Add like
Add dislike
Add to saved papers

Distinct HLA-C/KIR genotype profile associates with guttate psoriasis.

Psoriasis is a multifactorial disease with a strong genetic background. It associates strongly to HLA-Cw*0602. HLA-C interacts with killer immunoglobulin-like receptors (KIR) on natural killer (NK) and some natural killer-T (NKT) cells. KIR's function is triggered by specific binding to HLA ligands, which depends on the amino acid 80 of the MHC class I alpha-chain. This permits classifying all HLA-C alleles into two functional groups: asparagine (N80) or lysine (K80) carrying alleles. Psoriasis patients recruited at disease onset were categorized as guttate, vulgaris without arthropathy and vulgaris with arthropathy plus skin lesions. Patients and carefully matched controls were genotyped for position 80 of HLA-C and for KIR. Based on possible HLA/KIR combinations, individuals were classified according to expected NK/NKT cell responses: balanced (B), excess inhibition (EI), excess activation (EA), or undetermined (U). HLA-Cw6 and position 80 genotyping associated strongly to disease, whereas KIR2DS1 associated weakly. Individuals of the U and EI classes were more common among guttate psoriasis patients, which related to HLA-Cw*0602 status. These results suggest that different levels for NK/NKT cell activation thresholds, not only reduction, contribute to immune deregulation in psoriasis. In the guttate phenotype, balanced HLA-C/KIR interactions might be altered by the presence of concomitant streptococcal infections.

Full text links

We have located links that may give you full text access.
Can't access the paper?
Try logging in through your university/institutional subscription. For a smoother one-click institutional access experience, please use our mobile app.

For the best experience, use the Read mobile app

Mobile app image

Get seemless 1-tap access through your institution/university

For the best experience, use the Read mobile app

All material on this website is protected by copyright, Copyright © 1994-2024 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.

By using this service, you agree to our terms of use and privacy policy.

Your Privacy Choices Toggle icon

You can now claim free CME credits for this literature searchClaim now

Get seemless 1-tap access through your institution/university

For the best experience, use the Read mobile app