Abstract
Genetic dissection of human systemic lupus erythematosus (SLE) has been under intense studies during the past decade. Although the complexity inherent to polygenic, multifactorial diseases is challenging, several new insights have been obtained in the past several years using linkage and association studies of families containing SLE patients as well as case-control studies of populations. In addition, recent advances in our understanding of the human genome and emerging technology have been providing new tools in analyses of complex traits, such as SLE. An overview of our current understanding of the genetic basis of SLE and a brief review of findings of linkage and association studies are described here.
Publication types
-
Research Support, Non-U.S. Gov't
-
Research Support, U.S. Gov't, P.H.S.
-
Review
MeSH terms
-
Animals
-
Antigens, CD
-
Antigens, Surface / genetics
-
Apoptosis Regulatory Proteins
-
Chromosome Mapping
-
Complement System Proteins / genetics
-
Epistasis, Genetic
-
Female
-
Genetic Linkage
-
Humans
-
Lupus Erythematosus, Systemic / genetics*
-
Major Histocompatibility Complex
-
Male
-
Mice
-
Models, Genetic
-
Peptidyl-Dipeptidase A / genetics
-
Poly(ADP-ribose) Polymerases / genetics
-
Programmed Cell Death 1 Receptor
-
Receptors, IgG / genetics
Substances
-
Antigens, CD
-
Antigens, Surface
-
Apoptosis Regulatory Proteins
-
PDCD1 protein, human
-
Pdcd1 protein, mouse
-
Programmed Cell Death 1 Receptor
-
Receptors, IgG
-
Complement System Proteins
-
Poly(ADP-ribose) Polymerases
-
Peptidyl-Dipeptidase A