Antigens in the context of "Serovar"

A serotype or serovar is a distinct variation within a species of bacteria or virus or among immune cells of different individuals. These microorganisms, viruses, or cells are classified together based on their shared reactivity between their surface antigens and a particular antiserum, allowing the classification of organisms to a level below the species. A group of serovars with common antigens is called a serogroup or sometimes serocomplex.

Serotyping often plays an essential role in determining species and subspecies. The Salmonella genus of bacteria, for example, has been determined to have over 2600 serotypes. Vibrio cholerae, the species of bacteria that causes cholera, has over 200 serotypes, based on cell antigens. Only two of them have been observed to produce the potent enterotoxin that results in cholera: O1 and O139.

Crohn's disease is a type of inflammatory bowel disease (IBD) that may affect any segment of the gastrointestinal tract. Symptoms often include abdominal pain, diarrhea, fever, abdominal distension, and weight loss. Complications outside of the gastrointestinal tract may include anemia, skin rashes, arthritis, inflammation of the eye, and fatigue. The skin rashes may be due to infections, as well as pyoderma gangrenosum or erythema nodosum. Bowel obstruction may occur as a complication of chronic inflammation, and those with the disease are at much greater risk of colorectal cancer and small bowel cancer.

Although the precise causes of Crohn's disease (CD) are unknown, it is believed to be caused by a combination of environmental, immune, and bacterial factors in genetically susceptible individuals. It results in a chronic inflammatory disorder, in which the body's immune system defends the gastrointestinal tract, possibly targeting microbial antigens. Although Crohn's is an immune-related disease, it does not seem to be an autoimmune disease (the immune system is not triggered by the body itself). The exact underlying immune problem is not clear; however, it may be an immunodeficiency state.

Cancer immunotherapy (immuno-oncotherapy) is the stimulation of the immune system to treat cancer, improving the immune system's natural ability to fight the disease. It is an application of the fundamental research of cancer immunology (immuno-oncology) and a growing subspecialty of oncology.

Cancer immunotherapy exploits the fact that cancer cells often have tumor antigens, molecules on their surface that can bind to antibody proteins or T-cell receptors, triggering an immune system response. The tumor antigens are often proteins or other macromolecules (e.g., carbohydrates). Normal antibodies bind to external pathogens, but the modified immunotherapy antibodies bind to the tumor antigens marking and identifying the cancer cells for the immune system to inhibit or kill. The clinical success of cancer immunotherapy is highly variable between different forms of cancer; for instance, certain subtypes of gastric cancer react well to the approach whereas immunotherapy is not effective for other subtypes.

The Rh blood group system is a human blood group system. It contains proteins on the surface of red blood cells. After the ABO blood group system, it is most likely to be involved in transfusion reactions. The Rh blood group system consists of over 50 defined blood group antigens, of which the five antigens D, C, c, E, and e are among the most prominent. There is no d antigen. Rh(D) status of an individual is normally described with a positive (+) or negative (−) suffix after the ABO type (e.g., someone who is A+ has the A antigen and Rh(D) antigen, whereas someone who is A− has the A antigen but lacks the Rh(D) antigen). The terms Rh factor, Rh positive, and Rh negative refer to the Rh(D) antigen only. Antibodies to Rh antigens can be involved in hemolytic transfusion reactions and antibodies to the Rh(D) and Rh antigens confer significant risk of hemolytic disease of the newborn.

Molecular mimicry is the theoretical possibility that sequence similarities between foreign and self-peptides are enough 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, just a few crucial residues can activate a single antibody or TCR (T cell receptor). This highlights the importance of structural homology in the theory of molecular mimicry. Upon activation, these "peptide mimic" specific T or B cells can cross-react with self-epitopes, thus leading to tissue pathology (autoimmunity). Molecular mimicry is one of several ways in which autoimmunity can be evoked. A molecular mimicking event is more than an epiphenomenon despite its low probability, and these events have serious implications in the onset of many human autoimmune disorders.

One possible cause of autoimmunity, the failure to recognize self antigens as "self", is a loss of immunological tolerance, the ability for the immune system to discriminate between self and non-self. Other possible causes include mutations governing programmed cell death or environmental products that injure target tissues, thus causing a release of immunostimulatory alarm signals. Growth in the field of autoimmunity has resulted in more frequent diagnosis of autoimmune diseases. The resulting 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 more research comes 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 similar amino acid sequences or the homologous three-dimensional crystal structure of immunodominant epitopes remains a mystery.