Premium
Linkage Disequilibrium within the HLA Complex does not extend into HLA‐DP
Author(s) -
BAISCH J. M.,
CAPRA J. D.
Publication year - 1993
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/j.1365-3083.1993.tb03325.x
Subject(s) - linkage disequilibrium , human leukocyte antigen , genetics , biology , allele , haplotype , disequilibrium , population , gene , antigen , medicine , environmental health , ophthalmology
It is well known that certain alleles from different loci within the Human Leucocyte Antigen (HLA) complex are in linkage disequilibrium. This linkage phenomenon is relatively well characterized for haplotypes that include specific class I and class II alleles such as HLA‐B8 and HLA‐DR3. However, the HLA‐DP genes are located at the centromeric end of the HLA complex and are less well characterized with regard to linkage disequilibrium. The availability of a large population of healthy subjects and sequence‐specific oligonucleotide (SSO) typing enabled us to assess the degree of linkage between HLA‐DPBl and HLA‐DQBl genes. Using the polymerase chain reaction and a series of oligonucleotide probes which define seven DQβ alleles and twenty DPβ alleles, we studied 180 unrelated, normal Caucasian individuals and found only weak or negative associations between HLA‐DPBl and HLA‐DQBl. These data demonstrate that the association between HLA‐DQ and DP is weak and also imply that DP extended haplotypes related to particular diseases may not reflect normal associations. Implications of these results might impact on the concept of linkage disequilibrium in general as well as the evolution of the HLA complex. In addition, extensions of this work may have clinical ramifications with regard to bone marrow transplantation and founder effects in certain diseases.