T-cell reactivity to GAD65 peptide sequences shared with coxsackie virus protein in recent-onset IDDM, post-onset IDDM patients and control subjects
Schloot, N. C. ; Roep, B. O. ; Wegmann, D. R. ; Yu, L. ; Wang, T. B. ; Eisenbarth, G. S.
Springer
Published 1997
Springer
Published 1997
| ISSN: |
1432-0428
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|---|---|
| Keywords: |
Keywords Autoreactivity ; autoimmunity ; human T-cells ; GAD65 ; GAD autoantibodies ; insulin-dependent diabetes ; molecular mimicry.
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| Source: |
Springer Online Journal Archives 1860-2000
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| Topics: |
Medicine
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| Notes: |
Summary GAD65 is one of the major autoantigens associated with insulin-dependent diabetes mellitus (IDDM). The two peptides p17 and p18 of GAD65 that share sequence similarity with coxsackie virus (amino acid sequence identity: PEVKEK) appeared to be the major determinants of GAD65 recognized preferably by T cells from new-onset IDDM patients and their first degree relatives. In contrast, in our study unrelated control subjects frequently recognized the two GAD peptides (55 %, 16/29), similar to first degree relatives (41 %, 12/29) and IDDM patients post-onset (68 %, 15/22). However, recent-onset IDDM patients, responded less frequently (25 %, 4/16) compared with IDDM patients post-onset (p 〈 0.03) or unrelated control subjects (borderline significant) confirming previous observations in humans and NOD mice that T-cell reactivity to GADp17/p18 at diabetes onset is decreased. Moreover, this study demonstrated a positive correlation of T-cell proliferation to GAD p17 (amino acid 247–266) and p18 (amino acid 260–279) with simultaneous responses to both peptides in 13 % of all subjects tested (n = 97) (p 〈 0.001). T-cell proliferation to GAD p17 was higher than to p18 in recent-onset diabetic patients, first degree relatives and unrelated control subjects (p 〈 0.02, p 〈 0.004, p 〈 0.002, respectively). However, in post-onset IDDM patients, the two peptides were recognized equally well. Our results show that T-cell reactivity to GAD65 peptides homologous with coxsackie protein is very frequently observed, but not primarily associated with IDDM. The temporary decline of T-cell proliferation is not associated with the beta-cell destruction process, but with clinical manifestation. The positive correlation of reactivity to the two peptides in the viral motif implicates that PEVKEK is an immunogenic epitope. [Diabetologia (1997) 40: 332–338]
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| Type of Medium: |
Electronic Resource
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| URL: |
| _version_ | 1798295381671411712 |
|---|---|
| autor | Schloot, N. C. Roep, B. O. Wegmann, D. R. Yu, L. Wang, T. B. Eisenbarth, G. S. |
| autorsonst | Schloot, N. C. Roep, B. O. Wegmann, D. R. Yu, L. Wang, T. B. Eisenbarth, G. S. |
| book_url | http://dx.doi.org/10.1007/s001250050683 |
| datenlieferant | nat_lic_papers |
| hauptsatz | hsatz_simple |
| identnr | NLM199941130 |
| issn | 1432-0428 |
| journal_name | Diabetologia |
| materialart | 1 |
| notes | Summary GAD65 is one of the major autoantigens associated with insulin-dependent diabetes mellitus (IDDM). The two peptides p17 and p18 of GAD65 that share sequence similarity with coxsackie virus (amino acid sequence identity: PEVKEK) appeared to be the major determinants of GAD65 recognized preferably by T cells from new-onset IDDM patients and their first degree relatives. In contrast, in our study unrelated control subjects frequently recognized the two GAD peptides (55 %, 16/29), similar to first degree relatives (41 %, 12/29) and IDDM patients post-onset (68 %, 15/22). However, recent-onset IDDM patients, responded less frequently (25 %, 4/16) compared with IDDM patients post-onset (p 〈 0.03) or unrelated control subjects (borderline significant) confirming previous observations in humans and NOD mice that T-cell reactivity to GADp17/p18 at diabetes onset is decreased. Moreover, this study demonstrated a positive correlation of T-cell proliferation to GAD p17 (amino acid 247–266) and p18 (amino acid 260–279) with simultaneous responses to both peptides in 13 % of all subjects tested (n = 97) (p 〈 0.001). T-cell proliferation to GAD p17 was higher than to p18 in recent-onset diabetic patients, first degree relatives and unrelated control subjects (p 〈 0.02, p 〈 0.004, p 〈 0.002, respectively). However, in post-onset IDDM patients, the two peptides were recognized equally well. Our results show that T-cell reactivity to GAD65 peptides homologous with coxsackie protein is very frequently observed, but not primarily associated with IDDM. The temporary decline of T-cell proliferation is not associated with the beta-cell destruction process, but with clinical manifestation. The positive correlation of reactivity to the two peptides in the viral motif implicates that PEVKEK is an immunogenic epitope. [Diabetologia (1997) 40: 332–338] |
| package_name | Springer |
| publikationsjahr_anzeige | 1997 |
| publikationsjahr_facette | 1997 |
| publikationsjahr_intervall | 8004:1995-1999 |
| publikationsjahr_sort | 1997 |
| publisher | Springer |
| reference | 40 (1997), S. 332-338 |
| schlagwort | Keywords Autoreactivity autoimmunity human T-cells GAD65 GAD autoantibodies insulin-dependent diabetes molecular mimicry. |
| search_space | articles |
| shingle_author_1 | Schloot, N. C. Roep, B. O. Wegmann, D. R. Yu, L. Wang, T. B. Eisenbarth, G. S. |
| shingle_author_2 | Schloot, N. C. Roep, B. O. Wegmann, D. R. Yu, L. Wang, T. B. Eisenbarth, G. S. |
| shingle_author_3 | Schloot, N. C. Roep, B. O. Wegmann, D. R. Yu, L. Wang, T. B. Eisenbarth, G. S. |
| shingle_author_4 | Schloot, N. C. Roep, B. O. Wegmann, D. R. Yu, L. Wang, T. B. Eisenbarth, G. S. |
| shingle_catch_all_1 | Schloot, N. C. Roep, B. O. Wegmann, D. R. Yu, L. Wang, T. B. Eisenbarth, G. S. T-cell reactivity to GAD65 peptide sequences shared with coxsackie virus protein in recent-onset IDDM, post-onset IDDM patients and control subjects Keywords Autoreactivity autoimmunity human T-cells GAD65 GAD autoantibodies insulin-dependent diabetes molecular mimicry. Keywords Autoreactivity autoimmunity human T-cells GAD65 GAD autoantibodies insulin-dependent diabetes molecular mimicry. Summary GAD65 is one of the major autoantigens associated with insulin-dependent diabetes mellitus (IDDM). The two peptides p17 and p18 of GAD65 that share sequence similarity with coxsackie virus (amino acid sequence identity: PEVKEK) appeared to be the major determinants of GAD65 recognized preferably by T cells from new-onset IDDM patients and their first degree relatives. In contrast, in our study unrelated control subjects frequently recognized the two GAD peptides (55 %, 16/29), similar to first degree relatives (41 %, 12/29) and IDDM patients post-onset (68 %, 15/22). However, recent-onset IDDM patients, responded less frequently (25 %, 4/16) compared with IDDM patients post-onset (p 〈 0.03) or unrelated control subjects (borderline significant) confirming previous observations in humans and NOD mice that T-cell reactivity to GADp17/p18 at diabetes onset is decreased. Moreover, this study demonstrated a positive correlation of T-cell proliferation to GAD p17 (amino acid 247–266) and p18 (amino acid 260–279) with simultaneous responses to both peptides in 13 % of all subjects tested (n = 97) (p 〈 0.001). T-cell proliferation to GAD p17 was higher than to p18 in recent-onset diabetic patients, first degree relatives and unrelated control subjects (p 〈 0.02, p 〈 0.004, p 〈 0.002, respectively). However, in post-onset IDDM patients, the two peptides were recognized equally well. Our results show that T-cell reactivity to GAD65 peptides homologous with coxsackie protein is very frequently observed, but not primarily associated with IDDM. The temporary decline of T-cell proliferation is not associated with the beta-cell destruction process, but with clinical manifestation. The positive correlation of reactivity to the two peptides in the viral motif implicates that PEVKEK is an immunogenic epitope. [Diabetologia (1997) 40: 332–338] 1432-0428 14320428 Springer |
| shingle_catch_all_2 | Schloot, N. C. Roep, B. O. Wegmann, D. R. Yu, L. Wang, T. B. Eisenbarth, G. S. T-cell reactivity to GAD65 peptide sequences shared with coxsackie virus protein in recent-onset IDDM, post-onset IDDM patients and control subjects Keywords Autoreactivity autoimmunity human T-cells GAD65 GAD autoantibodies insulin-dependent diabetes molecular mimicry. Keywords Autoreactivity autoimmunity human T-cells GAD65 GAD autoantibodies insulin-dependent diabetes molecular mimicry. Summary GAD65 is one of the major autoantigens associated with insulin-dependent diabetes mellitus (IDDM). The two peptides p17 and p18 of GAD65 that share sequence similarity with coxsackie virus (amino acid sequence identity: PEVKEK) appeared to be the major determinants of GAD65 recognized preferably by T cells from new-onset IDDM patients and their first degree relatives. In contrast, in our study unrelated control subjects frequently recognized the two GAD peptides (55 %, 16/29), similar to first degree relatives (41 %, 12/29) and IDDM patients post-onset (68 %, 15/22). However, recent-onset IDDM patients, responded less frequently (25 %, 4/16) compared with IDDM patients post-onset (p 〈 0.03) or unrelated control subjects (borderline significant) confirming previous observations in humans and NOD mice that T-cell reactivity to GADp17/p18 at diabetes onset is decreased. Moreover, this study demonstrated a positive correlation of T-cell proliferation to GAD p17 (amino acid 247–266) and p18 (amino acid 260–279) with simultaneous responses to both peptides in 13 % of all subjects tested (n = 97) (p 〈 0.001). T-cell proliferation to GAD p17 was higher than to p18 in recent-onset diabetic patients, first degree relatives and unrelated control subjects (p 〈 0.02, p 〈 0.004, p 〈 0.002, respectively). However, in post-onset IDDM patients, the two peptides were recognized equally well. Our results show that T-cell reactivity to GAD65 peptides homologous with coxsackie protein is very frequently observed, but not primarily associated with IDDM. The temporary decline of T-cell proliferation is not associated with the beta-cell destruction process, but with clinical manifestation. The positive correlation of reactivity to the two peptides in the viral motif implicates that PEVKEK is an immunogenic epitope. [Diabetologia (1997) 40: 332–338] 1432-0428 14320428 Springer |
| shingle_catch_all_3 | Schloot, N. C. Roep, B. O. Wegmann, D. R. Yu, L. Wang, T. B. Eisenbarth, G. S. T-cell reactivity to GAD65 peptide sequences shared with coxsackie virus protein in recent-onset IDDM, post-onset IDDM patients and control subjects Keywords Autoreactivity autoimmunity human T-cells GAD65 GAD autoantibodies insulin-dependent diabetes molecular mimicry. Keywords Autoreactivity autoimmunity human T-cells GAD65 GAD autoantibodies insulin-dependent diabetes molecular mimicry. Summary GAD65 is one of the major autoantigens associated with insulin-dependent diabetes mellitus (IDDM). The two peptides p17 and p18 of GAD65 that share sequence similarity with coxsackie virus (amino acid sequence identity: PEVKEK) appeared to be the major determinants of GAD65 recognized preferably by T cells from new-onset IDDM patients and their first degree relatives. In contrast, in our study unrelated control subjects frequently recognized the two GAD peptides (55 %, 16/29), similar to first degree relatives (41 %, 12/29) and IDDM patients post-onset (68 %, 15/22). However, recent-onset IDDM patients, responded less frequently (25 %, 4/16) compared with IDDM patients post-onset (p 〈 0.03) or unrelated control subjects (borderline significant) confirming previous observations in humans and NOD mice that T-cell reactivity to GADp17/p18 at diabetes onset is decreased. Moreover, this study demonstrated a positive correlation of T-cell proliferation to GAD p17 (amino acid 247–266) and p18 (amino acid 260–279) with simultaneous responses to both peptides in 13 % of all subjects tested (n = 97) (p 〈 0.001). T-cell proliferation to GAD p17 was higher than to p18 in recent-onset diabetic patients, first degree relatives and unrelated control subjects (p 〈 0.02, p 〈 0.004, p 〈 0.002, respectively). However, in post-onset IDDM patients, the two peptides were recognized equally well. Our results show that T-cell reactivity to GAD65 peptides homologous with coxsackie protein is very frequently observed, but not primarily associated with IDDM. The temporary decline of T-cell proliferation is not associated with the beta-cell destruction process, but with clinical manifestation. The positive correlation of reactivity to the two peptides in the viral motif implicates that PEVKEK is an immunogenic epitope. [Diabetologia (1997) 40: 332–338] 1432-0428 14320428 Springer |
| shingle_catch_all_4 | Schloot, N. C. Roep, B. O. Wegmann, D. R. Yu, L. Wang, T. B. Eisenbarth, G. S. T-cell reactivity to GAD65 peptide sequences shared with coxsackie virus protein in recent-onset IDDM, post-onset IDDM patients and control subjects Keywords Autoreactivity autoimmunity human T-cells GAD65 GAD autoantibodies insulin-dependent diabetes molecular mimicry. Keywords Autoreactivity autoimmunity human T-cells GAD65 GAD autoantibodies insulin-dependent diabetes molecular mimicry. Summary GAD65 is one of the major autoantigens associated with insulin-dependent diabetes mellitus (IDDM). The two peptides p17 and p18 of GAD65 that share sequence similarity with coxsackie virus (amino acid sequence identity: PEVKEK) appeared to be the major determinants of GAD65 recognized preferably by T cells from new-onset IDDM patients and their first degree relatives. In contrast, in our study unrelated control subjects frequently recognized the two GAD peptides (55 %, 16/29), similar to first degree relatives (41 %, 12/29) and IDDM patients post-onset (68 %, 15/22). However, recent-onset IDDM patients, responded less frequently (25 %, 4/16) compared with IDDM patients post-onset (p 〈 0.03) or unrelated control subjects (borderline significant) confirming previous observations in humans and NOD mice that T-cell reactivity to GADp17/p18 at diabetes onset is decreased. Moreover, this study demonstrated a positive correlation of T-cell proliferation to GAD p17 (amino acid 247–266) and p18 (amino acid 260–279) with simultaneous responses to both peptides in 13 % of all subjects tested (n = 97) (p 〈 0.001). T-cell proliferation to GAD p17 was higher than to p18 in recent-onset diabetic patients, first degree relatives and unrelated control subjects (p 〈 0.02, p 〈 0.004, p 〈 0.002, respectively). However, in post-onset IDDM patients, the two peptides were recognized equally well. Our results show that T-cell reactivity to GAD65 peptides homologous with coxsackie protein is very frequently observed, but not primarily associated with IDDM. The temporary decline of T-cell proliferation is not associated with the beta-cell destruction process, but with clinical manifestation. The positive correlation of reactivity to the two peptides in the viral motif implicates that PEVKEK is an immunogenic epitope. [Diabetologia (1997) 40: 332–338] 1432-0428 14320428 Springer |
| shingle_title_1 | T-cell reactivity to GAD65 peptide sequences shared with coxsackie virus protein in recent-onset IDDM, post-onset IDDM patients and control subjects |
| shingle_title_2 | T-cell reactivity to GAD65 peptide sequences shared with coxsackie virus protein in recent-onset IDDM, post-onset IDDM patients and control subjects |
| shingle_title_3 | T-cell reactivity to GAD65 peptide sequences shared with coxsackie virus protein in recent-onset IDDM, post-onset IDDM patients and control subjects |
| shingle_title_4 | T-cell reactivity to GAD65 peptide sequences shared with coxsackie virus protein in recent-onset IDDM, post-onset IDDM patients and control subjects |
| sigel_instance_filter | dkfz geomar wilbert ipn albert fhp |
| source_archive | Springer Online Journal Archives 1860-2000 |
| timestamp | 2024-05-06T09:35:17.894Z |
| titel | T-cell reactivity to GAD65 peptide sequences shared with coxsackie virus protein in recent-onset IDDM, post-onset IDDM patients and control subjects |
| titel_suche | T-cell reactivity to GAD65 peptide sequences shared with coxsackie virus protein in recent-onset IDDM, post-onset IDDM patients and control subjects |
| topic | WW-YZ |
| uid | nat_lic_papers_NLM199941130 |