| Objective: OX40(CD134) and its cognate receptor OX40L belong to the TNF(Tumor Necrosis Factor) and TNF receptor Superfamilies, respectively. OX40 and OX40L is an important pair of costimulator, playing a critical role in the immune response,tumor immunity,host vs graft reaction and autoimmune diseases. OX40 is preferentially expressed by activated CD4~+T cells, it can remarkably stimulate CD4~+T cells proliferation and maintain its long-time survival, and also it can induce Thl/Th2 unbalance and stimulate B cells differentiation to produce IgE by secreting cytokines. The potential mechanism is that they can stimulate the expression of antiapoptotic factor Bcl-2 (B-cell lymphoma / leukemia-2)and then lead to inflammation sustained existence by inhibiting apoptotic of the CD4~+T cells and some other cells related to inflammation. Bcl-2 family is an important intra-cellular antiapoptotic genes, which is a critical mediator in the proliferation and its dynamic equilibrium of lymphocyte. The objective of this study is to approach the pathogenesis and mechanism of allergic rhinitis(AR) and investigate the expression of OX40 and Bcl-2 in the middle turbinate in the patients with AR by immunohistochemical method. The aim is to find a new immune therapeutic approach for the treatment of AR patients.Methods: Strictly according to allergic rhinitis patients selected standard published in Lanzhou meeting in 2004, 23 subjects with allergic rhinitis as experimental group were collected with 20 subjects of deflection of nasal septum as control group except the ones with allergic inflammatory diseases. Immunohistochemistry was used to examine the expression of OX40 and Bcl-2 in the two groups. The experimental data were expessed with (X|-)±S and the comparison between two groups was detected by t-test. The correlation of two variable between OX40 and Bcl-2 was detected by correlation analysis.Results: OX40 and Bcl-2 both showed strong expression in epithelium, glandular epithelium cell, vascular endotheliocyte, plasmocyte and CD4~+T cell. OX40 mainly expessed in cytomembrance and cytoplasm (OD=0.2394±0.0335), while OX40 was stained a little in control group. Also Bcl-2 had positive staining in cytomembrance and cytoplasm (OD=0.2373±0.0421) while expessed little in control group. There was statistically significant deviation between allergic rhinitis and control group (P<0.01). Correlation analysis showed that the expression of OX40 was significantly correlated with that of Bcl-2 (r=0.8690, P<0.05).Conclusions: OX40 and Bcl-2 play a critical role in the development of AR. The potential mechanism is as follows: Owning to the sustaining present of allergens, the expression of OX40 is increased on the cell envelope. The interaction between OX40 and its ligand OX40L may promote the expression of Bcl-2 to inhibit apoptos, and then sustain CD4~+T cells long-time survival, cytokines such as IL-4, TNF-r et al secretion, TH1/TH2 losing banlance, and finally promote the differentiation and secretion of the plasma cells. While Bcl-2 may inhibit the apoptos of epithelium, glandular epithelium cell and vascular endotheliocyte, and then lead to hyperplasia of epithelium, hypersecretion of glandular epithelium, hyperaemia of local nasal tissue and so on. All that result in local pathological changes of the AR and cause a series of corresponding clinical symptoms.
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