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2015 ; 64
(ä): 13-25
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The immunogenetics of multiple sclerosis: A comprehensive review
#MMPMID26142251
Hollenbach JA
; Oksenberg JR
J Autoimmun
2015[Nov]; 64
(ä): 13-25
PMID26142251
show ga
Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous
system and common cause of non-traumatic neurological disability in young adults.
The likelihood for an individual to develop MS is strongly influenced by her or
his ethnic background and family history of disease, suggesting that genetic
susceptibility is a key determinant of risk. Over 100 loci have been firmly
associated with susceptibility, whereas the main signal genome-wide maps to the
class II region of the human leukocyte antigen (HLA) gene cluster and explains up
to 10.5% of the genetic variance underlying risk. HLA-DRB1*15:01 has the
strongest effect with an average odds ratio of 3.08. However, complex allelic
hierarchical lineages, cis/trans haplotypic effects, and independent protective
signals in the class I region of the locus have been described as well. Despite
the remarkable molecular dissection of the HLA region in MS, further studies are
needed to generate unifying models to account for the role of the MHC in disease
pathogenesis. Driven by the discovery of combinatorial associations of
Killer-cell Immunoglobulin-like Receptor (KIR) and HLA alleles with infectious,
autoimmune diseases, transplantation outcome and pregnancy, multi-locus
immunogenomic research is now thriving. Central to immunity and critically
important for human health, KIR molecules and their HLA ligands are encoded by
complex genetic systems with extraordinarily high levels of sequence and
structural variation and complex expression patterns. However, studies to-date of
KIR in MS have been few and limited to very low resolution genotyping.
Application of modern sequencing methodologies coupled with state of the art
bioinformatics and analytical approaches will permit us to fully appreciate the
impact of HLA and KIR variation in MS.
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