Abstract
The effector mechanisms responsible for autoimmune β cell destruction in insulin dependent (type 1) diabetes (IDD) remain elusive. In order to investigate whether T lymphocytes bearing the gamma-delta T cell receptor (γδ+ T cells) could be involved in this process, we measured percentages of peripheral blood γδ+ T cells in IDD patients, relatives of IDD probands and controls. High levels of γδ+ T cells strongly differentiated 23 relatives at high risk for IDD on the basis of positive islet cell autoantibodies (ICA positive relatives) from 59 controls (P = 0.0013), whereas 26 ICA negative relatives, 14 recent-onset and nine long term IDD patients could not be distinguished from controls on the basis of percentages of γδ+ T cells. These data suggest that increased levels of circulating γδ+ T cells correlate with the ongoing autoimmune process in pancreatic islets of subjects at high risk for IDD and may thus represent an additional marker for the development of the disease.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 925-933 |
| Number of pages | 9 |
| Journal | Journal of Autoimmunity |
| Volume | 4 |
| Issue number | 6 |
| DOIs | |
| State | Published - 1991 |
| Externally published | Yes |
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ASJC Scopus subject areas
- Immunology
- Immunology and Allergy
Cite this
Increased T lymphocytes bearing the gamma-delta T cell receptor in subjects at high risk for insulin dependent diabetes. / Lang, Francois P.; Schatz, Desmond A.; Pollock, Bradley H; Riley, William J.; Maclaren, Noel K.; Dumont-Driscoll, Marilyn; Barrett, Douglas J.
In: Journal of Autoimmunity, Vol. 4, No. 6, 1991, p. 925-933.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Increased T lymphocytes bearing the gamma-delta T cell receptor in subjects at high risk for insulin dependent diabetes
AU - Lang, Francois P.
AU - Schatz, Desmond A.
AU - Pollock, Bradley H
AU - Riley, William J.
AU - Maclaren, Noel K.
AU - Dumont-Driscoll, Marilyn
AU - Barrett, Douglas J.
PY - 1991
Y1 - 1991
N2 - The effector mechanisms responsible for autoimmune β cell destruction in insulin dependent (type 1) diabetes (IDD) remain elusive. In order to investigate whether T lymphocytes bearing the gamma-delta T cell receptor (γδ+ T cells) could be involved in this process, we measured percentages of peripheral blood γδ+ T cells in IDD patients, relatives of IDD probands and controls. High levels of γδ+ T cells strongly differentiated 23 relatives at high risk for IDD on the basis of positive islet cell autoantibodies (ICA positive relatives) from 59 controls (P = 0.0013), whereas 26 ICA negative relatives, 14 recent-onset and nine long term IDD patients could not be distinguished from controls on the basis of percentages of γδ+ T cells. These data suggest that increased levels of circulating γδ+ T cells correlate with the ongoing autoimmune process in pancreatic islets of subjects at high risk for IDD and may thus represent an additional marker for the development of the disease.
AB - The effector mechanisms responsible for autoimmune β cell destruction in insulin dependent (type 1) diabetes (IDD) remain elusive. In order to investigate whether T lymphocytes bearing the gamma-delta T cell receptor (γδ+ T cells) could be involved in this process, we measured percentages of peripheral blood γδ+ T cells in IDD patients, relatives of IDD probands and controls. High levels of γδ+ T cells strongly differentiated 23 relatives at high risk for IDD on the basis of positive islet cell autoantibodies (ICA positive relatives) from 59 controls (P = 0.0013), whereas 26 ICA negative relatives, 14 recent-onset and nine long term IDD patients could not be distinguished from controls on the basis of percentages of γδ+ T cells. These data suggest that increased levels of circulating γδ+ T cells correlate with the ongoing autoimmune process in pancreatic islets of subjects at high risk for IDD and may thus represent an additional marker for the development of the disease.
UR - http://www.scopus.com/inward/record.url?scp=0026318198&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0026318198&partnerID=8YFLogxK
U2 - 10.1016/0896-8411(91)90055-H
DO - 10.1016/0896-8411(91)90055-H
M3 - Article
C2 - 1839880
AN - SCOPUS:0026318198
VL - 4
SP - 925
EP - 933
JO - Journal of Autoimmunity
JF - Journal of Autoimmunity
SN - 0896-8411
IS - 6
ER -