| Bronchial asthma is a kind of chronic allergic inflammatory disease of airway. Studies have verified that the pathologic foundation of asthma is allergic airway inflammation (AAI). With the stimulation of allergen, Many kinds of inflammatory cells, relied mainly on easinophilia, trend and assemble to the airway to be activccted, and release many kinds of inflammatory factors to destroy the epithelium of the airway, which cause AAI and airway hyper responsiveness. The theory of airway inflammation thinks that the asthma is a kind of chronic airway inflammatory disease, which involves the interactive of many inflammatory cells and factors. Airway inflammation is the pathologic foundation of airway hyperten siveness, which is the patho physiologic character of the asthma. Nowadays, many scholars think that the onset of asthma has close relation with excessively activation of CD4 and the out of 13alance of CD4/CD8, and they propose regarding CD4 as the target of immunoregulation of asthma. CD4+T cells can be divided into subgroups of Th1 and Th2. when the subgroup of Th2 is preponderant, it is easy for the increase of 1gE in blood and so eosinophilia to take place. The subgroup of Th1 mainly secrete IFN-r, and IL-12, however, the subgroup of Th2 secrete IL-4, IL-5, IL-13 and other cellular factors. Studies in recent ten years have mediated that no matter whether the proportion of Th1/Th2 polarizing to Th2 in patients of asthma or the excessively secreting of IL-4, IL-5, IL-13, etc, the costimulatory molecules play an important role. CD28 is a receptor expressed on the surface of T cell and recepting costimulatory signal, which is matched by the molecules of BT-1 and BT-2 expressed on the surface of APC. CTLA4 which has the same structure with CD28 and can also be combined with the molecules of CD80 and CD86, is also expressed on the surface of T cell, however the CTLA4 is so times the affinity to them of CD28. CTLA4 is not expressed in static T cell, and just expressed with a lower level in fresh activated T cell. The expression of CTLA4 is just in a lower level in 24hs after the activation of T cell and reaches the peak in 48h and resumes to the original level in 96 hours. The inhibition (suppression) of costimulatory signal can prevent the activation of T cell, and can make T cell in a strode of no response for a long time or apoptosis. CTLA4 that promotes the activation of T cell can inhibit the increase of T cell, promote the peculiar apoptosis of antigen, and inhibit Th1 and Th2 cell producing cellular factors. CTLA-4Ig, which is a structure part of CTLA4 out of cell, is a kind of soluble protein that can merge with the Fc segment of IgG, so it can combine with CD80 and CD86 too. In the mouse model of antigen-induced airway inflammation mouse, blocking the costimulatory way of CD80 and /or CD86 with CTLA-4Ig, can suppress the activation of T cell. Recently, a group of new molecules named as CD45 are found on the surface of cell membrane with the using of monoclonal antibody. The isoforms of CD45 are called as CD45R, as they are normally expressed on the surface of certain cells limitedly. T cells can be divided into two subgroups with this isoforms. The T cell without the stimulation of antigen is called naive T cell (Tn), which belongs to the group of CD45RA+T cell. However, The T cell with the strangulation of antigen is called memory T cell (Tm) which belongs to the group of CD45RO+cell. There are difference in the effect of secreting cellular factors and in allxiliary effect to B cell between the two. Tm secretes kinds of Th1. and Th2 lymph factors, such as IL-4, IL-6, IFN-r, IL-13, and a little IL-2, and has auxiliary function to produce Ig on B cell. 1. The influence of costimulatory molecules CTLA4-Ig on the expression of IL-13 by T cell in the patients of asthma. Using 16 cases of asthmatic patients as the research objects, 12 healthy persons as contrast, fetching peripheral veinal blood 6ml respectively, carrying on the separation and culture of PBMC, The PBMC of ea... |
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