Abstract

The immune system is an interacting network of cells and mediators that serves to defend the host against invasion by either infectious agents or malignant cells. The system discerns self from nonself; when this recognition breaks down, pathologic inflammatory states or autoimmune disease may develop. In considering the role of hormones in modulating immune function in health and disease, it is useful to consider two main functional arms of the immune system (Table 1). The first might be described as innate immunity, and probably represents, from the evolutionary perspective, the most primitive components of the system (1). Innate or natural immunity is not dependent on prior recognition of a foreign antigen and generally serves as an early line of defense against invasion. Innate responses lack high degrees of specificity, but are rapidly deployed. When such innate immune responses are mobilized in error or in excess, inflammatory damage may result. Components of innate or natural immune reactions include the complement proteins and macrophages along with their secreted products, such as interleukin 1 (IL-1) and tumor necrosis factor α (TNF-α). Innate or natural immune responses may be activated during sepsis and shock or when a malignancy is Table 1 Cellular and Soluble Mediators of Innate and Acquired Immunity Immune system components Cellular mediators Soluble mediators Innate immunity Macrophages NK cells IL-1, IL-6, IL-12,TNF-α — Adaptive immunity T lymphocytes B lymphocytes IL-2, IL-4, IL-10, other Antibodies present. The second major functional arm of the immune system is more specific, and may be referred to as “adaptive” because previous exposure to an antigen has taken place. Major components of this aspect of immune function include T and B lymphocytes, along with their respective secreted products, cytokines and antibodies. Chronic infectious diseases usually activate adaptive immune responses. Overresponsiveness or inappropriate triggering of the various components of the immune system may result in autoimmune diseases, such as rheumatoid arthritis, thyroiditis, or systemic lupus erythematosus. In some clinical situations, both innate and specific responses contribute to pathogenesis of autoimmune disorders. For example, rheumatoid arthritis is an autoimmune process that is most dependent on antigen-specific T cells. However, innate immune mediators such as IL-1 and TNF-α also contribute to ongoing tissue damage.

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