The role of IFN-gamma in systemic lupus erythematosus: a challenge to the Th1/Th2 paradigm in autoimmunity
Cytokines play a critical role in regulating lymphoid cell responses to most antigenic stimuli, and it is therefore very likely that these molecules profoundly affect the pathogenesis of autoimmune diseases. Consequently, investigations of the role of cytokines as effectors or predisposing elements in these diseases have received prominent attention for many years. Early findings from such studies, however, were frequently contradictory and, more importantly, difficult to incorporate into a conceptual framework. A new impetus in this area was provided by the discovery of Mosmann and colleagues that T cells could be conveniently divided into two main subsets, ie Th1 and Th2, with distinct arrays of cytokine secretion patterns and functions [1,2]. A hypothesis was subsequently formulated according to which cell-mediated autoimmune diseases, such as insulin-dependent diabetes mellitus, are induced by Th1 cells and their cytokines, and humorally-mediated autoimmune diseases, such as systemic lupus erythematosus, are induced by Th2 cells and their cytokines. As reviewed below, findings on the primary role of IFN-γ in the pathogenesis of murine lupus and other observations clearly refute this hypothesis.
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| description | Cytokines play a critical role in regulating lymphoid cell responses to most antigenic stimuli, and it is therefore very likely that these molecules profoundly affect the pathogenesis of autoimmune diseases. Consequently, investigations of the role of cytokines as effectors or predisposing elements in these diseases have received prominent attention for many years. Early findings from such studies, however, were frequently contradictory and, more importantly, difficult to incorporate into a conceptual framework. A new impetus in this area was provided by the discovery of Mosmann and colleagues that T cells could be conveniently divided into two main subsets, ie Th1 and Th2, with distinct arrays of cytokine secretion patterns and functions [1,2]. A hypothesis was subsequently formulated according to which cell-mediated autoimmune diseases, such as insulin-dependent diabetes mellitus, are induced by Th1 cells and their cytokines, and humorally-mediated autoimmune diseases, such as systemic lupus erythematosus, are induced by Th2 cells and their cytokines. As reviewed below, findings on the primary role of IFN-γ in the pathogenesis of murine lupus and other observations clearly refute this hypothesis. |
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| title | The role of IFN-gamma in systemic lupus erythematosus: a challenge to the Th1/Th2 paradigm in autoimmunity |
