SwePub
Sök i SwePub databas

  Utökad sökning

Träfflista för sökning "L773:0896 8411 OR L773:1095 9157 srt2:(2005-2009)"

Sökning: L773:0896 8411 OR L773:1095 9157 > (2005-2009)

  • Resultat 11-14 av 14
Sortera/gruppera träfflistan
   
NumreringReferensOmslagsbildHitta
11.
  • Bjornvold, M., et al. (författare)
  • FOXP3 polymorphisms in type 1 diabetes and coeliac disease
  • 2006
  • Ingår i: J Autoimmun. - : Elsevier BV. - 0896-8411. ; 27:2, s. 140-4
  • Tidskriftsartikel (refereegranskat)abstract
    • The FOXP3 gene encodes a transcription factor thought to be essential for the development and function of T regulatory cells. Two previous studies have tested common polymorphisms in FOXP3 for association with type 1 diabetes (T1D) with conflicting results. The aim of our study was to see whether there is any evidence of association between the FOXP3 polymorphisms previously reported to be associated with T1D, in a Caucasian population regarding T1D and coeliac disease (CD). We further looked for evidence of interaction between FOXP3 polymorphisms and HLA-DR3 in conferring susceptibility to T1D. Initially, we analysed two microsatellites in the FOXP3 gene in 363 T1D nuclear families. Our results indicated an association between FOXP3 and T1D (global p=0.004) and a possible interaction between FOXP3 and the HLA-DR3-DQ2 susceptibility haplotype. We then genotyped an additional independent set of 826 T1D patients and 1459 controls as well as one CD dataset consisting of 325 families. A similar tendency was revealed in the CD family material (pnc=0.055 for the associated allele). On the other hand, we were unable to reproduce our initial findings in the T1D case-control dataset (global p=0.6). Our results suggest that the tested FOXP3 markers do not have any major impact on susceptibility for these diseases.
  •  
12.
  •  
13.
  • Persson-Sjögren, Solveig, et al. (författare)
  • Expression of the NK-1 receptor on islet cells and invading immune cells in the non-obese diabetic mouse
  • 2005
  • Ingår i: Journal of Autoimmunity. - : Elsevier. - 0896-8411. ; 24:4, s. 269-279
  • Tidskriftsartikel (refereegranskat)abstract
    • The underlying mechanistic causes of immune cell infiltration in the islets of Langerhans and beta cell failure in the non-obese diabetic (NOD) mouse is still to be completely revealed. Substance P (SP) is a substance known to have pro-inflammatory, endocrine, neuromodulatory and trophic effects, and its preferred receptor, the neurokinin receptor 1 (NK-1 R), is reported to be involved in extravasation of granulocytes and in inflammation and tissue derangement. Therefore, we have investigated the expression of NK-1 R during development of insulitis in the NOD mouse. We show that the magnitude of immunoreactivity scoring NK-1 R expression in the islets was increased in the 12-week-old NOD mouse. Expression of NK-1 R co-localized with expression of glucagon. In line with this expression pattern, we did not detect any effect of SP on glucose-induced insulin release. NK-1 R expression was particularly observed in islet cells in association with the clusters of immune cells. Expression of NK-1 R was also demonstrated in a fraction of the infiltrating B and T lymphocytes, as well as on infiltrating macrophages and dendritic cells. The observations show that the level of NK-1 R expression is increased in 12-week-old NOD mice, being correlated with the occurrence of islet mononuclear infiltration. Our data suggest that SP may act as a chemoattractant, contributing to the pathogenic mononuclear infiltration process in the NOD mouse. On the whole, the observations suggest that SP and the NK-1 R to certain extents are involved in the changes that occur during the development of insulitis in the NOD mouse.
  •  
14.
  •  
Skapa referenser, mejla, bekava och länka
  • Resultat 11-14 av 14
Typ av publikation
tidskriftsartikel (13)
forskningsöversikt (1)
Typ av innehåll
refereegranskat (13)
populärvet., debatt m.m. (1)
Författare/redaktör
Kämpe, Olle (2)
Vaarala, Outi, 1962- (2)
Johansson, Boo (2)
Lejon, Kristina (2)
Ernerudh, Jan (1)
Alarcón-Riquelme, Ma ... (1)
visa fler...
Padyukov, L (1)
Lundberg, IE (1)
Gudjonsdottir, Audur ... (1)
Ascher, Henry, 1953 (1)
Amundsen, S. S. (1)
Dastmalchi, M (1)
Rorsman, Fredrik (1)
Dahle, Charlotte (1)
Dahle, Charlotte, 19 ... (1)
Ludvigsson, Johnny, ... (1)
Nilsson, Bengt-Olof (1)
Holmberg, Dan (1)
Kleinau, Sandra (1)
Forsgren, Sture (1)
Ekwall, Olov, 1968 (1)
Fathi, M (1)
Martinsson, Klara (1)
Alimohammadi, Mohamm ... (1)
Pöntynen, Nora (1)
Peltonen, Leena (1)
Betterle, Corrado (1)
Hultman, Per (1)
Soderberg-Naucler, C (1)
Skogh, Thomas (1)
Dumanski, Jan P (1)
Lie, B. A. (1)
Ek, J. (1)
Sollid, L. M. (1)
Hyöty, Heikki (1)
Knip, Mikael (1)
Ilonen, Jorma (1)
Löfgren, Sture (1)
Wikby, Anders (1)
Bruder, Carl E G (1)
Dahl-Jorgensen, K. (1)
Simell, Olli (1)
Ernerudh, Jan, 1952- (1)
Ardesjö, Brita (1)
Hansson, Caisa M (1)
Rahbar, A (1)
Lofgren, S (1)
Lejon, Kristina, 196 ... (1)
Holmberg, Dan, 1954- (1)
Motta, Vinicius (1)
visa färre...
Lärosäte
Linköpings universitet (5)
Uppsala universitet (4)
Göteborgs universitet (3)
Umeå universitet (3)
Karolinska Institutet (2)
Jönköping University (1)
Språk
Engelska (14)
Forskningsämne (UKÄ/SCB)
Medicin och hälsovetenskap (3)
Naturvetenskap (1)
Samhällsvetenskap (1)

År

Kungliga biblioteket hanterar dina personuppgifter i enlighet med EU:s dataskyddsförordning (2018), GDPR. Läs mer om hur det funkar här.
Så här hanterar KB dina uppgifter vid användning av denna tjänst.

 
pil uppåt Stäng

Kopiera och spara länken för att återkomma till aktuell vy