Priming and effector dependence on insulin B:9-23 peptide in NOD islet autoimmunity.

Priming and effector dependence on insulin B:9-23 peptide in NOD islet autoimmunity. Research Abstract Details 

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Priming and effector dependence on insulin B:9-23 peptide in NOD islet autoimmunity. Abstract Text:

Maki Nakayama,Joshua N Beilke,Jean M Jasinski,Masakazu Kobayashi,Dongmei Miao,Marcella Li,Marilyne G Coulombe,Edwin Liu,John F Elliott,Ronald G Gill,George S Eisenbarth,

NOD mice with knockout of both native insulin genes and a mutated proinsulin transgene, alanine at position B16 in preproinsulin (B16:A-dKO mice), do not develop diabetes. Transplantation of NOD islets, but not bone marrow, expressing native insulin sequences (tyrosine at position B16) into B16:A-dKO mice rapidly restored development of insulin autoantibodies (IAAs) and insulitis, despite the recipients' pancreatic islets lacking native insulin sequences. Splenocytes from B16:A-dKO mice that received native insulin-positive islets induced diabetes when transferred into wild-type NOD/SCID or B16:A-dKO NOD/SCID mice. Splenocytes from mice immunized with native insulin B chain amino acids 9-23 (insulin B:9-23) peptide in CFA induced rapid diabetes upon transfer only in recipients expressing the native insulin B:9-23 sequence in their pancreata. Additionally, CD4(+) T cells from B16:A-dKO mice immunized with native insulin B:9-23 peptide promoted IAAs in NOD/SCID mice. These results indicate that the provision of native insulin B:9-23 sequences is sufficient to prime anti-insulin autoimmunity and that subsequent transfer of diabetes following peptide immunization requires native insulin B:9-23 expression in islets. Our findings demonstrate dependence on B16 alanine versus tyrosine of insulin B:9-23 for both the initial priming and the effector phase of NOD anti-islet autoimmunity.

Priming and effector dependence on insulin B:9-23 peptide in NOD islet autoimmunity. Publishing Authors By Initials

M Nakayama,JN Beilke,JM Jasinski,M Kobayashi,D Miao,M Li,MG Coulombe,E Liu,JF Elliott,RG Gill,GS Eisenbarth,

For similar investigative techniques: epidemiologic methods: data collection: vital statistics: mortality: survival rate research abstracts see: investigative techniques: epidemiologic methods: data collection: vital statistics: mortality: survival rate research

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Priming and effector dependence on insulin B:9-23 peptide in NOD islet autoimmunity. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: The Journal of clinical investigation

VOLUME: 117

Page Numbers: 1835-43

Journal Abbreviation: J. Clin. Invest.

ISSN: 0021-9738

DAY: 3

MONTH: Jul

YEAR: 2007

Priming and effector dependence on insulin B:9-23 peptide in NOD islet autoimmunity. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 7802877

Priming and effector dependence on insulin B:9-23 peptide in NOD islet autoimmunity. Keywords Mesh Terms:

KEYWORDS: Survival Rate

MESH TERMS: transplantation

Chemical & Substance for Abstract: Priming and effector dependence on insulin B:9-23 peptide in NOD islet autoimmunity. Information

Substance Name: Insulin

Registry Number: 11061-68-0

Grant and Affiliation Information for Priming and effector dependence on insulin B:9-23 peptide in NOD islet autoimmunity.

AFFILIATION: Barbara Davis Center for Childhood Diabetes, University of Colorado Health Sciences Center (UCHSC), Aurora, CO 80045-6511, USA.

Country: United States

AGENCY: United States NIDDK

GRANT: P30 DK57516

ACRONYM: DK

MEDLINETA: J Clin Invest

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