Innate immune responses to infection

The human host survives many infectious challenges in the absence of preexisting specific (adaptive) immunity because of the existence of a separate set of protective mechanisms that do not depend on specific antigenic recognition. These antigen-independent mechanisms constitute innate immunity. Antimicrobial peptides are released at epithelial surfaces and disrupt the membranes of many microbial pathogens. Toll-like receptors on epithelial cells and leukocytes recognize a range of microbial molecular patterns and generate intracellular signals for activation of a range of host responses. Cytokines released from leukocytes and other cells exhibit a vast array of regulatory functions in both adaptive and innate immunity. Chemokines released from infected tissues recruit diverse populations of leukocytes that express distinct chemokine receptors. Natural killer cells recognize and bind virus-infected host cells and tumor cells and induce their apoptosis. Complement, through the alternative and mannose-binding lectin pathways, mediates antibody-independent opsonization, phagocyte recruitment, and microbial lysis. Phagocytes migrate from the microcirculation into infected tissue and ingest and kill invading microbes. These innate immune mechanisms and their interactions in defense against infection provide the host with the time needed to mobilize the more slowly developing mechanisms of adaptive immunity, which might protect against subsequent challenges.

Key words: Innate immunity, antimicrobial peptides, Toll-like receptors, chemokines, natural killer cells, complement, phagocytes

Abbreviations used: CXCL, CXC ligand, HBD, Human β-defensin, ICAM-1, Intercellular adhesion molecule 1, LFA-1, Lymphocyte function-associated antigen 1, MAC, Membrane attack complex, Mac-1, Macrophage antigen-1, MBL, Mannan-binding lectin, NADPH, Reduced nicotinamide adenine dinucleotide phosphate, NF, Nuclear factor, NK, Natural killer, PMN, Polymorphonuclear leukocyte, TLR, Toll-like receptor