G. Aust et al., DIFFERENT IMMUNOPHENOTYPE AND AUTOANTIBODY PRODUCTION BY PERIPHERAL-BLOOD AND THYROID-DERIVED LYMPHOCYTES IN PATIENTS WITH GRAVES-DISEASE, EXPERIMENTAL AND CLINICAL ENDOCRINOLOGY & DIABETES, 104(1), 1996, pp. 50-58
Direct multi-colour flow cytometric analysis was employed in patients
with Graves' disease (n = 10) to determine the immunophenotype in peri
pheral blood lymphocytes (PBL) at the time of diagnosis without treatm
ent (PBLw) and prior to operation (PBLp) and in thyroid-derived lympho
cytes (TL). Additionally, the secretion of anti-thyroperoxidase antibo
dies (anti-TPO) was measured during culture of isolated peripheral or
thyroid-derived B cells. Among TL from patients with high serum levels
of anti-TPO (6/10) a significantly (p < 0.01) higher percentage of B
cells were detected compared to PBLp (TL: 21.7 +/- 7.2%; PBLp: 13.2 +/
- 4.5%). Enriched thyroid-derived B cells only from these patients als
o showed high spontaneous anti-TPO secretion during culture. The diffe
rence between peripheral and thyroid-derived natural killer (NK) cells
was highly significant (p < 0.001; TL: 5.6 +/- 6.3%; PBLp: 13.6 +/- 5
.5%). Two patients were found with a higher number of NK cells within
TL. These patients were among those who had a low number of B cells in
filtrating the thyroid gland. Regarding the expression of several othe
r differentiation antigens, i.e. CD4 and CD8, gamma/delta TCR bearing
T cells and CD45RO on CD4(+) T cells as a marker for memory cells, on
TL no differences could be detected between patients with or without a
nti-TPO. In TL 31.5 +/- 7.7% of CD3(+) cells expressed the HLA-DR anti
gen (vs. 6.1 +/- 2.4% in PBLp; p < 0.001). Half of these cells simulta
neously expressed the activation antigen CD69. Surprisingly, the numbe
r of CD3(+) TL bearing the Il-2 receptor (CD25) and transferrin recept
or (CD71) was not increased. Taken together, the proportional distribu
tion of B and NK cells within the thyroid correlates with the anti-TPO
secretion in vivo and in vitro, suggesting different immune response
regulation processes of TL.