 4.59 g/d, and the S‐Cr level had increased to more than 2.0 mg/dL. Based on the allograft biopsy, we diagnosed nephrotic syndrome because of recurrence of IgAN with CAAMR. Subsequently, we performed a tonsillectomy, administered three sessions of steroid pulse therapy, and added losartan for the recurrence of IgAN. We also changed his immunosuppressant from mizoribine to mycophenolate mofetil to treat the CAAMR. The nephrotic syndrome improved with the multiple therapeutic approaches; however, the S‐Cr level did not decrease below 2.0 mg/dL. We possibly could have performed additional treatments such as rituximab and intravenous immunoglobulin for the CAAMR, but therapeutic strategies for CAAMR have not yet been established.
Overlapped glomerular lesions of chronic rejection and recurrent lupus nephritis in transplanted kidney: a case report
Authors: Masuzawa Naoko , Urasaki Koji , Okamoto Masahiko , Nobori Shuji , Ushigome Hidetaka , Yoshimura Norio , Yanagisawa Akio 
Published: June 2011

Masuzawa N, Urasaki K, Okamoto M, Nobori S, Ushigome H, Yoshimura N, Yanagisawa A. Overlapped glomerular lesions of chronic rejection and recurrent lupus nephritis in transplanted kidney: a case report. Clin Transplant 2011: 25 (Suppl. 23): 49–52. © 2011 John Wiley & Sons A/S.Abstract:  We describe a renal transplant recipient with systemic lupus erythematosus (SLE) who showed continuous proteinuria and low complement levels without clinical evidence of active SLE. Her first renal allograft biopsy, performed nine yr and eight months after transplantation, revealed unusual histological change of glomeruli, and it initially led us to make a contradictory diagnosis based on light and electron microscopic examinations. Diffuse global double‐ or multi‐contour glomerular basement membrane was caused by chronic endothelial injury owing to chronic rejection, and mesangial proliferation associated with mesangial electron‐dense deposit was a histological change characteristic of recurrent lupus nephritis (RLN). Immunofluorescence study displayed weak mesangial staining of IgM and C1q. We concluded that this case presented overlapped chronic rejection and RLN. Because both transplant nephropathy and lupus nephritis present constellations of various histologies, it is difficult to diagnose their overlap. Complete morphologic studies with both immunofluorescence and electron microscopic evaluations in addition to microscopic examination should be performed to elucidate complex histological findings.
BK polyomavirus nephropathy complicated with acute T‐cell‐mediated rejection in a kidney transplant recipient: a case report
Authors: Tanabe Tatsu , Shimizu Tomokazu , Sai Keiko , Miyauchi Yuki , Shirakawa Hiroki , Ishida Hideki , Honda Kazuho , Koike Junki , Yamaguchi Yutaka , Tanabe Kazunari 
Published: June 2011

Tanabe T, Shimizu T, Sai K, Miyauchi Y, Shirakawa H, Ishida H, Honda K, Koike J, Yamaguchi Y, Tanabe K. BK polyomavirus nephropathy complicated with acute T‐cell‐mediated rejection in a kidney transplant recipient: a case report. Clin Transplant 2011: 25 (Suppl. 23): 39–43. © 2011 John Wiley & Sons A/S.Abstract:  We present a case of severe BK polyomavirus nephropathy (BKVN) complicated with persistent acute T‐cell‐mediated rejection (ATMR) that progressed to allograft failure. A 54‐yr‐old man received a living donor kidney transplant from his wife. Approximately four months after transplantation, the patient’s serum creatinine (SCr) increased from a baseline value of 1.5–2.4 mg/dL. A histological analysis showed BKVN, and the SV40 antigen was detected in the tubular nuclei. The doses of immunosuppressants were reduced, and immunoglobulin was administered intravenously. The SCr increased further, to 5.3 mg/dL, and a second renal biopsy revealed the presence of severe ATMR. Antirejection treatment was performed, and low‐dose cidofovir was started. The SCr decreased, to 3 mg/dL, and BK virus antigen in the serum and urine samples became negative at the time of hospital discharge. However, the histological findings subsequently showed gradually progressive interstitial fibrosis and tubular atrophy, and the SCr increased gradually. Two years after the transplantation, the patient resumed hemodialysis. BK polyomavirus nephropathy is usually treated with a reduction in immunosuppressant therapy, although in some patients, the reduction in immunosuppressants induces a subsequent exacerbation of acute rejection and results in progressive graft failure, which suggests difficulty in treating BKVN after kidney transplantation.
The case of BK virus infection in which it was difficult to differentiate from acute rejection
Authors: Ito Yumi , Nishi Shinichi , Imai Naofumi , Yoshita Kazuhiro , Saito Kazuhide , Nakagawa Yuki , Takahashi Kota , Narita Ichiei 
Published: June 2011

Ito Y, Nishi S, Imai N, Yoshita K, Saito K, Nakagawa Y, Takahashi K, Narita I. The case of BK virus infection in which it was difficult to differentiate from acute rejection. Clin Transplant 2011: 25 (Suppl. 23): 44–48. © 2011 John Wiley & Sons A/S.Abstract:  BK virus (BKV) nephropathy is one of the major causes of allograft dysfunction or graft loss in kidney transplant recipients. Early diagnosis and timely reduction in immunosuppressant is important for proper treatment. We report a 35‐yr‐old male case of cadaveric renal transplantation with BK viral related tubulointerstitial nephritis complicated by acute rejection. The diagnostic biopsy showed severe inflammatory infiltrates, tubulitis, and peritubular capillaritis. Discontinuation of mycophenolate mofetil, prednisone pulse therapy, and r‐globulin was successful in relieving allograft dysfunction.