Adenoids are part of the MALT. In the present study, we analyzed cell surface markers and cytolytic activity of adenoidal NK (A-NK) cells and compared them with NK cells derived from blood of the same donors (B-NK). NK cells comprised 0.67% (0.4-1.2%) of the total lymphoid population isolated from adenoids. The majority (median=92%) of the A-NK cells was CD56(bright)CD16(-). A-NK cells were characterized by the increased expression of activation-induced receptors. NKp44 was detected on >60%, CD25 on >40%, and HLA-DR on >50% of freshly isolated A-NK cells. Functional assays indicated that the cytotoxic machinery of A-NK is intact, and sensitive target cells are killed via natural cytotoxicity receptors, such as NKG2D. Carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1; CD66) expression was up-regulated in 23% (median) of the A-NK cells by IL-2 activation but unchanged in B-NK cells. CEACAM1 inhibited the A-NK killing of target cells. CXCR4 was expressed on more than 40% A-NK cells prior to activation. Its ligand, CXCL12, was found in endothelial cells of the capillaries within the adenoid and in cells of the epithelial lining. In addition, A-NK cells migrated in vitro toward a gradient of CXCL12 in a dose-responsive manner, suggesting a role for this chemokine in A-NK cell recruitment and trafficking. We conclude that the A-NK cells are unique in that they display an activated-like phenotype and are different from their CD16(-) B-NK cell counterparts. This phenotype presumably reflects the chronic interaction of A-NK cells with antigens penetrating the body through the nasal route.
Hearing loss may be another EIM of IBD. It is found in 38 % of IBD patients and in up to 52 % of patients with other EIMs and increases over the age of 40. Early hearing evaluation should be recommended to these high-risk IBD patients.
Presentation schedule is subject to change. For the most up-to-date information, visit www.entnet.org/annual_meeting. Results: Before intratympanic methylprednisolone perfusion, the level of HDAC2 protein were significantly depressed in all SSNHL patients (F = 13.291,<.0001), while the HDAC2 mRNA expressing much higher than the control group (F = 6.047, =.007). The expression level of HDAC2 mRNA increased significantly after intratympanic methylprednisolone (GC sensitive group: t = 3.941, P = .006; GC insensitive group: t = 2.57, P = .026). The HDAC2 protein level in GC sensitive group increased significantly (t = 6.148, P < .001).Conclusions: Knockdown of HDAC2 expression induces corticosteroid insensitivity. Glucocorticoids can increase the expression of HDAC2 mRNA. HDAC2 can be downregulated by posttranslational modifications.
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