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Ingebjørg Knutsen

Researcher at University of Oslo

Publications -  8
Citations -  553

Ingebjørg Knutsen is an academic researcher from University of Oslo. The author has contributed to research in topics: Allele & Haplotype. The author has an hindex of 7, co-authored 8 publications receiving 541 citations.

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HLA-Encoded Genetic Predisposition in IDDM: DR4 Subtypes May Be Associated With Different Degrees of Protection

TL;DR: It is suggested that disease susceptibility is mainly conferred by DQ8 while DR4 subtypes confer different degrees of protection, and features of a protective peptide that fit such a model are briefly discussed.
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HLA class II haplotypes in primary sclerosing cholangitis patients from five European populations

TL;DR: The association of primary sclerosing cholangitis (PSC) to HLA class II genes was studied by comparing patients from five different European populations and PSC was found to be positively associated to three different HLAclass II haplotypes.
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Dermatitis herpetiformis and celiac disease are both primarily associated with the HLA-DQ (α1*0501, (β1*02) or the HLA-DQ (α1*03, (β1*0302) heterodimers

TL;DR: It is concluded that dermatitis herpetiformis and celiac disease are associated to the very same HLA-DQ alpha beta heterodimers.
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A K‐ras 13GLY → ASP mutation is recognized by HLA‐DQ7 restricted T cells in a patient with colorectal cancer. Modifying effect of DQ7 on established cancers harbouring this mutation?

TL;DR: On the basis of analysis of 251 colonic carcinomas, the presence of HLA‐DQ7 did not seem to protect against the establishment of carcinomas carrying the 13Asp mutation, since the frequency of the DQ7 haplotype was not decreased among patients having this mutation.
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The HLA‐DQ(α1*0102, β1*0602) heterodimer may confer susceptibility to multiple sclerosis in the absence of the HLA‐DR(α1*01, β1*1501) heterodimer

TL;DR: The findings indicate that the genes encoding the DQ(alpha 1*0102, beta 1*0602) heterodimer may confer susceptibility to developing multiple sclerosis in the absence of the DRB1*1501 allele.