By M. Eric Gershwin, John M. Vierling, Michael P. Manns
Immunology is a vast department of biomedical technological know-how that covers the research of all facets of the immune approach in all organisms. It offers with, between different issues, the physiological functioning of the immune method in states of either health and wellbeing and affliction; malfunctions of the immune process in immunological issues (autoimmune ailments, hypersensitivities, immune deficiency, allograft rejection); the actual, chemical and physiological features of the parts of the immune process in vitro, in situ, and in vivo. Immunology has numerous functions in numerous disciplines of technological know-how, and as such is extra divided.
Liver Immunology: rules and Practice covers bacterial, parasitic and viral infections of the liver, autoimmune liver affliction, alcoholic and nonalcoholic fatty liver illnesses, and transplantation in an easy-to-read and thorough structure. Authors additionally handle the main matters that experience arisen during this box in recent times, together with physiological roles of hepatocytes, sinusoidal lining cells, activated macrophages (Kupffer cells), cholangiocytes and stellate cells, and their modulation of T cells, average killer (NK) cells and NKT cells. This quantity turns into a must-read for clinicians, investigators and scholars, beginner and specialist alike.
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Additional info for Liver Immunology: Principles and Practice
However, a number of mechanisms are operative in LSECs to protect this cell population from damage. Expression of granzyme B inhibitors protects from induction of apoptosis (152), and various forms of preconditioning induce hyporesponsive states in LSECs that render them resistant to damage (38,153,154). Taken together, these experimental findings provide evidence that the barrier function of LSECs is instrumental in maintaining hepatic organ integrity. Destruction of this barrier leads to microcirculatory disturbances and exposure of other hepatic cell populations to circulating leukocytes, all of which contributes to hepatocellular damage either by tissue hypoxia resulting from perfusion failure or direct immune-mediated attack.
This may ensure that physiological concentrations of endotoxin do not induce activation and cytokine release from LSECs or Kupffer cells and thus fail to induce an acute-phase response or local inflammatory reactions in the liver during the physiological situation. Constitutive exposure to gut-derived bacterial degradation products in portal venous blood contributes to the unique hepatic microenvironment. Endothelial cells from mice raised under germ-free conditions do not express CD54 constitutively.
Intravenous injection of a T-cell mitogen, concanavalin A (Con A), leads to development of fulminant hepatic injury with death of mice ensuing from liver failure (141). The local release of tumor necrosis factor-F (TNF-F) from activated T cells and other cells in the liver plays a pivotal role in the mediation of liver injury, as neutralizing antibodies to TNF-F prevent induction of liver injury (142). Similarly, TNF-R knockout mice fail to develop ConA-mediated liver injury (143). It was shown that ConA localized to LSECs following intravenous injection and that LSECs served as competent accessory cells to induce T-cell activation and TNF-F release (144).