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Recent advances in autoimmunity

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Abstract

Although autoimmunity in terms of immune reaction of an organism against itself has been postulated as a significant cause of human disease for many years, only in the past few years have advances in our understanding of immunoregulation brought us to the point where we feel we may speculate intelligently on pathogenesis. The immune system is divided broadly into cell-mediated immunity, which is influenced early in life by the thymus and humoral immunity. T- or thymic-dependent lymphocytes are effector organs of cell-mediated immunity and B- or bursal-equivalent (referring to an avian organ that influences humoral immunity) lymphocytes are responsible for humoral immunity. In order to secrete antibody, B-lymphocytes undergo differentiation into plasma cells that are antibody-secreting cells. B-lymphocytes only differentiate into antibody-secreting plasma cells in the presence of a subpopulation of T-lymphocytes that give a “signal” that antibody to a particular antigen should be secreted. These lymphocytes are referred to as helper T cells and represent one limb of immunoregulation. The other limb of immunoregulation is that of suppressor T cells that can suppress antibody synthesis. In the presence of normal B-lymphocytes, whether antibody will be secreted in response to exposure of the system to a given antigen will therefore be a summation of the helper and suppressor T cell influences on the B cell. One may therefore presume that in a normal organism foreign or bacterial antigens will result in a net helper effect and antibody synthesis, whereas self-antigens will result in a net suppressor effect and little or . . .


 

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