Hypothesis for the pathogenesis of type 1A diabetes

Drugs of Today

Volumn 41, Issue 2, 2005, Pages 141-149

  Jasinski, Jean M ^a   Eisenbarth, George S ^b  

^a UNIVERSITY OF COLORADO   (United States)

^b UNIVERSITY OF COLORADO DENVER   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

C PEPTIDE; GLUTAMATE DECARBOXYLASE 65; HLA ANTIGEN; HLA DQ ANTIGEN; HLA DR ANTIGEN; INSULIN; INTERLEUKIN 13; PANCREAS ISLET CELL ANTIBODY; POLYCYTIDYLIC ACID; T LYMPHOCYTE RECEPTOR; T LYMPHOCYTE RECEPTOR BETA CHAIN; TOLL LIKE RECEPTOR; TRANSCRIPTION FACTOR FOXP3; VITAMIN D RECEPTOR;

ANIMAL EXPERIMENT; ANIMAL MODEL; AUTOIMMUNE DISEASE; CELL DESTRUCTION; CONGENITAL RUBELLA SYNDROME; CONTROLLED STUDY; DIABETES MELLITUS TYPE 1A; DIABETIC KETOACIDOSIS; ENTEROVIRUS; ENVIRONMENTAL FACTOR; FEMALE; GENE MUTATION; GENETIC POLYMORPHISM; GENETIC SUSCEPTIBILITY; HAPLOTYPE; HUMAN; IMMUNE MEDIATED DIABETES MELLITUS; IMMUNE RESPONSE GENE; IMMUNOSUPPRESSIVE TREATMENT; IMMUNOTHERAPY; INSULIN DEPENDENT DIABETES MELLITUS; INSULIN RELEASE; MAJOR HISTOCOMPATIBILITY COMPLEX; MOUSE; NONHUMAN; ONTOGENY; PANCREAS ISLET BETA CELL; PATHOGENESIS; RAT; REVIEW; T LYMPHOCYTE;

ANIMALS; DIABETES MELLITUS, TYPE 1; HUMANS; IMMUNOTHERAPY;

EID: 16244420705     PISSN: 16993993     EISSN: 16994019     Source Type: Journal    
DOI: 10.1358/dot.2005.41.2.882664     Document Type: Review

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