Sökning: id:"swepub:oai:DiVA.org:umu-41996" >
The prolonged and e...
-
Sundström, Mia,1980-Umeå universitet,Immunologi/immunkemi,Lejon
(författare)
The prolonged and enhanced immune response in the non-obese diabetic mouse is dependent on genes in the Idd1/24, Idd12 and Idd18 regions
- Artikel/kapitelEngelska2010
Förlag, utgivningsår, omfång ...
-
Elsevier BV,2010
-
printrdacarrier
Nummerbeteckningar
-
LIBRIS-ID:oai:DiVA.org:umu-41996
-
https://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-41996URI
-
https://doi.org/10.1016/j.jaut.2010.08.002DOI
Kompletterande språkuppgifter
-
Språk:engelska
-
Sammanfattning på:engelska
Ingår i deldatabas
Klassifikation
-
Ämneskategori:ref swepub-contenttype
-
Ämneskategori:art swepub-publicationtype
Anmärkningar
-
In non-obese diabetic (NOD) mice B cells are an absolute requirement for T1D development. NOD mice display various B cell related immune deviations when compared to normal mice such as an enhanced and prolonged immune response towards several antigens, including non-self immunoglobulins. We hypothesized that this trait contributes to diabetes pathogenesis, and investigated the genetic factor(s) governing the altered immune response. A (NODxC57BL/6)F(2) cohort (n = 214) were analyzed for its primary immune response against a BALB/c derived monoclonal antibody, and a genome wide linkage analysis was performed. Significant linkage to the Idd1/Idd24, Idd12 and Idd18.1 regions as well as to a proximal region (marker D2Mit367, 33.5 Mb) on chromosome 2 was detected. We verified the observed linkage by analyzing a set of H2 congenic NOD and C57BL/6 mice and narrowed down the region to 8 Mb. Interaction between Idd1/24 and Idd12, as well as the novel locus on chromosome 2 was observed. However, the action by Idd18.1 was not influenced by any of the other loci. In addition to the known H2 I-Aβ(g7) allelic variant of Idd1 in NOD, candidate gene analysis revealed a significant difference in the transcription of the H2-O/DO molecule. We hypothesize that multiple mechanisms contribute to the loss of immune response control, including that peptide loading on MHC class II in B cells of NOD is altered.
Ämnesord och genrebeteckningar
Biuppslag (personer, institutioner, konferenser, titlar ...)
-
Lejon, KristinaUmeå universitet,Immunologi/immunkemi,Lejon(Swepub:umu)krle0001
(författare)
-
Umeå universitetImmunologi/immunkemi
(creator_code:org_t)
Sammanhörande titlar
-
Ingår i:Journal of Autoimmunity: Elsevier BV35:4, s. 375-3820896-84111095-9157
Internetlänk
Hitta via bibliotek
Till lärosätets databas