Autoimmunity : Molecular Pathogenesis And Associated Oral Disease.

Autoimmunity can be defined as an immune response against self –antigens so called self-tolerance. The etiology is considered as multifactorial. Humoral or cellular immune mechanisms are responsible for various systemic and organ specific autoimmune diseases. Advances made in this field to know the immunopathology of autoimmune diseases affecting the oral tissues.

Autoimmunity / 소아과

Self/non-self discrimination and unresponsiveness to self is the fundamental properties of the immune system. Self-tolerance is a state in which the individual is incapable of developing an immune response to an individual's own antigens and it underlies the ability to remain tolerant of individual's own tissue components. Several mechanisms have been postulated to explain the tolerant state. They can be broadly classified into two groups: central tolerance and peripheral tolerance. Several mechanisms exist, some of which are shared between T cells and B cells. In central tolerance, the recognition of self-antigen by lymphocytes in bone marrow or thymus during development is required, resulting in receptor editing (revision), clonal deletion, anergy or generation of regulatory T cells. Not all self-reactive B or T cells are centrally purged from the repertoire. Additional mechanisms of peripheral tolerance are required, such as anergy, suppression, deletion or clonal ignorance. Tolerance is antigen specific. Generating and maintaining the self-tolerance for T cells and B cells are complex. Failure of self-tolerance results in immune responses against self-antigens. Such reactions are called autoimmunity and may give rise to autoimmune diseases. Development of autoimmune disease is affected by properties of the genes of the individual and the environment, both infectious and non-infectious. The host's genes affect its susceptibility to autoimmunity and the environmental factors promote the activation of self-reactive lymphocytes, developing the autoimmunity. The changes in participating antigens (epitope spreading), cells, cytokines or other inflammatory mediators contribute to the progress from initial activation to a chronic state of autoimmune diseases.

Construction of T7 phage display cDNA library from synovium of rheumatoid arthritis patients / 中国免疫学杂志

Objective:To construct and evaluate T7 phage display cDNA library from synovium of rheumatoid arthritis patients.Methods:Total RNA was extracted from pooled RA synovium by Trizol reagents.Messenger RNA was isolated from total RNA by oligo (dT)-conjugated Oligotex particles,and then,the agarose gel electrophoresis showed the range of mRNA size.After mRNA was reverse-transcribed into double-stranded cDNA,end modification,adaptors ligation and EcoR Ⅰ and Hind Ⅲ digestion were performed.After eliminating excess adaptors and small fragments(less than 300 bp),the cDNA was ligated into T7Select 10-3 vector.The RA synovium phage display cDNA library was constructed by package reaction in vitro and plate proliferation.Plaque assay and PCR were used to evaluate the library.Results:We showed that complexity of the library was about 2?107,and the phage titer of the amplified library was 8.9?10 10 pfu/ml.Insert ratio was proved to be 90% with the range of 300-2 000 bp inserts.Meanwhile,a target cDNA gene of BiPwas probed with PCR amplification.Conclusion:The phage display cDNA library from synovium was construted with high quality and can be used as a valuable source in screening of RA self-antigens.