caa a22 4500 465804136 CHVBK 20180323112059.0 cr unu---uuuuu 170327e19901001xx s 000 0 eng 10.1007/BF03349608 doi (NATIONALLICENCE)springer-10.1007/BF03349608 CD4 cells from patients with autoimmune thyroid disease secrete interferon γ after stimulation by thyroid microsomal antigen; CD8 cells suppress this secretion [Elektronische Daten] [Y. Sakatsume, S. Matsubayashi, Y. Kasuga, M. Iitaka, Y. Iwatani, Robert Volpé] The production of interferon gamma (IFNγ) by peripheral blood mononuclear cells (PBMC) from normal persons and patients with autoimmune thyroid disease (AITD) has been studied in vitro either spontaneously or after stimulation with thyroid microsomal antigen (TMc) or liver microsomal antigen (LMc). The numbers of IFNγ secreting cells were measured by a spot-ELISA technique. AITD PBMC spontaneously contained significantly more IFNγ secreting cells than did normal control PBMC. Moreover, TMc antigen caused a significantly greater number of IFNγ secreting cells in AITD PBMC than did LMc antigen, whereas there was no significant difference between the two antigens in the normal control PBMC preparations. Thus TMc antigen caused a stimulation of the number of IFNγ secreting cells only in the AITD PBMC and not in the normal PBMC. CD4 plus B cells or CD4 cells alone (with monocytes in both instances) contained more IFNγ secreting cells under unstimulated conditions than did CD8 cells in both groups. AITD CD4 plus B cells (or CD4 cells) contained more IFNγ secreting cells than did normal cells, but there was no significant difference between both groups in terms of the number of CD8 IFNγ secreting cells. Normal CD4 plus B cells (or CD4 cells) responded to TMc antigen significantly more than did total normal PBMC at 10 and 1,000 ng/ml TMc. This was not the case when patients' CD4 plus B cells (or CD4 cells) were compared with patients' total PBMC, in which there were no significant differences. This suggests that CD8 suppressor activity was inadequate in AITD and thus the deletion of CD8 cells did not result in an increase in IFNγ secreting cells. When TMc antigen was added to AITD CD8 cells, there was a significant diminution of IFNγ secreting cell numbers at 10 and 1,000 ng/ml TMc. Moreover, adding autologous CD8 cells to CD4 plus B cells resulted in a significant suppression of IFNγ production at 100 and 1,000 ng/ml TMc in both groups. AITD CD8 cells appeared to be somewhat less effective than normal CD8 cells, but this did not reach significance. It is thus concluded that AITD CD4 cells respond specifically to TMc antigen. CD4 production of IFNγ appears to be suppressed by CD8 cells activated with antigen and the CD8 cells appear to be involved in the regulation of IFNγ production by the CD4 cells. Italian Society of Endocrinology (SIE), 1990 CD4 cells nationallicence autoimmune thyroid disease nationallicence interferon gamma nationallicence CD8 cells nationallicence Sakatsume Y. Endocrinology Research Laboratory, The Wellesley Hospital, 160 Wellesley Street East, M4Y 1J3, Toronto, Ontario, Canada aut Matsubayashi S. Endocrinology Research Laboratory, The Wellesley Hospital, 160 Wellesley Street East, M4Y 1J3, Toronto, Ontario, Canada aut Kasuga Y. Endocrinology Research Laboratory, The Wellesley Hospital, 160 Wellesley Street East, M4Y 1J3, Toronto, Ontario, Canada aut Iitaka M. Endocrinology Research Laboratory, The Wellesley Hospital, 160 Wellesley Street East, M4Y 1J3, Toronto, Ontario, Canada aut Iwatani Y. Endocrinology Research Laboratory, The Wellesley Hospital, 160 Wellesley Street East, M4Y 1J3, Toronto, Ontario, Canada aut Volpé Robert Endocrinology Research Laboratory, The Wellesley Hospital, 160 Wellesley Street East, M4Y 1J3, Toronto, Ontario, Canada aut Journal of Endocrinological Investigation Springer International Publishing 13/9(1990-10-01), 717-726 0391-4097 13:9<717 1990 13 40618 https://doi.org/10.1007/BF03349608 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/BF03349608 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Sakatsume Y. Endocrinology Research Laboratory, The Wellesley Hospital, 160 Wellesley Street East, M4Y 1J3, Toronto, Ontario, Canada aut NATIONALLICENCE 700 1- Matsubayashi S. Endocrinology Research Laboratory, The Wellesley Hospital, 160 Wellesley Street East, M4Y 1J3, Toronto, Ontario, Canada aut NATIONALLICENCE 700 1- Kasuga Y. Endocrinology Research Laboratory, The Wellesley Hospital, 160 Wellesley Street East, M4Y 1J3, Toronto, Ontario, Canada aut NATIONALLICENCE 700 1- Iitaka M. Endocrinology Research Laboratory, The Wellesley Hospital, 160 Wellesley Street East, M4Y 1J3, Toronto, Ontario, Canada aut NATIONALLICENCE 700 1- Iwatani Y. Endocrinology Research Laboratory, The Wellesley Hospital, 160 Wellesley Street East, M4Y 1J3, Toronto, Ontario, Canada aut NATIONALLICENCE 700 1- Volpé Robert Endocrinology Research Laboratory, The Wellesley Hospital, 160 Wellesley Street East, M4Y 1J3, Toronto, Ontario, Canada aut NATIONALLICENCE 773 0- Journal of Endocrinological Investigation Springer International Publishing 13/9(1990-10-01), 717-726 0391-4097 13:9<717 1990 13 40618 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer