Immune Reactions Against Heat Shock Proteins and Arthritis

摘要: During the last decade our insight into aetiology and pathogenesis of supposedly autoimmune diseases like rheumatoid arthritis made considerable progress: they seem to be helper T lymphocyte (T cell) mediated; possible triggering and/or target antigens have been identified aberrant expression human leucocyte (products HLA system, major histocompatibility complex) may involved in presentation these cells. The cell, which is a class II-restricted CD4 positive plays central role orchestrating immune response. way it does so by producing cytokines or lymphokines, regulate, at least, all other activated (by antigen) players system. Thus most specific efficient immunotherapy for an disease shut off button that specifically turns on autoreactive cell. That molecule presenting autoantigen cell receptor How this cells (Th) indeed turned very efficiently, has shown experimental animal models further discussed previous chapter Kingsley Panayi Immunotherapy. One such model stimulated lot research direction adjuvant (AA), induced susceptible animals (Lewis rats) injection Mycobacterium tuberculosis oil. In model, from affected Lewis rats isolated are capable transferring naive animals. These recognize epitopes mycobacterial heat shock protein 65 kDa (hsp65). we will review studies performed 6 7 years, addressed proteins, particular hsp65, of, respectively, reactive arthritis.