About: Barriers of the Human Organism and Their Achilles’ Heels

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Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Barriers of the Human Organism and Their Achilles’ Heels
Source	PMC
abstract	The human body is covered by barriers separating it from the external and internal surroundings. The “milieu enterieur” has to be stabilised in spite of the variable external and internal conditions of toxic, osmotic, microbial and climatic environmental circumstances. This first line of barriers is composed of skin and mucous membranes of complicated structures. A second line of barrier system is present in our organisms. Certain organs have to be separated from the immune system and other parts of the body because of evolutionary reasons (eye-bulb and testicles) because of unique proteins “unknown” for the acquired immune system. The blood-brain barrier (BBB) is providing enhanced safety circumstances for the central nervous system. The second line of barriers is represented by the special properties of the capillary endothelial system. The maternal-fetal barrier is the most complex. At the maternal fetal interface two individuals of two different haplotypes has to be live 9 months separated by a very complicated dynamic barrier. The placenta is the organ, which is separating the maternal and fetal tissues. Similar to others the bidirectional transport of gasses, metabolites, cells, proteins, regulatory substances, are transported by active or passive transcellular and intercellular mechanisms. The fetal immune system develops immunotolerance to all maternal cells and antigens transferred transplacentally. The problem is to mitigate the maternal immune system to tolerate the paternal haplotype of the fetus. In the case of normal pregnancy a complex series of physiological modifications can solve the problem without harmful consequences to the mother and fetus. The outermost contact cells of trophoblasts express instead of HLA-class Ia and class II antigens non-variable HLA-C, HLA-E, HLA-F and HLA-G antigens. The first consequence of this is reduction of the activity of maternal natural killer cells and maternal dendritic cells; Progesteron, micro-RNA and mediators influence the development of T effector-cells. The production of soluble HLA-G(5 and 6) and IL-10 supports the differentiation of Th-2 CD4(+) helper cells, reducing the ability of maternal cells to kill fetal cells. Series of receptors and costimulators are expressed by the different lines of semi-allogenic trophoblast cells to bind HLA-G and mitigate maternal immune response; The maternal immunotolerance is further facilitated by the activation of CD4(+)CD25(bright)Foxp3(+) regulatory T (T(REG)) cells. Infections have to be prevented during pregnancy. The cells of placenta express 10 Toll-like receptors a group of pattern recognition receptors responsible for innate immunity. The interferon level is also higher in the placental tissues than in the somatic fetal or maternal cells. The complement system is also adapted to the requirements of the pregnancy and fetal damage is inhibited by the production of “assymmetric IgG antibodies” under hormonal and placental-regulation. These modifications prevent the activation of complement, cytotoxic activity, opsonising ability, antigen clearance and precipitating activity of the molecules. The Achilles’ heels of the different barriers are regularly found by virus infections. Lamina cribrosa of the blood-brain barrier, optical nerve of the eyes, etc. the risk factors of the maternal-fetal barrier has been summarised in Table 1.1.
has issue date	2012-03-08(xsd:dateTime)
bibo:doi	10.1007/978-94-007-4216-1_1
has license	no-cc
sha1sum (hex)	207f90f000d19d0c72e3cdac5b31117b3a3ae562
schema:url	https://doi.org/10.1007/978-94-007-4216-1_1
resource representing a document's title	Barriers of the Human Organism and Their Achilles’ Heels
has PubMed Central identifier	PMC7121758
schema:publication	Maternal Fetal Transmission of Human Viruses and their Influence on Tumorigenesis
resource representing a document's body	covid:207f90f000d19d0c72e3cdac5b31117b3a3ae562#body_text
is schema:about of	named entity 'THEIR' named entity 'HEELS' named entity 'ORGANISM' named entity 'ACHILLES' named entity 'CONTENTS' named entity 'TAK' named entity 'MARIA' named entity 'III' named entity 'HUMAN' named entity 'pregnancy' named entity 'autologous' named entity 'HIV-1' named entity 'CD25' named entity 'apoptosis' named entity 'Foxp3' named entity 'immune response' named entity 'IgA' named entity 'DAF' named entity 'vasculitis' named entity 'chemokines' named entity 'IgE' named entity 'sIL-2R' named entity 'epithelium' named entity 'preterm deliveries' named entity 'trophoblast cells' named entity 'virus' named entity 'CD4 +' named entity 'assay' named entity 'IgG' named entity 'metastasis' named entity 'secretion' named entity 'viruses' named entity 'HLA-G' named entity 'effector/memory T cells' named entity 'syncytiotrophoblast' named entity 'azobenzene' named entity 'correlation' named entity 'NK cells' named entity 'infection' named entity 'fetal growth restriction' named entity 'receptor-mediated endocytosis' named entity 'neonates' named entity 'virus' named entity 'MAMPs' named entity 'IFN-g' named entity 'TNF-a' named entity 'antibodies' named entity 'cytotoxic T lymphocyte' named entity 'Complement' named entity 'Plasma cells' named entity 'TGF-b1' named entity 'colitis' named entity 'oxidative stress' named entity 'antigens' named entity 'IL-10' named entity 'Virus infection' named entity 'HLA' named entity 'PD-1' named entity 'CD4 +' named entity 'Antibacterial' named entity 'IL-17A' named entity 'adhesion' named entity 'lipopolysaccharides' named entity 'gestation' named entity 'Keskin' named entity 'polymorphic' named entity 'lentiviruses' named entity 'immune defence' named entity 'claudin-4' named entity 'high levels' named entity 'Human cytomegalovirus' named entity 'paracellular transport' named entity 'interact' named entity 'defensins' named entity 'ICOS' named entity 'complement' named entity 'fetal' named entity 'gene expression' named entity 'postpartum' named entity 'transplacental' named entity 'morbidity' named entity 'cytolysis' named entity 'Th2' named entity 'Achilles' heel'

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