PMID- 19474733
OWN - NLM
STAT- MEDLINE
DCOM- 20091007
LR  - 20171116
IS  - 1531-698X (Electronic)
IS  - 1040-8703 (Linking)
VI  - 21
IP  - 4
DP  - 2009 Aug
TI  - Autoimmune thyroid disease: unlocking a complex puzzle.
PG  - 523-8
LID - 10.1097/MOP.0b013e32832cf824 [doi]
AB  - PURPOSE OF REVIEW: The autoimmune thyroid diseases (AITD), Graves' disease and 
      chronic lymphocytic thyroiditis (CLT) are amongst the most common endocrine 
      diseases in childhood and adolescence. The application of molecular biology has 
      permitted an unparalleled insight into susceptibility genes that predispose to 
      their development and has allowed enhanced understanding of their complex immune 
      pathophysiology. RECENT FINDINGS: The susceptibility genes that predispose to 
      AITD can be subdivided into those that affect the immune response in general and 
      thyroid-specific antigens. Both known and new susceptibility genes have been the 
      focus of recent attention. Although there is no known human leukocyte antigen 
      (HLA) association in CLT, recent work has demonstrated an association with a 
      specific amino acid pocket signature irrespective of the HLA-DR class. In Graves' 
      disease a specific combination of polymorphisms for thyroglobulin and HLA-DR 
      markedly increases the odds ratio for developing disease. The availability of 
      recombinant antigen [particularly thyroid peroxidase and thyrotropin (TSH) 
      receptor] and of high affinity monoclonal antibodies has provided insight into 
      the specific epitopes recognized by antibodies in AITD and has confirmed the 
      increased affinity of stimulating TSH receptor antibodies for the shed A subunit 
      rather than the holoreceptor. SUMMARY: Powerful molecular tools have been 
      developed that have shed light on the nature of the susceptibility genes for and 
      the pathophysiology of AITD. These have already led to improved diagnostic tools 
      and, hopefully, will permit the development of more specific immune therapy in 
      the future.
FAU - Brown, Rosalind S
AU  - Brown RS
AD  - Children's Hospital Boston and Harvard University, Boston, Massachusetts 02115, 
      USA. Rosalind.Brown@childrens.harvard.edu
LA  - eng
PT  - Journal Article
PT  - Review
PL  - United States
TA  - Curr Opin Pediatr
JT  - Current opinion in pediatrics
JID - 9000850
RN  - 0 (Antigens, CD)
RN  - 0 (CD40 Antigens)
RN  - 0 (CTLA-4 Antigen)
RN  - 0 (CTLA4 protein, human)
RN  - 0 (HLA Antigens)
RN  - EC 3.1.3.48 (PTPN22 protein, human)
RN  - EC 3.1.3.48 (Protein Tyrosine Phosphatase, Non-Receptor Type 22)
SB  - IM
MH  - Adolescent
MH  - Animals
MH  - Antibody Formation
MH  - Antigens, CD/genetics
MH  - Apoptosis/immunology
MH  - CD40 Antigens/genetics
MH  - CTLA-4 Antigen
MH  - Child
MH  - Child, Preschool
MH  - Gene Expression Regulation
MH  - Genetic Predisposition to Disease
MH  - Graves Disease
MH  - HLA Antigens/genetics
MH  - Hashimoto Disease/*genetics/*immunology
MH  - Humans
MH  - Immunity, Cellular
MH  - Protein Tyrosine Phosphatase, Non-Receptor Type 22/genetics
MH  - Th1 Cells/immunology
MH  - Th2 Cells/immunology
MH  - Thyroiditis, Autoimmune/*genetics/*immunology
RF  - 39
EDAT- 2009/05/29 09:00
MHDA- 2009/10/08 06:00
CRDT- 2009/05/29 09:00
PHST- 2009/05/29 09:00 [entrez]
PHST- 2009/05/29 09:00 [pubmed]
PHST- 2009/10/08 06:00 [medline]
AID - 10.1097/MOP.0b013e32832cf824 [doi]
PST - ppublish
SO  - Curr Opin Pediatr. 2009 Aug;21(4):523-8. doi: 10.1097/MOP.0b013e32832cf824.