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2018 ; 9
(3
): 336
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The role of the mitochondria and the endoplasmic reticulum contact sites in the
development of the immune responses
#MMPMID29491398
Martinvalet D
Cell Death Dis
2018[Feb]; 9
(3
): 336
PMID29491398
show ga
Mitochondria and endoplasmic reticulum (ER) contact sites (MERCs) are dynamic
modules enriched in subset of lipids and specialized proteins that determine
their structure and functions. The MERCs regulate lipid transfer, autophagosome
formation, mitochondrial fission, Ca(2+) homeostasis and apoptosis. Since these
functions are essential for cell biology, it is therefore not surprising that
MERCs also play a critical role in organ physiology among which the immune system
stands by its critical host defense function. This defense system must
discriminate and tolerate host cells and beneficial commensal microorganisms
while eliminating pathogenic ones in order to preserve normal homeostasis. To
meet this goal, the immune system has two lines of defense. First, the fast
acting but unspecific innate immune system relies on anatomical physical barriers
and subsets of hematopoietically derived cells expressing germline-encoded
receptors called pattern recognition receptors (PRR) recognizing conserved motifs
on the pathogens. Second, the slower but very specific adaptive immune response
is added to complement innate immunity. Adaptive immunity relies on another set
of specialized cells, the lymphocytes, harboring receptors requiring somatic
recombination to be expressed. Both innate and adaptive immune cells must be
activated to phagocytose and process pathogens, migrate, proliferate, release
soluble factors and destroy infected cells. Some of these functions are strongly
dependent on lipid transfer, autophagosome formation, mitochondrial fission, and
Ca(2+) flux; this indicates that MERCs could regulate immunity.