The monocyte-macrophage network is an important component of the immune surveillance system. In autoimmune diseases such as lupus erythematosus, this network is deregulated. The monocyte-macrophage network has several functions: 1) destroys microorganisms and tissue debris formed during inflammation; 2) removes dead or dying red blood cells, denatured plasma proteins, and microorganisms that enter the blood; 3) plays a role in the recognition of allogeneic proteins; and 4) promotes the secretion of cytokines. Antigens or heterogeneous proteins do not usually activate T cells directly. Antigens or allosteric proteins are often given to T cells by macrophages. Antigens are present on the surface of macrophages, but in order to respond to antigens, T cells must recognize codes on the surface of macrophages. The human leukocyte antigen, or histocompatibility antigen (HLA) system, takes on the task of recognizing antigens. The histocompatibility antigen system functions when it binds to T cell surface markers and subsequently activates T cells. Class Ⅱ determinants recognize surface antigens for CD4 or helper lymphocytes. Class I (histocompatibility antigen A, B or C) determinants recognize markers for CD8 or suppressor lymphocytes. In summary, the inflammatory process involves an extremely complex set of pathophysiological processes. Inflammatory initiators or stimulators cause capillary dilation, increased permeability or disruption of capillary wall integrity, plasma exudation and leukocyte migration outside the capillaries, and in severe cases cells can also leak out of the damaged vessel wall and into the tissues. Cells and tissues then undergo degeneration and necrosis and are phagocytosed and digested by the monocyte-megakaryocyte system and eventually replaced by granulation and connective tissue. All of these processes are closely associated with leukocytes, especially neutrophils, lymphocytes and monocytes-macrophages, as well as many cytokines.