Abstract

Background Our immune system is composed of an innate (germ-line encoded) and adaptive (acquired) arm. It involves specialized hematopoietic cells but also cell-intrinsic (non-hematopoietic) mechanisms, antigen-specific receptors (T and B cell receptors/immunoglobulins), microbial sensors (pattern recognition receptors), and a complex network of signaling molecules that cooperatively work together to prevent or control infection by invading microorganisms via a variety of effector mechanisms. Both innate and adaptive immune defense mechanisms are tightly regulated, to avoid potentially harmful consequences such as tissue damage to the host, and to maintain tolerance to self as well as to harmless foreign antigens. An imbalance or insufficiency of these immune defense and regulatory mechanisms becomes apparent as clinical disease, either in the form of symptomatic infections (in which case the host immune defense was insufficient to prevent or control infection, dysregulated, or even deficient), or during ...

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