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Digitale Medien

Autoantibodies to the islet antigen ICA 69 occur in IDDM and in rheumatoid arthritis (1995)

Martin, S. ; Kardorf, J. ; Schulte, B. ; [weitere]

Springer

Diabetologia 38 (1995), S. 351-355

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ISSN: 1432-0428

Schlagwort(e): ICA 69 ; insulin-dependent diabetes mellitus ; rheumatoid arthritis

Quelle: Springer Online Journal Archives 1860-2000

Thema: Medizin

Notizen: Summary Islet cell antigen (ICA) 69 is a newly-recognized islet cell antigen to which autoantibodies have been observed in prediabetic relatives of patients with insulin-dependent-diabetes mellitus (IDDM). Here we extend the earlier analysis of ICA 69 antibodies to patients with recent-onset IDDM and to patients with other immune-mediated diseases. ICA 69 antibodies were determined by Western blot using an affinity purified recombinant fusion protein of ICA 69 and maltose binding protein. ICA 69 antibody quantities were determined as titres using a titration curve of a standard serum as reference. Mean logarithmic ICA 69 antibody titres were 3.4 (±1.4) in 99 patients with acute IDDM compared to 2.8 (±0.9) in 49 healthy blood donors (p〈0.001). A higher mean ICA 69 antibody titre of 4.1 (±0.8) was observed in 16 patients with rheumatoid arthritis in comparison to acute IDDM (p〈0.01) and healthy control subjects (p〈0.001). The percentage of sera with ICA 69 antibody titres above the 2 SD level of normal subjects was 21% in IDDM, 31% in rheumatoid arthritis and 6% in healthy blood donors. None of the patients with autoimmune thyroid disease (n=20), inflammatory bowel disease (n=9) or multiple sclerosis (n=7) had elevated ICA 69 antibodies. In IDDM, presence of ICA 69 antibodies persisted and the titre remained the same over 18 months of follow-up. The relationship of ICA 69 antibodies to islet cell antibodies (ICA) or insulin autoantibodies (IAA) was tested. The production of ICA 69 antibodies was not associated in diabetic patients with the presence of any of the two other autoantibodies. In conclusion, this study describes ICA 69 antibodies in acute IDDM and finds them to be independent of other islet autoantibodies. In addition ICA 69 is a target of humoural autoimmunity not only in IDDM but also in rheumatoid arthritis.

Materialart: Digitale Medien

URL: http://dx.doi.org/10.1007/BF00400641

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Digitale Medien

T-cell reactivity to GAD65 peptide sequences shared with coxsackie virus protein in recent-onset IDDM, post-onset IDDM patients and control subjects (1997)

Schloot, N. C. ; Roep, B. O. ; Wegmann, D. R. ; [weitere]

Springer

Diabetologia 40 (1997), S. 332-338

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ISSN: 1432-0428

Schlagwort(e): Keywords Autoreactivity ; autoimmunity ; human T-cells ; GAD65 ; GAD autoantibodies ; insulin-dependent diabetes ; molecular mimicry.

Quelle: Springer Online Journal Archives 1860-2000

Thema: Medizin

Notizen: 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]

Materialart: Digitale Medien

URL: http://dx.doi.org/10.1007/s001250050683

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Digitale Medien

Autoreactive and immunoregulatory T-cell subsets in insulindependent diabetes mellitus (1999)

Douglas Petersen, L. ; van der Keur, M. ; de Vries, R. R. P. ; [weitere]

Springer

Diabetologia 42 (1999), S. 443-449

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ISSN: 1432-0428

Schlagwort(e): Keywords Autoreacitivity ; autoimmune disease ; regulation ; suppression ; T-cell subset ; CD45.

Quelle: Springer Online Journal Archives 1860-2000

Thema: Medizin

Notizen: Abstract Aims/hypothesis. Type I (insulin-dependent) diabetes mellitus is a T-cell mediated autoimmune disease. Several subsets of T-cells, in particular CD4+ and in vivo activate CD45RA+RO+ T-cells, have been shown to be increased at disease onset. The functional implications of these relative increases in CD4 T-cells were investigated. Methods. Subsets of T-cells were sorted on the basis of their activation status (CD45RA+ naïve cells, CD45RA+RO+ recently activated cells and CD45RO+ memory cells) and stimulated with autoantigens or recall antigen in vitro. Results. Proliferative responses to tetanus toxoid were primarily or exclusively observed in resting memory T-cells (CD45RO+). Autoimmune T-cell responses were, however, primarily measured in activated T-cells (CD45RA+RO+) in newly diagnosed Type I diabetic patients, whereas those with longer disease duration reacted to autoantigens with memory T-cells (CD45RO+) (p 〈 0.004). Interestingly, in non-diabetic control subjects not responding to autoantigens in the regular assay, considerable autoreactive T-cell responses were detectable after sorting in the CD45RO+ or CD45RA+RO+ lymphocyte subsets. Remixing these subsets showed that these autoimmune responses in activated cells could be down-modulated by CD45RA+ lymphocytes, whereas resting memory cells appeared unaffected by the suppressive CD45RA subset. Conclusion/interpretation. These results show that autoimmune T-cell responses can be linked to particular subsets which differ depending on clinical status. Furthermore, the CD45RA T-cell subset harbours lymphocytes potentially capable of suppressing autoimmune T-cell responses. The changes in responsiveness to exogenous insulin may help to unravel the mechanism by which isohormonal therapy could prevent the onset of Type I diabetes. [Diabetologia (1999) 42: 443–449]

Materialart: Digitale Medien

URL: http://dx.doi.org/10.1007/s001250051177

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