what is difference between endoplasmic reticulum and mitochondria
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HeY maTe....
HeY maTe....Among the various intracellular organelles that interact with the ER, which include the Golgi apparatus, mitochondria, peroxisomes, endosomes and lysosomes, the mitochondria has one of the most extensively studied and well-characterized connections with the ER.
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The role of the mitochondria and the endoplasmic reticulum contact sites in the development of the immune responses
Review Article | OPEN | Published: 28 February 2018
The role of the mitochondria and the endoplasmic reticulum contact sites in the development of the immune responses
Denis Martinvalet
Cell Death & Diseasevolume 9, Article number: 336 (2018) | Download Citation
Abstract
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, Ca2+ 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 Ca2+ flux; this indicates that MERCs could regulate immunity.
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