SwePub
Sök i SwePub databas

  Utökad sökning

Träfflista för sökning "WFRF:(Lindehammer Sabina) "

Sökning: WFRF:(Lindehammer Sabina)

  • Resultat 1-10 av 12
  • [1]2Nästa
Sortera/gruppera träfflistan
   
NumreringReferensOmslagsbildHitta
1.
  • Lindehammer, Sabina, et al. (författare)
  • Seroconversion to islet autoantibodies between early pregnancy and delivery in non-diabetic mothers
  • 2011
  • Ingår i: Journal of Reproductive Immunology. - Elsevier. - 1872-7603. ; 88:1, s. 72-79
  • Tidskriftsartikel (refereegranskat)abstract
    • Islet autoantibodies are currently used to classify type 1 diabetes at diagnosis as they reflect the autoimmune pathogenesis of the disease. The presence of maternal autoantibodies reactive with pancreatic islet antigens is thought to increase the risk for type 1 diabetes in the offspring. The objective of this study was to determine seroconversion to islet autoantibodies in non-diabetic mothers during pregnancy. Screening of 33,682 mothers between September 2000 and August 2004 in the Diabetes Prediction in Skane (DiPiS) study showed that at delivery, 242 non-diabetic mothers had increased titers of islet autoantibodies reactive with glutamic acid decarboxylase (GADA), islet antigen-2 (IA-2A) or insulin (IAA), alone or in combination. Control mothers (n = 1419), who were islet autoantibody negative at delivery, were randomly selected and matched by age, parity and pregnancy sampling date. Mothers positive for GADA (92%), IA-2A (84%) or IAA (65%) at delivery had increased titers already evident in early pregnancy. Titers declined for GADA (p<0.0001). IA-2A (p<0.0001) and IAA (p<0.0001). Seroconversion during pregnancy was observed for GADA in 10 (8%), IA-2A in 3 (16%) and IAA in 37 (35%) mothers. It is concluded that non-diabetic mothers with islet autoantibodies at delivery had significantly higher titers during early pregnancy than at delivery. As the statistical power in the seroconverting mothers was insufficient, further studies are needed to determine if the risk for type 1 diabetes in the offspring differs between mothers who already had increased titers of islet autoantibodies during early pregnancy or acquired them during pregnancy. (C) 2010 Elsevier Ireland Ltd. All rights reserved.
2.
  • Lindehammer, Sabina, et al. (författare)
  • Temporal trends of HLA genotype frequencies of type 1 diabetes patients in Sweden from 1986 to 2005 suggest altered risk
  • 2008
  • Ingår i: Acta Diabetologica. - 1432-5233. ; 45:4, s. 231-5
  • Tidskriftsartikel (refereegranskat)abstract
    • The aim of this study was to compare the frequency of human leukocyte antigen (HLA) genotypes in 1-18-year-old patients with type 1 diabetes newly diagnosed in 1986-1987 (n = 430), 1996-2000 (n = 342) and in 2003-2005 (n = 171). We tested the hypothesis that the HLA DQ genotype distribution changes over time. Swedish type 1 diabetes patients and controls were typed for HLA using polymerase chain reaction amplification and allele specific probes for DQ A1* and B1* alleles. The most common type 1 diabetes HLA DQA1*-B1*genotype 0501-0201/0301-0302 was 36% (153/430) in 1986-1987 and 37% (127/342) in 1996-2000, but decreased to 19% (33/171) in 2003-2005 (P < 0.0001). The 0501-0201/0501-0201 genotype increased from 1% in 1986-1987 to 7% in 1996-2000 (P = 0.0047) and to 5% in 2003-2005 (P > 0.05). This study in 1-18-year-old Swedish type 1 diabetes patients supports the notion that there is a temporal change in HLA risk.
  •  
3.
  • Björck, Sara, et al. (författare)
  • Serum cytokine pattern in young children with screening detected celiac disease.
  • 2015
  • Ingår i: Clinical and Experimental Immunology. - British Society for Immunology. - 0009-9104. ; 179:2, s. 230-235
  • Tidskriftsartikel (refereegranskat)abstract
    • Celiac disease is an autoimmune disease characterized by inflammation localized to the small bowel, but less is known about systemic signs of inflammation. The aim was to measure cytokines of the T helper 1 (Th1) and T helper 2 (Th2) cell patterns in children with screening detected celiac disease before and after treatment with a gluten free diet.
  •  
4.
  •  
5.
  • Lindehammer, Sabina, et al. (författare)
  • Early human pregnancy serum cytokine levels predict autoimmunity in offspring.
  • 2011
  • Ingår i: Autoimmunity. - Taylor & Francis. - 0891-6934. ; 44, s. 445-452
  • Tidskriftsartikel (refereegranskat)abstract
    • It is generally believed that pregnancy is mediated by a Th2 response, which includes cytokines that promote placental growth and are involved in inducing tolerance to the foetus. If the balance between Th1/and Th2-mediated cytokines is disrupted, systemic and local changes could predispose the foetus to future disease. Therefore, a shift in the Th1/Th2 balance during pregnancy, possibly caused by underlying environmental factors, could be associated with post-partum autoimmune disease in the offspring. Based on this presumption, we used celiac disease as a model to investigate whether autoimmunity is triggered in the foetus during early pregnancy, observed as changes in the mother's cytokine profile. Ten cytokines were measured by electro-chemi-luminescent multiplex ELISA in serum samples obtained from mothers during early pregnancy. Cases included women with children who had developed verified celiac disease before the age of 5, who were compared with other women as matched controls. We observed that 7 out of 10 cytokine levels were significantly increased in our case mothers when compared to controls. Five of these belonged to what is generally known as a Th1-mediated response (TNF?, IFN?, IL-2, IL-1? and IL-12) and two were Th2 cytokines (IL-13 and IL-10). However, the IL-10 cytokine is known to have features from both arms of the immune system. These results were confirmed in a logistic regression model where five out of the initial seven cytokines remained. This study suggests that increase in Th1 serum cytokines may be associated with celiac disease in offspring.
  •  
6.
  • Lindehammer, Sabina, et al. (författare)
  • Early-Pregnancy Cytokines in Mothers to Children Developing Multiple, Persistent Islet Autoantibodies, Type 1 Diabetes, or Both Before 7 Years of Age.
  • 2011
  • Ingår i: American Journal of Reproductive Immunology. - Wiley-Blackwell. - 1600-0897. ; 66, s. 495-503
  • Tidskriftsartikel (refereegranskat)abstract
    • Citation Lindehammer SR, Fex M, Maziarz M, Hanson I, Marsal K, Lernmark Å on behalf of the Diabetes Prediction in Skåne (DiPiS) Study Group. Early-pregnancy cytokines in mothers to children developing multiple, persistent islet autoantibodies, type 1 diabetes, or both before 7 years of age. Am J Reprod Immunol 2011 Problem Increased levels of serum cytokines in early pregnancy may increase the risk of type 1 diabetes in the offspring. Method of study Early-pregnancy (between 10 and 16 gestational weeks) serum samples from non-diabetic index mothers (n = 48) of children who developed islet autoimmunity, type 1 diabetes, or both before 7 years of age were analyzed for IFN-γ, IL-10, IL-12, IL-13, IL-1β, IL-2, IL-4, IL-5, CXCL8, and TNF. Control mothers (n = 93) were matched for age, sampling date, and HLA-DQ genotypes. Results IFN-γ (P = 0.02) and IL-1β (P = 0.04) were elevated in the index mothers. All cytokines except IL-4 were highly correlated (P < 0.0001). IFN-γ [OR 1.39 (1.04, 1.85), P = 0.026] and possibly IL-2 [OR 1.21 (0.99, 1.48), P = 0.057] in early pregnancy were associated with an increased risk of multiple, persistent islet autoantibodies, type 1 diabetes, or both before 7 years of age in the offspring. However, the statistical significance for IL-2 was lost in the logistic regression when adjusted for gestational length at delivery and parity. Conclusion Increased Th1 cytokine levels during early pregnancy might contribute to an increased risk of islet autoimmunity, type 1 diabetes, or both in the offspring.
  •  
7.
  • Lindehammer, Sabina Resic, et al. (författare)
  • Viruses, diabetes, and autoimmunity : Studies of subjects at genetic risk for type 1 diabetes
  • 2013
  • Ingår i: Diabetes and Viruses. - Springer. - 9781461440505 - 9781461440512 ; 9781461440512, s. 187-194
  • Bokkapitel (refereegranskat)abstract
    • The possible importance of virus infections before the development of islet autoimmunity and then for the appearance of clinical type 1 diabetes is reviewed. There is a lack of specific data on the role of virus to induce islet autoimmunity. There is also a paucity of data to demonstrate that virus infections may contribute to an accelerated disease process resulting in clinical onset of type 1 diabetes. In contrast, there is a plethora of studies on virus infections at the time of clinical onset. However, these studies have made the understanding of virus in type 1 diabetes less easy. Future studies need to address further gestational infections and the risk of the offspring for islet autoimmunity. Such studies should also investigate the mechanisms by which gestational infections may alter the ability of the offspring to respond to future virus infections related to the development of islet autoimmunity or accelerator of the clinical onset of diabetes.
  •  
8.
  • Lindehammer, Sabina (författare)
  • Triggers of autoimmunity. Studies on gestational events.
  • 2011
  • Doktorsavhandling (övrigt vetenskapligt)abstract
    • Popular Abstract in Swedish Typ 1-diabetes är en allvarlig, autoimmun, sjukdom och Sverige har världens näst högsta antal nya insjuknanden. Varje år diagnostiseras ca 700 individer i Sverige med sjukdomen som kan debutera i alla åldrar. Senare studier tyder dock på att barn med typ 1-diabetes blir allt yngre. Vi vet idag att ärftligheten är kopplad till en specifik gen vilket förklarar ca 30-50% av sjukdomsförekomsten. Detta tyder på att inte bara ärftlighet kan förklara sjukdomen utan någon form av miljöfaktor också krävs för att sjukdomen ska bryta ut. Glutenintolerans är en annan autoimmun sjukdom som har samma ärftliga faktor som typ 1-diabetes, fast i denna sjukdom känner vi till antigenet, nämligen gluten - en samling proteiner som finns i vete, råg och korn. I populationsstudien DiPiS (Diabetes Prediktion i Skåne) samlade man in blodprover från kvinnor (DiPiS mammor) i samband med förlossning. Dessa prover påvisade en säsongsberoende variation i mammor som födde barn med autoantikroppar. Dessa autoantikroppar är så kallade markörer för typ 1-diabetes. Dessutom har man visat att mammor som rapporterade infektioner tidigt under graviditeten samt under vintermånaderna, påvisade en ökad risk att föda barn med autoantikroppar. Detta skulle kunna betyda att infektioner är en faktor som påverkar förekomsten av typ 1-diabetes. Med hjälp av en biobank vid Mikrobiologen i Malmö har vi lyckats identifiera DiPiS-mammor och hämta ut deras blodprov vilka samlades in under deras första besök hos mödravården. Det övergripande målet med denna avhandling är att undersöka sambandet mellan miljöfaktorer under tidig graviditet och senare förekomst av autoimmunitet hos barnet. Vi testar också möjligheten att exponering för vissa virusstammar (som tillhör gruppen enterovirus) skulle kunna vara en utlösande faktor för autoimmunitet hos barnet. DiPiS-studien och mikrobiologens biobank möjliggjorde våra studier som undersöker förändringar i immunförsvaret hos mamman under tidig graviditet, som senare födde barn vilka utvecklade typ 1-diabetes eller glutenintolerans. I den första delstudien av avhandlingen undersöker vi förekomst och utveckling av autoantikroppar kopplade till typ 1-diabetes i den gravida mamman. I detta arbete undersöktes inskrivningsprovet från Mikrobiologen i Malmö hos 242 friska mammor vid förlossning av sitt barn, för autoantikroppar mot insulin, GAD65 eller IA-2. Huvudfyndet var att de flesta mammor som födde barn med autoantikroppar hade dessa redan i inskrivningsprovet och nivån av dessa sjönk sedan under resten av graviditeten. Detta är också vanligt med autoantikroppar för andra autoimmuna sjukdomar, där det är välkänt att de sjunker under graviditeten, till exempel ledgångsreumatism. I vår studie var det totalt 50 mammor som utvecklade autoantikroppar under graviditeten. I det andra delarbetet undersökte vi förändringar i immunförsvaret hos mamman under tidig graviditet, samt om dessa förändringar var kopplade till glutenintolerans hos barnet senare i livet. Inskrivningsprovet från Mikrobiologen i Malmö analyserades för nio cytokiner och en chemokin, vilka alla är immunologiska markörer. Totalt visade sig sju av nio cytokiner vara förhöjda i inskrivningsprovet hos de mammor som födde ett barn som utvecklade glutenintolerans före fem års ålder. I delarbete tre undersöktes 48 mammor som fött ett barn vilket utvecklade typ-1 diabetes före sju års ålder. Dessa mammors inskrivningsprov undersöktes tillsammans med 93 kontrollmammor för samma immunologiska markörer som i delarbete två. Huvudfynden var att cytokiner som ofta uttrycks i samband med infektioner och som aktiverar den cellulära delen av immunförsvaret återfanns i förhöjda koncentrationer hos de mammor som födde ett barn som utvecklade diabetes före sju års ålder. I det sista delarbetet analyserades samtliga inskrivningsprover för IgM-antikroppar mot en specifik virusgrupp som kallas för enterovirus. Resultaten visar att ca 10% av mammorna visade tecken på virusexponering redan i inskrivningsprovet. Autoantikroppar återfanns oftare hos de mammor som hade den ärftliga riskfaktorn för både typ-1 diabetes och glutenintolerans. Ett viktigt fynd var att mammor som utvecklade autoantikroppar under graviditeten dvs. var negativa i inskrivningsprovet men positiva vid födseln, var i högre utsträckning positiva för enterovirus IgM-antikroppar i inskrivningsprovet än de som inte utvecklade autoantikroppar under graviditeten. Dessa resultat påvisar att en enterovirusinfektion tidig under graviditeten kan förklara att mammor med ärftlig risk för typ 1-diabetes utvecklar autoantikroppar som är karakteristiska för typ 1-diabetes. Avhandlingen som presenteras här är den första av sitt slag då den direkt undersöker hur autoantikroppar uppstår under graviditeten och att det finns ett samband mellan inflammatoriska processer vid virusinfektioner och förekomsten av autoimmuna sjukdomar såsom glutenintolerans och typ 1-diabetes hos barnet. Detta fynd stödjer hypotesen att miljöfaktorer som påverkar mamman under tidig graviditet också påverkar det ofödda fostrets framtida hälsa.
9.
  • Löfroos, Ann-Britt, et al. (författare)
  • Colorectal cancer-infiltrating T lymphocytes display a distinct chemokine receptor expression profile
  • 2017
  • Ingår i: European Journal of Medical Research. - BioMed Central (BMC). - 0949-2321. ; 22:1
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: T lymphocytes exert important homeostatic functions in the healthy intestinal mucosa, whereas in case of colorectal cancer (CRC), infiltration of T lymphocytes into the tumor is crucial for an effective anti-tumor immune response. In both situations, the recruitment mechanisms of T lymphocytes into the tissues are essential for the immunological functions deciding the outcome. The recruitment of T lymphocytes is largely dependent on their expression of various chemokine receptors. The aim of this study was to identify potential chemokine receptors involved in the recruitment of T lymphocytes to normal human colonic mucosa and to CRC tissue, respectively, by examining the expression of 16 different chemokine receptors on T lymphocytes isolated from these tissues. Methods: Tissues were collected from patients undergoing bowel resection for CRC. Lymphocytes were isolated through enzymatic tissue degradation of CRC tissue and nearby located unaffected mucosa, respectively. The expression of a broad panel of chemokine receptors on the freshly isolated T lymphocytes was examined by flow cytometry. Results: In the normal colonic mucosa, the frequencies of cells expressing CCR2, CCR4, CXCR3, and CXCR6 differed significantly between CD4+ and CD8+ T lymphocytes, suggesting that the molecular mechanisms mediating T lymphocyte recruitment to the gut differ between CD4+ and CD8+ T lymphocytes. In CRC, the frequencies of cells expressing CCR2 and CXCR5 were significantly lower in both the CD4+ and CD8+ T lymphocyte populations compared to unaffected colonic mucosa, and the frequency of CCR9+ cytotoxic T lymphocytes was significantly decreased in CRC tissue. Conclusions: With regard to the normal gut mucosa, the results suggest that the molecular mechanisms mediating T lymphocyte recruitment differ between CD4+ and CD8+ T lymphocytes, which are important for understanding gut homeostasis. Importantly, T lymphocytes from CRC compared to normal colonic tissue displayed a distinct chemokine receptor expression profile, suggesting that mechanisms for recruitment of T lymphocytes to CRC tissue are skewed compared to normal colonic mucosa. Understanding these mechanisms could help in developing new strategies in cancer immunotherapy and to optimize already available alternatives such as immune checkpoint inhibitors.
10.
  • Rešić Lindehammer, Sabina, et al. (författare)
  • Seroconversion to Islet Autoantibodies After Enterovirus Infection in Early Pregnancy.
  • 2012
  • Ingår i: Viral Immunology. - Mary Ann Liebert, Inc.. - 0882-8245. ; 25:4, s. 254-261
  • Tidskriftsartikel (refereegranskat)abstract
    • Gestational enterovirus (EV) infections have been associated with an increased risk for type 1 diabetes in the offspring. We therefore analyzed non-diabetic mothers for EV exposure in early pregnancy in relation to type 1 diabetes HLA-DQ risk genotypes and seroconversion to islet autoantibodies during pregnancy. Non-diabetic mothers who had islet autoantibodies (n=365) against glutamic acid decarboxylase (GADA), islet antigen-2 autoantibodies (IA-2A), or insulin autoantibodies (IAA), in early pregnancy and at delivery were compared to islet autoantibody-negative mothers (n=1457) matched for age and sampling date. Mothers were genotyped for HLA-DQ and analyzed for both EV-RNA and EV-IgM. EV-IgM, but not EV-RNA, was detected during early pregnancy in 12% of islet autoantibody-positive mothers compared to 11% of the controls. In early pregnancy, mothers with HLA-DQ 2/2 or 2/X genotypes showed an increased risk for islet autoantibodies at delivery (OR 1.85; p=0.001). After adjusting for parity, maternal age, year of birth, and season of early pregnancy, early pregnancy EV-IgM combined with DQ2/2 or 2/X increased the risk for islet autoantibodies (OR 3.10; 95% CI 1; p=0.008). EV-IgM in early pregnancy increased the risk for islet autoantibodies at delivery in non-diabetic mothers with HLA-DQ 2/2 or 2/X type 1 diabetes risk genotypes.
Skapa referenser, mejla, bekava och länka
  • Resultat 1-10 av 12
  • [1]2Nästa
 
pil uppåt Stäng

Kopiera och spara länken för att återkomma till aktuell vy