The autologous-serum skin test (ASST) can cause a wheal-and-flare response in some cases of chronic idiopathic urticaria. We subjected 102 patients affected by chronic idiopathic urticaria to this test and studied some clinical parameters to detect any significant differences between ASST-positive and ASST-negative patients. The only significant difference we noted between the two groups was the incidence of angioedema (P = 0.01). We suggest that the ASST cannot be used alone either to predict the severity of urticaria or to define it as 'autoimmune'.
Hereditary Hemorrhagic Telangiectasia (HHT) is a rare genetic disease characterized by mutations occurring in the endoglin and ALK-1, two receptors of transforming growth factor-beta1. From a pathogenic point of view, a possible involvement of the immune system in HHT has been suggested since a mononuclear cell infiltrate was found around the area of telangiectases. Up until now, no information has been available about the role played by leukocytes in HHT and the mechanisms elicited by secretion of their mediators. However, the fact that a deficit of adaptive immunity in HHT has been reported in a companion paper in this issue will represent a great contribution to the understanding of HHT pathogenesis. The purpose of this study was to evaluate whether patients with HHT manifest also alterations in the innate immune response. Therefore, the phenotype of T, B and natural killer lymphocytes, serum immunoglobulin levels, phagocytosis and oxidative burst activity exerted by polymorphonuclear cells (PMN) and monocytes (MO) were analyzed in 22 patients. Twenty individuals demonstrated single or multiple deficits of PMN and MO functions, while the immunophenotype of lymphocytes and serum concentrations of immunoglobulins were normal. To the best of our knowledge, this is the first demonstration of a reduction in PMN and MO functions in HHT, thus suggesting a higher susceptibility to infectious complications in these patients. The relationship between innate immune deficits and T helper 1 and monocyte-derived cytokine dysfunction in HHT, as previously reported, is discussed.
In recent years an association between oral lichen planus (OLP) and HCV infection has been reported, but the frequency of this association seems to differ in the various geographic areas. It is clear, instead, that some abnormalities occur in the immune-regulation mechanisms of patients with OLP and it is thought to be due to the chronic antigenic stimulus of HCV that causes functional disorders of the immune system in infected patients. Possible immunologic difference between 17 patients with OLP and HCV+ and 17 patients with OLP and HCV-were investigated using standard immunofluorescence and flow cytometry techniques. The distribution of T and B cells was normal in all patients examined, while NK CD56+ cells were increased, above all in HCV-patients. About 65% ofT CD4+ lymphocytes coexpressed the CD45RO isoform (p=0.002), while approximately 32% expressed CD45RA, without significant differences in comparison to HCV+ subjects (p>0.05). Moreover, almost all the CD4+CD45RO+ subpopulation coexpressed CD29 in all patients examined. No significant differences between the two groups of patients were detected as to the increase of cytotoxic T CD8+CD57+ lymphocytes. The B cells CD19+CD5+ responsible for the production of "natural" antibodies were detectable in both the examined groups, even ifnot in all HCV+ subjects (30% ± 10.1 in HCV-and 27% ±19.4in HCV+ patients; p=0.47).These findings suggest the existence ofdifferences in lymphocyte subpopulations between OLP-HCV+ subjects and OLP-HCV-patients.
Circulating levels of EPCs were significantly lower in SSHL patients compared with controls. In particular, CD34+KDR+ cells and CD34+CD133+KDR+ cells were significantly reduced (p < 0.05).
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