Vitiligo is a common dermatological disorder characterized by the presence on the skin of depigmented macules resulting from the destruction of cutaneous melanocytes. Autoimmunity is an important hypothesis with regard to vitiligo aetiology and the evidence for autoimmune responses being involved in the pathogenesis of this disorder will be discussed in the present review. All immune system compartments, including innate and adaptive immunity have been implicated in vitiligo development. Particularly relevant are autoantibodies and autoreactive T cells in vitiligo patients that have cytotoxic effects upon pigment cells. Furthermore, predisposition to vitiligo appears to be associated with certain alleles of the major histocompatibility complex class II antigens as well as with other autoimmune-susceptibility genes. Moreover, the association of vitiligo with autoimmune disorders, the animal models of the disease, and the positive response to immunosuppressive therapeutic agents emphasize the role of autoimmunity in the development of this disorder.

CFDS could characterize two distinct subtypes in patients with AIT. Conversely, IL-6 seemed to be an unhelpful test in this context.

Iodide concentration by the thyroid gland, an essential step for thyroid hormone synthesis, is mediated by the Na + /I symporter (NIS). To identify factors that may regulate this process, we have studied NIS gene expression in the Fisher rat thyroid cell line (FRTL-5) by a semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) technique. Increasing concentrations of bovine TSH (0·1, 1, 10, 50 and 100 mU/l), with or without tumour necrosis factor-(TNF ), interferon-(IFN ) or interleukin-1 (IL-1 ) were added to FRTL-5 cells previously deprived of TSH for a minimum of 5 days. RNA was extracted and samples were studied for NIS expression. TSH enhanced NIS mRNA expression in a dose-dependent manner, with induction evident at 0·1 mU/l, reaching a peak at 50 mU/l, an effect detected after 6 h of stimulation, but not in the first 2 h. Both TNF and, to a lesser extent, IL-1 inhibited basal and TSH-induced NIS expression. High concentrations of IFN also downregulated TSH-stimulated NIS mRNA expression.Using the same technique, we also investigated NIS mRNA tissue distribution in two male and one female Wistar rats. High levels of NIS expression were detected in the thyroid, stomach, and mammary gland, lower levels were found in the intestine, adipose tissue and liver, borderline levels were expressed in the salivary gland, and no expression was detected in the kidneys.In summary, we have shown that TSH upregulates rat NIS gene expression in vitro, and this induction can be modulated by cytokines. Analysis of the distribution of rat NIS mRNA ex vivo demonstrated variable levels of NIS transcription in different tissue samples.

Intercellular adhesion molecule-1 (ICAM-1), hitherto identified on activated B cells, macrophages, dendritic cells, endothelia and certain epithelial cells, serves as a ligand for the lymphocyte function-associated antigen-1 (LFA-1). ICAM-1 binding by LFA-1 enhances the efficiency of lymphocyte-target cell and lymphocyte-accessory cell interactions. We have investigated the in-vitro expression of ICAM-1 by cultured thyroid cells from five patients with Graves' disease using indirect immunofluorescence analysis, and found that 30 +/- 11% (mean +/- S.D.) of cells were ICAM-1 positive under basal conditions. The proportion of cells which were ICAM-1 positive and the amount of ICAM-1 per cell (assessed by fluorescence intensity) were both increased in all cases by the cytokines gamma-interferon, interleukin-1 and tumour necrosis factor. Immunohistochemical analysis of frozen sections from thyroidectomy specimens demonstrated ICAM-1 on thyroid follicular cells in areas of lymphocytic infiltration in patients with Graves' disease (n = 2) or Hashimoto's thyroiditis (n = 2). ICAM-1 was not found in specimens from a patient with a toxic multinodular goitre or a patient with Graves' disease without focal lymphocytic accumulation. These results suggest that the thyroid epithelium may express ICAM-1 as well as major histocompatibility complex class II antigens, such as HLA-DR, in response to locally synthesized cytokines. The enhanced expression of ICAM-1 may render these cells more susceptible as targets for lymphocyte-mediated cytotoxicity, and together with HLA-DR antigen expression may increase the accessory cell capability of the thyroid follicular cells.