Immunoexpression of the CD30 ligand/CD30 and IL-6/IL-6R signals in thyroid autoimmune diseases.
To elucidate the role of Th2 cytokines in autoimmune thyroid diseases, we have studied by immunohistochemistry the expression of two Th2 ligand/receptor systems (CD30-L/CD30 and IL-6/IL-6R) in goitrous Graves' disease (GD) and Hashimoto's thyroiditis (HT). A total number of 50 nodular goiters (NG), including 10 GD showing a lymphoid aggregate grade I, 30 HT 8 of which had a lymphoid aggregate of grade I, 12 of grade II and 10 grade III, and 10 colloid goiters have been evaluated. In addition, 5 normal thyroids were included in the study as controls. Reactivity of ligand and cognate receptor of both CD30-L/CD30 and IL-6/IL-6R pathways was observed in a greater proportion of GD, compared to HT (P<0.005). In HT, the expression of CD30-L/CD30 system was detected more frequently than IL-6/IL-6R (P<0.05) and showed an inverse correlation with the grade of lymphoid aggregate, whereas IL-6/IL-6R correlated positively with lymphocyte infiltration (P<0.05). Based on our results concerning a dominance of Th2 cytokines in GD, we postulate that CD30-L/CD30 and IL-6/IL-6R systems could play a major role in the pathogenesis of GD. However, the expression of CD30L/CD30 and IL-6/IL-6R in HT suggests that Th2 mechanisms are involved also in tissue damage of HT. The two systems could contribute to drive the autoimmune response skewing toward a Th2 phenotype and this appears to be correlated with the lymphoid aggregate grade.
Ruggeri
R M
RM
Clinical/Experimental Department of Medicine and Pharmacology, University of Messina, Italy.
Barresi
G
G
Sciacchitano
S
S
Trimarchi
F
F
Benvenga
S
S
Trovato
M
M
D000328:Adult; D000368:Aged; D015703:Antigens, CD / Q000235:genetics / Q000378:metabolism*; D015551:Autoimmunity; D053285:CD30 Ligand; D002449:Cell Aggregation; D049109:Cell Proliferation; D005260:Female; D005786:Gene Expression Regulation; D006111:Graves Disease / Q000235:genetics / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D050031:Hashimoto Disease / Q000235:genetics / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D006801:Humans; D007150:Immunohistochemistry; D015850:Interleukin-6 / Q000235:genetics / Q000378:metabolism*; D017730:Ki-1 Antigen / Q000235:genetics / Q000378:metabolism*; D008214:Lymphocytes / Q000473:pathology / Q000502:physiology; D008297:Male; D008875:Middle Aged; D019947:Receptors, Interleukin-6 / Q000235:genetics / Q000378:metabolism*; D015398:Signal Transduction; D018418:Th2 Cells / Q000473:pathology / Q000502:physiology; D013961:Thyroid Gland / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D048069:Tumor Necrosis Factors / Q000235:genetics / Q000378:metabolism*
D015703:Antigens, CD; D053285:CD30 Ligand; D015850:Interleukin-6; D017730:Ki-1 Antigen; D019947:Receptors, Interleukin-6; C505774:TNFSF8 protein, human; D048069:Tumor Necrosis Factors