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  • Title: In vivo levels of IL-4, IL-10, TGF-beta1 and IFN-gamma mRNA of the peripheral blood mononuclear cells in patients with alopecia areata in comparison to those in patients with atopic dermatitis.
    Author: Katagiri K, Arakawa S, Hatano Y.
    Journal: Arch Dermatol Res; 2007 Jan; 298(8):397-401. PubMed ID: 17021766.
    Abstract:
    Alopecia areata (AA) has been considered to be supported by an aberrant expression of IFN-gamma as a result of antigen dependent immune response. On the other hand, AA sometimes concurs with atopic diseases, although the mechanism of the concurrence is not clear. This study was designed to elucidate the immune status of AA and the similarity between AA and atopic dermatitis (AD) by analysis of in vivo levels of mRNA of Th1, Th2, and suppressive cytokines of peripheral blood mononuclear cells (PBMC). Using semiquantitative RT-PCR, the levels of cytokine mRNA were measured in freshly isolated PBMC of 47 patients with AA, 15 patients with AD, and 12 healthy controls (HC). The levels of IL-4, IFN-gamma, and TGF-beta1 mRNA were lower in patients with AA than those in HC. The levels of IL-10 mRNA in AA were comparable with those in HC. Decreased levels of IFN-gamma and TGF-beta1 were also shown in patients with AD. These results indicated a similarity (decreased levels of IFN-gamma and TGF-beta1) between AD and AA based on the cytokine profile. In addition, decreased levels of IL-4 mRNA in AA might also explain the experience that the severity of atopic disease coincident with AA is mild in the most of cases. Next, we compared the levels of these cytokine mRNA among the three subgroups of AA that were categorized based on the severity of the symptoms: mild, severe and totalis. Although there was no significant difference between any combinations of the subgroups, there was a tendency to increase the levels of IFN-gamma mRNA and to decrease the levels of IL-4 mRNA according to the severity of alopecia. However, the levels of IFN-gamma mRNA in any subgroups were less than those of HC. These results suggest that IFN-gamma is therefore involved in the pathogenesis of AA, although the information from PBMC is limited. In conclusion, AA might be induced by an aberrant expression of IFN-gamma in individuals whose PBMC produce low amounts of IFN-gamma and TGF-beta1. Further analysis is therefore required to investigate the phenotypes of the population in PBMC with or without reference to regulatory T cells.
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