The mechanisms of allergic rhinitis from sensitization to onset had not been well revealed. We had performed gene expression analysis of nasal epithelial cells by using microarray toward patients with seasonal allergic rhinitis by Japanese cedar pollen (SAR-JCP) and healthy, non-atopic subjects (control subjects). We found that Cystatin SN was up-regulated in SAR-JCP than control subjects. We also invited subjects who possess specific IgE against JCP in serum but had not experienced any SAR-JCP related symptoms “Sensitized subjects” and analyzed Cystatin SN expression. Because some showed higher expression pattern of Cystatin SN among sensitized subjects, it was suspected that Cystatin SN was one of the candidate genes that related the onset from sensitization phase. Cystatin SN belongs to Cystatin family and acts as protease inhibitor. Cystatins have anti-protease activity against not only exogenous protease such as pollen, bacteria, and fungi, but also endogenous protease such as cathepsin, which contribute to inflammation, tissue repair, and cell proliferation. This review summarize the functions of Cystatin SN in nasal epithelial cells and developing allergic rhinitis.

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Bullosis is a general term for a group of conditions causing blistering and erosion of musocutaneous lesions, which is classified into the congenital and autoimmune types. Pemphigus vulgaris (PV) is an autoimmune bullous disease, in which autoantibodies react with the cell–cell adhesion structure, and characterized by intractable oral and laryngopharyngeal lesions. Its varied symptoms and relatively incidence make early diagnosis difficult. Because PV initially presents with oral and laryngopharyngeal symptoms, otolaryngologists play an important role in early diagnosis in general practice. Determination of anti-desmoglein-1 and/or -3 autoantibody levels is useful not only in differential diagnosis and treatment evaluation but also in predicting the clinical course and disease severity. Complicated clinical manifestations of PV can be explained by the desmoglein theory, and the disease course in our 2 patients also fit with this theory. PV must be considered when patients develop intractable oropharyngolarygeal lesions.

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The hyper-immunoglobulin E syndrome is a primary immunodeficiency characterized by recurrent staphylococcal abscesses, recurrent cyst-forming pneumonia, and an elevated serum IgE level of >2000 IU/ml. We present the rare case to our knowledge of an association between hyper-IgE syndrome and chronic rhinosinusitis in a 34-year-old woman. Enodscopic sinus surgery was performed on both sides to control the recurrent sinus infections. 10 months after surgery, no sinusitis flare-ups have been confirmed. Patients with hyper-IgE show abnormal STAT3 activity. However, STAT 3 phosphorylation (STAT3 activation) is not defective, and mutations that cause inhibition of STAT3 nuclear import (DNA binding) have been observed. We examined her immunological back ground using her blood. Similarly, in our patient, it was considered unlikely that the level of STAT3 phosphorylation clearly differs from that of a healthy individual under any stimulation conditions. On the other hand, the phagocytic ability of neutrophils was lower. These results suggested that patients with hyper-IgE exhibit an imbalance between humoral and cell-mediated immunity, in that immune response is predominantly humoral. Moreover, a decline in cell-mediated immune function may manifest as the decreased phagocytic activity of neutrophils.

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