Effects of omalizumab treatment on serum cytokine concentrations of atopic patients with chronic spontaneous urticaria: a preliminary report.

SUMMARY: Omalizumab has recently obtained indication for chronic spontaneous urticaria both in the US and Europe. However, the mechanism of action of this drug has yet to be fully elucidated. Previous studies have shown elevations in cytokine serum levels in patients with chronic spontaneous urticaria, and it is not known whether omalizumab treatment may affect cytokine serum levels in this condition. Besides, a proportion of chronic spontaneous urticaria patients have concomitant atopy, which may be associated, at least in theory, with prevalence of serum Th2-type cytokines. In this study, serial serum samples from five patients (4 atopic and 1 nonatopic) with chronic spontaneous urticaria were assayed for cytokine concentrations by means of flow-cytometry-based multiplex bead assays, before and during omalizumab treatment. Omalizumab appeared to significantly affect the concentrations of multiple cytokines in a case of severe, long-lasting chronic spontaneous urticaria. Interestingly, IL-22 serum levels were found to progressively increase in three of five patients. Further studies are thus needed in larger patient populations, to conclusively establish whether the mechanism of action of omalizumab in chronic spontaneous urticaria also includes modulation of cytokine synthesis.

Lupus mastitis in systemic lupus erythematosus: a rare condition requiring a minimally invasive diagnostic approach.

Breast involvement is a rare event in SLE patients. The most frequent presentation is lupus panniculitis with skin erythema, tenderness, and parenchymal nodules. However, when breast masses are detected in SLE patients without significant superficial inflammation, it is mandatory to rule out breast carcinoma. Here, we report the case of a 47-year-old woman with an 18-year-long history of SLE, who presented with a suspicious breast mass. Since surgical trauma has been reported to be able to exacerbate breast inflammation in lupus mastitis, an ultrasound-guided minimally invasive Mammotome biopsy was performed to obtain tissue samples for histological and immunohistochemical examinations. Histology was consistent with lupus mastitis. The patient was already on mycophenolate mofetil and hydroxychloroquine. At the latest follow-up visit 6 years later, no progression of the breast lesion was observed.

T-helper cell type-2 regulation in allergic disease.

Substantial experimental evidence now supports the notion that allergic diseases are characterised by a skewing of the immune system towards a T-helper cell type-2 (Th2) phenotype. Studies using both human and mouse model systems have provided key evidence for the role that Th2 cytokines play in driving many of the hallmarks of allergic inflammation. Furthermore, the signalling pathways by which Th2 cytokines exert their effects on airway target cells are rapidly being elucidated, and antagonists of the Th2 pathway are under active development. In this review, the current knowledge of the role of T-helper cell type-2 cells in asthma is summarised, focusing on how and where T-helper cell type-2 cells differentiate from naïve precursors. The signalling molecules and transcription factors involved in T-helper cell type-2 differentiation will be reviewed in detail, in an attempt to translate studies using genetically modified mice into meaningful insights about asthma and other allergic diseases.

Direct or reverse correlations within the expression of activation, differentiation or T-B cooperation molecules on chronic lymphocytic leukemia B cells.

AIM: B-cell chronic lymphocytic leukemia (B-CLL) is characterized by homogeneous coexpression of CD19, CD23 and CD5, and poor expression of membrane Ig. The aim of this study was to evaluate, in B-CLL patients and in healthy subjects by flow cytometry, B cell expression of surface molecules involved in cell activation, differentiation, T-B cooperation and apoptosis. METHODS: The study population consisted of 29 patients (16 men and 13 women; mean age: 66.5 years) with B-CCL. The control group consisted of 16 sex- and age-matched healthy subjects. The results are reported as percentages and mean fluorescence intensity (MFI) of CD19+ cells coexpressing each analyzed molecule. RESULTS: We found that the lymphocyte activation markers, CD69, CD25 and CD11c, were more expressed in B-CLL patients than controls. CD38 and CD95 expressions were higher on normal B lymphocytes than leukemic B cells. Finally, CD80 and CD86, molecules involved in T-B cooperation, showed an inverse expression between lymphocytes of B-CLL patients and healthy subjects. CD80 was higher on normal than leukemic B cells, while CD86 expression was higher on CLL B cells. Linear regression analysis showed a positive correlation between CD80 and CD95 expression on leukemic B cells; a reverse correlation was observed between CD69 and CD11c. CONCLUSION: These results suggest that common mechanisms may regulate the simultaneous expression of CD80 and CD95 or the reverse expression of CD69 and CD11c, respectively, in different stages of B cell activation and/or differentiation.

[Late onset immunodeficiency with hypo-IgG and hyper-IgM, T CD4+ lymphocytopenia and vitiligo]. / Immunodeficienza ad insorgenza tardiva con ipo-IgG e iper-IgM, linfocitopenia T CD4+ e vitiligo.

The Authors report the clinical case of a patient with a deficit of humoral immunity who developed infections since puberty. The serum levels of IgG and IgA decreased progressively in the fourth decade of life, while serum IgM increased. Moreover, the patient developed a marked CD4+ T lymphocytopenia and a meager B lymphocytopenia, vitiligo, positivity for anti-SSA/Ro autoantibodies and granulomatous phlogosis of the knee. The heterogeneity of the clinical and laboratory data suggests that this patient might present an overlap immunodeficiency syndrome with some of the clinical and immunological features typical of the hyper-IgM syndrome (in the X-linked or autosomal forms) and others that can be referred to a nosologically distinct humoral immunodeficiency such as the common variable immunodeficiency.