Immune response to infection

Abstract 

The immune system in mammals has two facets – the innate and adaptive immune systems – which function as a complex, interdependent entity. This has only recently been fully appreciated when it was realized that the innate immune system has the ability to ‘sample’ microorganisms via its pattern recognition receptors (PRRs) that recognize pathogen-associated molecular patterns – structures present on pathogens but not on mammalian cells. Once activated, PRRs such as Toll-like receptors, C-type lectins and others activate signalling pathways and gene transcription programmes that lead to the production of chemical messengers (cytokines, chemokines, etc.) that activate the most appropriate immune responses for protection against a particular microorganism. The adaptive immune system mounts cell-mediated responses to deal with intracellular microorganisms (e.g. mycobacteria, viruses, etc.) and/or humoral (antibody) responses to combat extracellular microorganisms (Streptococcus, Haemophilus, etc.). Primary immune deficiencies predispose to different infections, depending on the nature of the underlying immune defect (e.g. combined immune deficiency, antibody deficiency, autoinflammatory syndromes). Recent recognition of how subtle immune defects predispose to infections with only selected, weak pathogens (‘non-classical primary immune deficiencies’) have enhanced our understanding of immunity to infection. Understanding the mechanisms underlying the immune response to infection will improve diagnosis and treatment.

Keywords: adaptive, immunity, infection, innate, non-classical primary immune deficiencies, pattern recognition receptors, Toll-like receptors