Macrophages as effectors of the immunoendocrinologic interactions in autoimmune rheumatic diseases.

An intricate balance between soluble mediators, released by activated cells of the immune/inflammatory systems, and products of the neuroendocrine system is implicated in the presence of an autoimmune rheumatic disease. Monocytes/macrophages contribute to autoimmune events in rheumatic diseases, such as rheumatoid arthritis (RA) or systemic lupus erythematosus (SLE), mainly acting as antigen-processing and presenting cells in the presence of an autoimmune rheumatic disease. Clinical symptoms such as morning stiffness and gelling, at least in RA, that peak during the late night and early morning, are consistent with the hypothesis that the immune function of activated cells (i.e., Th1 cells and monocytes/macrophages) and their mediators (cytokines and reactive oxygen intermediates) is increased at these times in relation to neuroendocrine pathway rhythmicity. Therefore, monocytes/macrophages seem to be the "link" between the steroid hormone environment (i.e., gonadal hormones) and the immune response effectors. If gonadal hormones, along with cytotoxic agents, do modulate macrophage apoptosis, such an approach might offer an important pathway to the control of autoimmune diseases. In conclusion, on the basis of a more complete understanding of macrophage effector and immunoregulatory activities, on both a local and systemic level, new hopes arise from the possible development of more sophisticated antimacrophage treatments for the management of autoimmune rheumatic diseases.