hh.sePublications
Change search
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf
Backcross and partial advanced intercross analysis of nonobese diabetic gene-mediated effects on collagen-induced arthritis reveals an interactive effect by two major loci
Lund University, Lund, Sweden; Cartela AB, Lund 22007, Sweden.
Lund University, Lund, Sweden.
Lund University, Lund, Sweden.
Lund University, Lund, Sweden.ORCID iD: 0000-0001-7790-8197
Show others and affiliations
2006 (English)In: Journal of Immunology, ISSN 0022-1767, E-ISSN 1550-6606, Vol. 177, no 6, p. 3952-3959Article in journal (Refereed) Published
Abstract [en]

Genetic segregation analysis between NOD and C57BL strains have been used to identify loci associated with autoimmune disease. Only two loci (Cia2 and Cia9) had earlier been found to control development of arthritis, whereas none of the previously identified diabetes loci was of significance for arthritis. We have now made a high-powered analysis of a backcross of NOD genes on to the B10.Q strain for association with collagen-induced arthritis. We could confirm relevance of both Cia2 and Cia9 as well as the interaction between them, but we did not identify any other significant arthritis loci. Immune cellular subtyping revealed that Cia2 was also associated with the number of blood macrophages. Congenic strains of the Cia2 and Cia9 loci on the B10.Q background were made and used to establish a partial advanced intercross (PAI). Testing the PAI mice for development of collagen-induced arthritis confirmed the loci and the interactions and also indicated that at least two genes contribute to the Cia9 locus. Furthermore, it clearly showed that Cia2 is dominant protective but that the protection is not complete. Because these results may indicate that the Cia2 effect on arthritis is not only due to the deficiency of the complement C5, we analyzed complement functions in the Cia2 congenics as well as the PAI mice. These data show that not only arthritis but also C5-dependent complement activity is dominantly suppressed, confirming that C5 is one of the major genes explaining the Cia2 effect. © 2006 by The American Association of Immunologists, Inc.

Place, publisher, year, edition, pages
Rockville, MD: American Association of Immunologists , 2006. Vol. 177, no 6, p. 3952-3959
National Category
Immunology in the medical area
Identifiers
URN: urn:nbn:se:hh:diva-48831DOI: 10.4049/jimmunol.177.6.3952ISI: 000240475300051PubMedID: 16951358Scopus ID: 2-s2.0-33748567828OAI: oai:DiVA.org:hh-48831DiVA, id: diva2:1719050
Available from: 2022-12-14 Created: 2022-12-14 Last updated: 2023-02-17Bibliographically approved

Open Access in DiVA

No full text in DiVA

Other links

Publisher's full textPubMedScopus

Authority records

Nandakumar, Kutty Selva

Search in DiVA

By author/editor
Nandakumar, Kutty Selva
In the same journal
Journal of Immunology
Immunology in the medical area

Search outside of DiVA

GoogleGoogle Scholar

doi
pubmed
urn-nbn

Altmetric score

doi
pubmed
urn-nbn
Total: 6 hits
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf