STUDIES OF HUMAN PERIPHERAL-BLOOD MONONUCLEAR-CELLS (PBMC) FROM PATIENTS WITH SUBACUTE THYROIDITIS IN SEVERE COMBINED IMMUNODEFICIENT (SCID) MICE - LESS PRODUCTION OF HUMAN INTERFERON-GAMMA THAN THAT SEEN FOR GRAVES-DISEASE

Citation
N. Yoshikawa et al., STUDIES OF HUMAN PERIPHERAL-BLOOD MONONUCLEAR-CELLS (PBMC) FROM PATIENTS WITH SUBACUTE THYROIDITIS IN SEVERE COMBINED IMMUNODEFICIENT (SCID) MICE - LESS PRODUCTION OF HUMAN INTERFERON-GAMMA THAN THAT SEEN FOR GRAVES-DISEASE, Hormone and Metabolic Research, 26(9), 1994, pp. 419-423
Citations number
29
Categorie Soggetti
Endocrynology & Metabolism
ISSN journal
00185043
Volume
26
Issue
9
Year of publication
1994
Pages
419 - 423
Database
ISI
SICI code
0018-5043(1994)26:9<419:SOHPM(>2.0.ZU;2-9
Abstract
Human peripheral blood mononuclear cells (PBMC) from 2 patients with d e Quervain's subacute thyroiditis (SAT), 2 with Graves' disease (GD), and 3 normal persons (N) were engrafted into severe combined immunodef icient (SCID) mice so as to study whether SAT PBMC would differ immuno logically from GD PBMC in vivo. Human IgG was detected in all mice eng rafted with PBMC from either group of patients or normal persons. Thyr oid Stimulating Antibody (TSAb) was detected in the sera of mice with PBMC from SAT or GD patients, but not N. Thyroperoxidase (TPO)-antibod y (Ab) and/or thyroglobulin (Tg)-Ab was detectable in the mice with GT ) PBMC only, but not in those with SAI or normal PBMC. The production of interferon gamma (IFN gamma) in mice engrafted with N PBMC was 8, 1 3 and 14 U/ml, similar to values found in sera of SCID mice with SAT P BMC (14 and 11 U/ml), i.e., much lower than that seen far GD PBMC (127 and 78 U/ml); this is consistent with the view that, compared to GD T lymphocytes, that there is probably a lower number of T lymphocytes s ensitized to the thyrotrophin (TSH) receptor antigen in SPIT patients. Another possibility is that the transient thyroidal antigenic release seen in the acute (hyperthyroid) phase may be insufficient for adequa te T cell sensitization. Still other possibilities include the effect of more severe hyperthyroidism of GD on T cell sensitization, and CD4/ CD8 cell ratios. In any event, these results are consistent with our p revious view that antigenic release in SAT will not itself lead to aut oimmune thyroid disease.