PMID- 21045701
OWN - NLM
STAT- MEDLINE
DCOM- 20110324
LR  - 20101215
IS  - 1531-6963 (Electronic)
IS  - 1040-8711 (Linking)
VI  - 23
IP  - 1
DP  - 2011 Jan
TI  - Pathogenesis of IgG4-related disease.
PG  - 114-8
LID - 10.1097/BOR.0b013e3283412f4a [doi]
AB  - PURPOSE OF REVIEW: To review studies that have examined underlying genetic and 
      immunological aspects of IgG4-related disease. RECENT FINDINGS: Genetic studies 
      have suggested that several human leukocyte antigen (HLA) and non-HLA 
      haplotypes/genotypes are associated with susceptibility to IgG4-related disease 
      or to disease relapse after steroid therapy. Among several autoantibodies 
      identified so far, autoantibodies against lactoferrin and carbonic anhydrase II 
      are most frequently detected in serum of IgG4-disease patients. However, it has 
      not been well clarified whether or not those autoantibodies belong to an IgG4 
      subclass. Studies that have demonstrated molecular mimicry between Helicobacter 
      pylori and constituents of pancreatic epithelial cells suggest that gastric H. 
      pylori infection triggers autoimmune pancreatitis in genetically predisposed 
      individuals through antibody cross-reactivity. Recently, T-helper 2 immune 
      reaction has been suggested to be predominant in IgG4-related disease. 
      Interestingly, regulatory immune reactions are activated in IgG4-related disease, 
      and regulatory cytokines interleukin-10 and transforming growth factor-b have 
      been suggested, respectively, to play important roles in IgG4 class switch and 
      fibroplasia. SUMMARY: Autoimmunity has been considered the most probable 
      pathogenesis of IgG4-related disease, but has not been completely proved so far. 
      A breakthrough study to detect a specific autoantigen, autoantibody, or pathogen 
      is necessary.
FAU - Zen, Yoh
AU  - Zen Y
AD  - Institute of Liver Studies, King's College Hospital, London, UK. 
      yoh.zen@kcl.ac.uk
FAU - Nakanuma, Yasuni
AU  - Nakanuma Y
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - United States
TA  - Curr Opin Rheumatol
JT  - Current opinion in rheumatology
JID - 9000851
RN  - 0 (Autoantigens)
RN  - 0 (Chemokines)
RN  - 0 (Cytokines)
RN  - 0 (Immunoglobulin G)
SB  - IM
MH  - Autoantigens/immunology
MH  - Autoimmune Diseases/*etiology/genetics/immunology/pathology
MH  - Chemokines/immunology
MH  - Cross Reactions
MH  - Cytokines/immunology
MH  - Genetic Predisposition to Disease
MH  - Helicobacter Infections/complications/immunology
MH  - Helicobacter pylori/immunology
MH  - Humans
MH  - Immunoglobulin G/*metabolism
MH  - Molecular Mimicry
MH  - Pancreatitis/etiology/genetics/immunology
MH  - T-Lymphocytes, Regulatory/immunology
EDAT- 2010/11/04 06:00
MHDA- 2011/03/25 06:00
CRDT- 2010/11/04 06:00
PHST- 2010/11/04 06:00 [entrez]
PHST- 2010/11/04 06:00 [pubmed]
PHST- 2011/03/25 06:00 [medline]
AID - 10.1097/BOR.0b013e3283412f4a [doi]
PST - ppublish
SO  - Curr Opin Rheumatol. 2011 Jan;23(1):114-8. doi: 10.1097/BOR.0b013e3283412f4a.