Abstract
The ability to recognize the presence of a pathogen and respond appropriately is a fundamental aspect of innate immunity. This chapter describes the types of receptors and their ligands that are used to detect microbes that have entered the body as well as responses. Some receptors recognize conserved structures unique to microbes and not present in mammalian cells, called pathogen-associated molecular patterns (PAMPs). Other receptors recognize nucleic acids that are unique to the microbe or are in the cytoplasm where nucleic acids are not normally found. Interestingly, certain disruptions to the cell, such as microbial invasion or cell stress, can be detected and are called danger-associated molecular patterns (DAMPs). The host makes multiple types of responses appropriate for eliminating the type of pathogen. The inflammatory response consists of fluid and cells entering tissues to fight the infection and secretion of cytokines and chemokines for cell–cell communication. The complement system is an ancient system of proteins for fighting infections. Once activated, complement proteins promote inflammation and directly kill pathogens. Other effector mechanisms such as the secretion of antimicrobial peptides are discussed. The breadth of receptors and responses reflects how important it is to recognize an invading microbe, make an appropriate response for the type of pathogen, and destroy it before being harmed. However, in some cases, it is not possible to eliminate the microbe or inducer of inflammation. A state of chronic inflammation is an adaption by the host to this situation.
Access this chapter
Tax calculation will be finalised at checkout
Purchases are for personal use only
References
Bosurgi L, Cao YG, Cabeza-Cabrerizo M, Tucci A, Hughes LD, Kong Y, et al. Macrophage function in tissue repair and remodeling requires IL-4 or IL-13 with apoptotic cells. Science. 2017;356(6342):1072–6.
Boxberger N, Hecker M, Zettl UK. Dysregulation of inflammasome priming and activation by MicroRNAs in human immune-mediated diseases. J Immunol. 2019;202(8):2177–87.
Broz P, Dixit VM. Inflammasomes: mechanism of assembly, regulation and signalling. Nat Rev Immunol. 2016;16(7):407–20.
Chen Q, Sun L, Chen ZJ. Regulation and function of the cGAS-STING pathway of cytosolic DNA sensing. Nat Immunol. 2016;17(10):1142–9.
Crowl JT, Gray EE, Pestal K, Volkman HE, Stetson DB. Intracellular nucleic acid detection in autoimmunity. Annu Rev Immunol. 2017;35:313–36.
Dantzer R, Kelley KW. Twenty years of research on cytokine-induced sickness behavior. Brain Behav Immun. 2007;21(2):153–60.
Evavold CL, Kagan JC. How inflammasomes inform adaptive immunity. J Mol Biol. 2018;430(2):217–37.
Foster SL, Medzhitov R. Gene-specific control of the TLR-induced inflammatory response. Clin Immunol. 2009;130(1):7–15.
Goldberg EL, Asher JL, Molony RD, Shaw AC, Zeiss CJ, Wang C, et al. Beta-hydroxybutyrate deactivates neutrophil NLRP3 inflammasome to relieve gout flares. Cell Rep. 2017;18(9):2077–87.
Hendricks DW, Balfour HH Jr, Dunmire SK, Schmeling DO, Hogquist KA, Lanier LL. Cutting edge: NKG2C(hi)CD57+ NK cells respond specifically to acute infection with cytomegalovirus and not Epstein-Barr virus. J Immunol. 2014;192(10):4492–6.
Ivashkiv LB. IFNgamma: signalling, epigenetics and roles in immunity, metabolism, disease and cancer immunotherapy. Nat Rev Immunol. 2018;18(9):545–58.
Kawai T, Akira S. Toll-like receptors and their crosstalk with other innate receptors in infection and immunity. Immunity. 2011;34(5):637–50.
Kieser KJ, Kagan JC. Multi-receptor detection of individual bacterial products by the innate immune system. Nat Rev Immunol. 2017;17(6):376–90.
Kotas ME, Medzhitov R. Homeostasis, inflammation, and disease susceptibility. Cell. 2015;160(5):816–27.
Liu Y, Olagnier D, Lin R. Host and viral modulation of RIG-I-mediated antiviral immunity. Front Immunol. 2016;7:662.
Maeda K, Caldez MJ, Akira S. Innate immunity in allergy. Allergy. 2019;00:1–15.
Magna M, Pisetsky DS. The role of HMGB1 in the pathogenesis of inflammatory and autoimmune diseases. Mol Med. 2014;20:138–46.
O’Neill LA, Golenbock D, Bowie AG. The history of Toll-like receptors - redefining innate immunity. Nat Rev Immunol. 2013;13(6):453–60.
Parham P, Guethlein LA. Genetics of natural killer cells in human health, disease, and survival. Annu Rev Immunol. 2018;36:519–48.
Ram S, Lewis LA, Rice PA. Infections of people with complement deficiencies and patients who have undergone splenectomy. Clin Microbiol Rev. 2010;23(4):740–80.
Ricklin D, Barratt-Due A, Mollnes TE. Complement in clinical medicine: clinical trials, case reports and therapy monitoring. Mol Immunol. 2017;89:10–21.
Serhan CN, Levy BD. Resolvins in inflammation: emergence of the pro-resolving superfamily of mediators. J Clin Invest. 2018;128(7):2657–69.
West EE, Kolev M, Kemper C. Complement and the regulation of T cell responses. Annu Rev Immunol. 2018;36:309–38.
Author information
Authors and Affiliations
Corresponding author
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 2019 Springer Nature Switzerland AG
About this chapter
Cite this chapter
Kavathas, P.B., Krause, P.J., Ruddle, N.H. (2019). Innate Immunity: Recognition and Effector Functions. In: Krause, P., Kavathas, P., Ruddle, N. (eds) Immunoepidemiology. Springer, Cham. https://doi.org/10.1007/978-3-030-25553-4_3
Download citation
DOI: https://doi.org/10.1007/978-3-030-25553-4_3
Published:
Publisher Name: Springer, Cham
Print ISBN: 978-3-030-25552-7
Online ISBN: 978-3-030-25553-4
eBook Packages: Biomedical and Life SciencesBiomedical and Life Sciences (R0)