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Enhanced production of γ-interferon by thyroid-derived T cell clones from patients with Hashimoto's thyroiditis.
- Source :
-
Clinical & Experimental Immunology . Aug1987, Vol. 69 Issue 2, p323-331. 9p. - Publication Year :
- 1987
-
Abstract
- T lymphocytes from thyroid infiltrate and peripheral blood (PB) of four patients with Hashimoto's thyroiditis (HT) were analysed at clonal level for their ability to secrete interleukin 2 (IL-2) and y-interferon (y-IFN), As controls, T cell clones from PB of four normal donors and from spleen of two trauma victims were used. While no abnormality was found in the capacity lo produce lL-2, the proportion of y-IFN-producing (IFN-P) T cell clones derived from HT infiltrates was significantly higher (p<0-0005) than that of IFN-P clones derived from normal or patient PB. Most of CD4 +and CD8 + IFN-P clones from thyroid infiltrates, as well as a proportion of CD4 + PB-derived clones of patients with HT, released higher amounts of v-IFN than control clones. A relationship could be demonstrated between high y-IFN production and natural killer (NK) activity in T cell clones from thyroid and PB of HT patients. In fact, the percentage of I FN-P clones with NK potential (NK + ) was remarkably higher (p<0.0005) in thyroid infiltrates than in normal spleen or PB. The proportion of IFN-P NK + clones from patient PB was also significantly increased (P<0.02) but, unlike thyroid-derived clones in which the majority of IFN-P NK + clones were CD8 +, most PB-derived IFN-P NK + clones from the same patients expressed the CD4 + phenolype. Almost all thyroid NK + clones could be triggered to produce more y-IFN, while y-IFN synthesis by NK-negative thyroid clones was comparable to that of control clones. In view of the multiple effects ascribed to y-IFN in the cascade of events leading to immune responses, the abnormal potential to y-lFN secretion shown by intrathyroidal T lymphocytes may be of importance in the pathogenesis of autoimmune throiditis. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 00099104
- Volume :
- 69
- Issue :
- 2
- Database :
- Academic Search Index
- Journal :
- Clinical & Experimental Immunology
- Publication Type :
- Academic Journal
- Accession number :
- 16141931