antigenic phenotype - ορισμός. Τι είναι το antigenic phenotype
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Τι (ποιος) είναι antigenic phenotype - ορισμός

STRUCTURE OF A MOLECULE THAT IMITATES OR SIMULATES THE STRUCTURE OF A DIFFERENT MOLECULE
Antigenic mimickry; Antigenic mimicry

Phenotype (clinical medicine)         
PRESENTATION OF A DISEASE IN CLINICAL MEDICINE
Clinical phenotype
In a nosological sense, the term phenotype can be used in clinical medicine for speaking about the presentation of a disease. The complementary concept in this regard is endotype, which refers to the pathogenesis of the disease ignoring its presentation.
Antigenic variation         
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PROCESSES INVOLVED IN THE BIOLOGICAL STRATEGY OF CHANGING ANTIGENIC DETERMINANTS ON THE SURFACE THAT ARE EXPOSED TO ANOTHER ORGANISM'S IMMUNE SYSTEM
Antigenic alteration; Variable surface antigen
Antigenic variation or antigenic alteration refers to the mechanism by which an infectious agent such as a protozoan, bacterium or virus alters the proteins or carbohydrates on its surface and thus avoids a host immune response, making it one of the mechanisms of antigenic escape. It is related to phase variation.
The Extended Phenotype         
  • A [[beaver dam]], an example of an organism altering the environment in which it evolves — the first form of extended phenotype
  • reed warbler]] raising the young of a common cuckoo
BOOK WRITTEN BY RICHARD DAWKINS, ABOUT THE EXTENSION OF THE PHENOTYPE TO ETHOLOGY
Extended phenotype; Extended Phenotype; The extended phenotype
The Extended Phenotype is a 1982 book by the evolutionary biologist Richard Dawkins, in which the author introduced a biological concept of the same name. The main idea is that phenotype should not be limited to biological processes such as protein biosynthesis or tissue growth, but extended to include all effects that a gene has on its environment, inside or outside the body of the individual organism.

Βικιπαίδεια

Molecular mimicry

Molecular mimicry is defined as the theoretical possibility that sequence similarities between foreign and self-peptides are sufficient to result in the cross-activation of autoreactive T or B cells by pathogen-derived peptides. Despite the prevalence of several peptide sequences which can be both foreign and self in nature, a single antibody or TCR (T cell receptor) can be activated by just a few crucial residues which stresses the importance of structural homology in the theory of molecular mimicry. Upon the activation of B or T cells, it is believed that these "peptide mimic" specific T or B cells can cross-react with self-epitopes, thus leading to tissue pathology (autoimmunity). Molecular mimicry is a phenomenon that has been just recently discovered as one of several ways in which autoimmunity can be evoked. A molecular mimicking event is, however, more than an epiphenomenon despite its low statistical probability of occurring and these events have serious implications in the onset of many human autoimmune disorders.

In the past decade the study of autoimmunity, the failure to recognize self antigens as "self", has grown immensely. Autoimmunity is thought by many researchers to be a result of a loss of immunological tolerance, the ability for an individual to discriminate between self and non-self, though others are beginning to think that many autoimmune diseases are due to mutations governing programmed cell death, or to environmental products that injure target tissues, thus causing a release of immunostimulatory alarm signals,. Growth in the field of autoimmunity has resulted in more and more frequent diagnosis of autoimmune diseases. Consequently, recent data show that autoimmune diseases affect approximately 1 in 31 people within the general population. Growth has also led to a greater characterization of what autoimmunity is and how it can be studied and treated. With an increased amount of research, there has been tremendous growth in the study of the several different ways in which autoimmunity can occur, one of which is molecular mimicry. The mechanism by which pathogens have evolved, or obtained by chance, similar amino acid sequences or the homologous three-dimensional crystal structure of immunodominant epitopes remains a mystery.