Stress Response and Immunity: Links and Trade Offs

Autonomous Immunity

Author(s): Nadia Danilova

Pp: 257-306 (50)

DOI: 10.2174/9789811437175120010010

* (Excluding Mailing and Handling)


Autonomous immunity is a set of immune mechanisms present in practically every cell of a multicellular organism. They include immune mechanisms based on nuclear acids, such as RNA interference (RNAi). Small RNAs generated from pathogen dsRNAs guide nucleases to the pathogenic nucleic acids. In addition, RNAi restricts the expression of transposable elements by establishing transcriptionrepressing chromatin over DNA regions that encode such elements. Other autonomous mechanisms prevent the entry of viruses into cells, detect and destroy non-self nucleic acids, restrict pathogen growth and replication, prevent pathogen release, and induce regulated cell death if the infection cannot be suppressed. Infected cells release interferons and other cytokines that alert neighboring cells and preventively induce defensive mechanisms in them. Pathogens express pathogen-associated molecular patterns (PAMPs), which are recognized by pattern-recognition receptors (PRRs). These receptors also recognize damaged “self” molecules expressing damageassociated molecular patterns. Infection can also be sensed indirectly through changes in the functioning of some key cellular molecules. Stress and infection can lead to the formation of inflammasomes triggering production and secretion of pro-inflammatory cytokines.

Keywords: Argonaute, Drosha, Dicer, Damage-associated molecular pattern, Danger theory, Effector immunity, Inflammasome, NLR, Pathogen-associated molecular patterns, Pattern recognition receptor, piRNAs, RNA interference, siRNAs, TLR.

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