NDLI: H2-E transgenic class II-negative mice can distinguish self from nonself in susceptibility to heterologous thyroglobulins in autoimmune thyroiditis

Please wait, while we are loading the content...

Generation of the primary antibody repertoire in rabbits: expression of a diverse set of Igk-V genes may compensate for limited combinatorial diversity at the heavy chain locus

Molecular analysis of complement component C8β and C9 cDNAs of Japanese flounder, Paralichthys olivaceus

Characterization of MHC class I and β2-microglobulin sequences in Atlantic cod reveals an unusually high number of expressed class I genes

Identification and characterization of a fish natural resistance-associated macrophage protein (NRAMP) cDNA

Genomic structure and chromosomal location of the mouse macrophage C-type lectin gene

Determination of the IgG2a allotype of CXB recombinant inbred mouse strains by a PCR-based method

Autoreactive T-cell receptor expression in mouse chronic graft-vs-host disease

Characterization of beta2-microglobulin in a primitive fish, the Siberian sturgeon (Acipenser baeri)

Cloning of two zebrafish cDNAs that share domains with the MHC class II-associated invariant chain

Marsupial Mhc class I: classical sequences from the opossum, Monodelphis domestica

Cloning and sequencing of horse interleukin-12 and interleukin-18 cDNAs

The structure of the llama heavy chain constant genes reveals a mechanism for heavy-chain antibody formation

Cloning and sequence analysis of the H2-K2 b gene reveals that it is a pseudogene

Human Helios, an Ikaros-related zinc finger DNA binding protein: cDNA cloning and tissue expression pattern

Identification of an enhancer element in the mouse B7-1 promoter

Erratum: Immunogenetics (1999) 49 : 256–265

Erratum: Immunogenetics (1998) 48 : 22–31

Immunogenetics : Volume 49

Immunogenetics : Volume 48

Immunogenetics : Volume 47

Immunogenetics : Volume 46

Immunogenetics : Volume 45

H2-E transgenic class II-negative mice can distinguish self from nonself in susceptibility to heterologous thyroglobulins in autoimmune thyroiditis

Content Provider	Springer Nature Link
Author	Wan, Qiang Shah, Rajal McCormick, Daniel J. Lomo, Lesley C. Giraldo, Alvaro A. David, Chella S. Kong, Y. M.
Copyright Year	1999
Abstract	Susceptibility to experimental autoimmune thyroiditis (EAT) is linked to H2-A class II genes;k and s haplotypes are susceptible, while b and f are resistant. EAT is inducible with thyroglobulins (Tgs) from several mammalian species which share portions of identical sequences. But cross-activation and cross-tolerance studies with mouse (m), human (h), and porcine (p) Tg have indicated mTg-unique T-cell epitope(s), in addition to conserved, in EAT induction. The recent introduction of the HLA-DRB1*0301 (DR3) transgene rendered major histocompatibility complex (MHC) class II-negative (Ab0) mice susceptible to EAT induction by both hTg and mTg, suggesting usage of conserved epitopes. Here, we introduced the H2-Ea k transgene into resistant B10 (H2 b ) or Ab0 mice with a defective Ea gene to provide functional surface H2E (b haplotype) expression. Surprisingly, both transgenic strains showed severe inflammation only after hTg, but not mTg, immunization, although the moderating influence of the A b gene in B10 was evident. In proliferative assays, hTg-primed cells did not respond to mTg, nor to conserved 12mer peptides from three primary hormonogenic sites, two of which can activate T cells for thyroiditis transfer and cytotoxicity. The vigorous response to hTg stimulation was reduced only by Eβb-specific monoclonal antibody. EAT induction with bovine and pTg showed responses similar to hTg, suggesting thyroiditogenic epitopes shared with hTg, but not mTg. This is the first demonstration of: (1) nonpermissiveness for EAT induction with mTg, normally the most thyroiditogenic Tg and the one with unique epitopes for susceptible mice, and (2) the separation of hTg from mTg in EAT induction in H2-E-transgenic mice.
Starting Page	22
Ending Page	30
Page Count	9
File Format	PDF
ISSN	00937711
Journal	Immunogenetics
Volume Number	50
Issue Number	1-2
e-ISSN	14321211
Language	English
Publisher	Springer-Verlag
Publisher Date	1999-10-11
Publisher Place	Berlin, Heidelberg
Access Restriction	One Nation One Subscription (ONOS)
Content Type	Text
Resource Type	Article
Subject	Genetics Immunology

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

HLA-DRB1 Polymorphism Determines Susceptibility to Autoimmune Thyroiditis in Transgenic Mice: Definitive Association with HLA-DRBI*0301 (DR3) Gene

Role of mouse and human class II transgenes in susceptibility to and protection against mouse autoimmune nhyroiditis

H2-M, a facilitator of MHC class II peptide loading, and its negative modulator H2-O are differentially expressed in response to proinflammatory cytokines

Autoimmune thyroiditis in Fcgamma receptor-deficient nonobese diabetic mice.

Autoimmune diabetes can be induced in transgenic major histocompatibility complex class II-deficient mice

HLA-DRB1 polymorphism determines susceptibility to autoimmune thyroiditis in transgenic mice: definitive association with HLA- DRB1*0301 (DR3) gene

HLA-DRB1 polymorphism determines susceptibility to autoimmune thyroiditis in transgenic mice: definitive association with HLA-DRB1*0301 (DR3) gene.

Discriminating self from nonself with short peptides from large proteomes

Inhibition of autoimmune diabetes in nonobese diabetic mice by transgenic restoration of H2-E MHC class II expression: additive, but unequal, involvement of multiple APC subtypes.

H2-E transgenic class II-negative mice can distinguish self from nonself in susceptibility to heterologous thyroglobulins in autoimmune thyroiditis

Similar Documents

HLA-DRB1 Polymorphism Determines Susceptibility to Autoimmune Thyroiditis in Transgenic Mice: Definitive Association with HLA-DRBI*0301 (DR3) Gene

Role of mouse and human class II transgenes in susceptibility to and protection against mouse autoimmune nhyroiditis

H2-M, a facilitator of MHC class II peptide loading, and its negative modulator H2-O are differentially expressed in response to proinflammatory cytokines

Autoimmune thyroiditis in Fcgamma receptor-deficient nonobese diabetic mice.

Autoimmune diabetes can be induced in transgenic major histocompatibility complex class II-deficient mice

HLA-DRB1 polymorphism determines susceptibility to autoimmune thyroiditis in transgenic mice: definitive association with HLA- DRB1*0301 (DR3) gene

HLA-DRB1 polymorphism determines susceptibility to autoimmune thyroiditis in transgenic mice: definitive association with HLA-DRB1*0301 (DR3) gene.

Discriminating self from nonself with short peptides from large proteomes

Inhibition of autoimmune diabetes in nonobese diabetic mice by transgenic restoration of H2-E MHC class II expression: additive, but unequal, involvement of multiple APC subtypes.

H2-E transgenic class II-negative mice can distinguish self from nonself in susceptibility to heterologous thyroglobulins in autoimmune thyroiditis