PMID- 15701924
OWN - NLM
STAT- MEDLINE
DCOM- 20050725
LR  - 20231213
IS  - 0007-1420 (Print)
IS  - 0007-1420 (Linking)
VI  - 71
DP  - 2004
TI  - Genetic insights into disease mechanisms of autoimmunity.
PG  - 93-113
AB  - Educating the immune system to distinguish between self and non-self is critical 
      to ensure that an immune response is mounted against foreign antigens and not 
      against self. A breakdown in these mechanisms can lead to the onset of autoimmune 
      disease. Clinical and molecular data suggest that shared immunogenetic mechanisms 
      lead to the autoimmune process. The most studied genes and molecules are the 
      human leukocyte antigen (HLA) region and the cytotoxic T-lymphocyte-associated 4 
      molecule (CTLA-4). Recently progress has been achieved in narrowing down the 
      primary variants within both gene regions, but further work is needed to 
      determine the function and extent of the aetiological variant(s) present. Recent 
      exciting results also suggest a role for the newly discovered lymphoid-specific 
      phosphatase (LYP) protein. As well as these general mechanisms, disease-specific 
      mechanisms are beginning to be elucidated, for example the role of autoimmune 
      regulatory element 1 (AIRE1) in autoimmune polyendocrinopathy-candidiasis 
      ectodermal dystrophy (APECED). Taken together, these data suggest that both 
      general and disease-specific mechanisms lead to the clinical outcome of 
      autoimmune disease and that increased understanding of these mechanisms will 
      improve our knowledge of how autoimmune disease occurs, eventually leading to the 
      development of novel therapeutic agents.
FAU - Simmonds, M J
AU  - Simmonds MJ
AD  - Division of Medical Sciences, University of Birmingham, Institute of Biomedical 
      Research, Birmingham B15 2TT, UK.
FAU - Gough, S C L
AU  - Gough SC
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20050208
PL  - England
TA  - Br Med Bull
JT  - British medical bulletin
JID - 0376542
RN  - 0 (Antigens, CD)
RN  - 0 (Antigens, Differentiation)
RN  - 0 (CTLA-4 Antigen)
RN  - 0 (CTLA4 protein, human)
RN  - 0 (HLA Antigens)
RN  - 0 (Histocompatibility Antigens Class I)
RN  - 0 (Histocompatibility Antigens Class II)
RN  - 0 (Immunosuppressive Agents)
RN  - 0 (Insulin)
RN  - 0 (Transcription Factors)
RN  - 9007-36-7 (Complement System Proteins)
SB  - IM
MH  - Antigens, CD
MH  - Antigens, Differentiation/genetics/immunology
MH  - Autoimmune Diseases/*genetics/immunology
MH  - Autoimmunity/*genetics/immunology
MH  - CTLA-4 Antigen
MH  - Complement System Proteins/genetics/immunology
MH  - HLA Antigens/*genetics/immunology
MH  - Histocompatibility Antigens Class I/genetics/immunology
MH  - Histocompatibility Antigens Class II/genetics/immunology
MH  - Humans
MH  - Immunosuppressive Agents/immunology
MH  - Insulin/genetics/immunology
MH  - Transcription Factors/genetics/immunology
MH  - AIRE Protein
RF  - 77
EDAT- 2005/02/11 09:00
MHDA- 2005/07/26 09:00
CRDT- 2005/02/11 09:00
PHST- 2005/02/11 09:00 [pubmed]
PHST- 2005/07/26 09:00 [medline]
PHST- 2005/02/11 09:00 [entrez]
AID - 71/1/93 [pii]
AID - 10.1093/bmb/ldh032 [doi]
PST - epublish
SO  - Br Med Bull. 2005 Feb 8;71:93-113. doi: 10.1093/bmb/ldh032. Print 2004.