INFLAMMATION
The inflammatory response (inflammation) occurs when tissues are injured by bacteria, trauma, toxins, heat, or any other cause. Chemicals including histamine, bradykinin, serotonin, and others are released by damaged tissue. These chemicals cause blood vessels to leak fluid into the tissues, causing swelling. This helps isolate the foreign substance from further contact with body tissues.
The chemicals also attract white blood cells that "eat" microorganisms and dead or damaged cells. The process in which these white blood cells surround, engulf, and destroy foreign substances is called phagocytosis, and the cells are called phagocytes. Phagocytes eventually die. Pus is formed from a collection of dead tissue, dead bacteria, and live and dead phagocytes.
2009年6月28日 星期日
The Human Immune Response System
The Human Immune Response System
An overview of the system
The human immune response system recognizes pathogens and acts to remove, immobilize, or neutralize them. The immune system is antigen-specific (responding to specific molecules on a pathogen) and has memory (its defense to a pathogen is encoded for future activation). The immune system relies on several components to fight an infecting pathogen. T cells are lymphocytes that circulate between the blood, lymph, and lymphoid organs to trigger a systemic immune response with antigen-receptors on the T cell membrane. B cells are lymphocytes that activate the primary immune response when antigens bind to their receptors, causing the B cells to proliferate. Daughter cells of B cells later differentiate into antibody-releasing plasma cells. B cells also comprise the immune system's memory (see diagram).
Antibodies, also called immunoglobulins, are divided into five classes by structure and function, enabling them to recognize a wide spectrum of antigens. Antibody functions include complement fixation that can lead to antigen-cell lysis (rupture) and can cause inflammation. Antibodies also generate a neutralization response where viruses and bacteria are destroyed by phagocytes. Agglutination, or clumping together, of foreign cells are caused by B cells' promotion of complex cross-linking of antibodies binding to antigens. These agglutinated cells are phagocytized. B cells are cloned in massive quantities for a single specific antigen.
Immune response to T. cruzi
The human immune response to T. cruzi infection is inadequate; it provides only a partial defense at best. The immune system's response at its worst causes the defense mechanisms to turn on the body it is intended to protect, thus often causing more harm to the person than does T. cruzi. As T. cruzi immunizes humans to their own antigens, human antibodies attack myocardial and neural cells.
Complement in humans does not become activated solely by T. cruzi invasion; antibodies must be present for complement to bind to a specific T. cruzi antigen. This allows T. cruzi to have time to infect human tissue. Parasite strain and an individual's immune competence are prime factors in determining the T. cruzi's pathology of an individual.
Once infected with T. cruzi, humans acquire partial immunity or resistance to the severe pathologies of Chagas' disease's acute phase through subsequent infections of T. cruzi. This guards many individuals who live in highly endemic areas from the acute symptoms of chagas. Complete removable of the parasite from these individuals would risk the onset of acute chagas through future infection, which is deadly - especially for children.
T. cruzi incorporates certain host cell membrane proteins onto its surface thereby masking its antigenic signal to the immune system's lymphocytes. T. cruzi can also cleave antibody molecules on its surface thereby escaping the immune response's detection. T. cruzi frequently invade monocytes, a circulating phagocyte. Intracellular phagocytosis bring amastigotic T. cruzi into tissue cells where they can proliferate. Once inside tissue cells, T. cruzi are undetected by immune response. Trypomastigotes remain in the blood stream for a short period of time so that the T. cruzi-specific immunoglobulins don't have sufficient time to be activated. T. cruzi employs successful strategies to escape the remarkably potent immune response system. By masking themselves or by eluding the response mechanisms, the parasite is able to adapt to survive and continue the life of the species.
Immune response that damages the human body
Unintentional damage is done to the body's otherwise healthy tissue as the response system attacks what it recognizes as a trigger for a defensive response but does not recognize that it is attacking itself. This is what's known as an autoimmune reaction. Autoimmune responses are responsible in large part for the destructive symptoms of Chagas disease. This pathology is referred to as immunopathology. Severe inflammation occurs around tissue that embody amastigotes as the amastigotes release themselves from the tissue's dead cells. Among the tissue most often encysted is myocardial neural plexes. Plexes are networks of nerves that serve a variety of organs and functions. Digestive system neural plexes are targets as well, namely in the colon and esophagus. During the acute phase of chagas, B and T cells are incited to produce antibodies. Since T. cruzi is able to mask its presence in the blood, these antibodies do not attack T. cruzi but instead go after cell membrane antigenic components called epitopes, that the body's healthy cells and T. cruzi share. Research is being done to isolate the epitope and how T. cruzi uses it to elude recognition by the immune system.
Scientists work to find a cure to T. cruzi's infecting the human species. As research continues into how T. cruzi uses the human body as a host, the disciplines of parasitology and immunology learn much about how these organisms adapt and thrive in changing environments. T. cruzi proves to be a formidable opponent in the fight.
An overview of the system
The human immune response system recognizes pathogens and acts to remove, immobilize, or neutralize them. The immune system is antigen-specific (responding to specific molecules on a pathogen) and has memory (its defense to a pathogen is encoded for future activation). The immune system relies on several components to fight an infecting pathogen. T cells are lymphocytes that circulate between the blood, lymph, and lymphoid organs to trigger a systemic immune response with antigen-receptors on the T cell membrane. B cells are lymphocytes that activate the primary immune response when antigens bind to their receptors, causing the B cells to proliferate. Daughter cells of B cells later differentiate into antibody-releasing plasma cells. B cells also comprise the immune system's memory (see diagram).
Antibodies, also called immunoglobulins, are divided into five classes by structure and function, enabling them to recognize a wide spectrum of antigens. Antibody functions include complement fixation that can lead to antigen-cell lysis (rupture) and can cause inflammation. Antibodies also generate a neutralization response where viruses and bacteria are destroyed by phagocytes. Agglutination, or clumping together, of foreign cells are caused by B cells' promotion of complex cross-linking of antibodies binding to antigens. These agglutinated cells are phagocytized. B cells are cloned in massive quantities for a single specific antigen.
Immune response to T. cruzi
The human immune response to T. cruzi infection is inadequate; it provides only a partial defense at best. The immune system's response at its worst causes the defense mechanisms to turn on the body it is intended to protect, thus often causing more harm to the person than does T. cruzi. As T. cruzi immunizes humans to their own antigens, human antibodies attack myocardial and neural cells.
Complement in humans does not become activated solely by T. cruzi invasion; antibodies must be present for complement to bind to a specific T. cruzi antigen. This allows T. cruzi to have time to infect human tissue. Parasite strain and an individual's immune competence are prime factors in determining the T. cruzi's pathology of an individual.
Once infected with T. cruzi, humans acquire partial immunity or resistance to the severe pathologies of Chagas' disease's acute phase through subsequent infections of T. cruzi. This guards many individuals who live in highly endemic areas from the acute symptoms of chagas. Complete removable of the parasite from these individuals would risk the onset of acute chagas through future infection, which is deadly - especially for children.
T. cruzi incorporates certain host cell membrane proteins onto its surface thereby masking its antigenic signal to the immune system's lymphocytes. T. cruzi can also cleave antibody molecules on its surface thereby escaping the immune response's detection. T. cruzi frequently invade monocytes, a circulating phagocyte. Intracellular phagocytosis bring amastigotic T. cruzi into tissue cells where they can proliferate. Once inside tissue cells, T. cruzi are undetected by immune response. Trypomastigotes remain in the blood stream for a short period of time so that the T. cruzi-specific immunoglobulins don't have sufficient time to be activated. T. cruzi employs successful strategies to escape the remarkably potent immune response system. By masking themselves or by eluding the response mechanisms, the parasite is able to adapt to survive and continue the life of the species.
Immune response that damages the human body
Unintentional damage is done to the body's otherwise healthy tissue as the response system attacks what it recognizes as a trigger for a defensive response but does not recognize that it is attacking itself. This is what's known as an autoimmune reaction. Autoimmune responses are responsible in large part for the destructive symptoms of Chagas disease. This pathology is referred to as immunopathology. Severe inflammation occurs around tissue that embody amastigotes as the amastigotes release themselves from the tissue's dead cells. Among the tissue most often encysted is myocardial neural plexes. Plexes are networks of nerves that serve a variety of organs and functions. Digestive system neural plexes are targets as well, namely in the colon and esophagus. During the acute phase of chagas, B and T cells are incited to produce antibodies. Since T. cruzi is able to mask its presence in the blood, these antibodies do not attack T. cruzi but instead go after cell membrane antigenic components called epitopes, that the body's healthy cells and T. cruzi share. Research is being done to isolate the epitope and how T. cruzi uses it to elude recognition by the immune system.
Scientists work to find a cure to T. cruzi's infecting the human species. As research continues into how T. cruzi uses the human body as a host, the disciplines of parasitology and immunology learn much about how these organisms adapt and thrive in changing environments. T. cruzi proves to be a formidable opponent in the fight.
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