T-cell mediated liver injury

Imose M, Nagaki M, Kimura K, Takai S, Imao M, Naiki T, Osawa Y, Asano T, Hayashi H, Moriwaki H. Leflunomide protects from T-cell-mediated liver injury in mice through inhibition of nuclear factor kappaB. Hepatology 2004 40(5) 1160-9. 

Fiorucci S, Santucci L, Antonelli E, Dis-trutti E, Del Sero G, et al. 2000. NO-aspirin protects from T cell-mediated liver injury by inhibiting caspase-dependent processing of Thl-like cytokines. Gastroenterology 118 404-21... 

V(38.3 elements [37]. A pathogenic role forYPM has been established in a number of studies and in vivo production of YPM has been detected in clinical patients infected with Y. pseudotuberculosis. Infection was accompanied by an IgG response and elevated levels of V(33 T cells in peripheral blood mononuclear cells and mesenteric lymph nodes [38]. In mice, YPM has been shown to induce an acute, T-cell-mediated, toxic shock response [39]. The toxic shock response was inducible in BALB/c mice but not inT-cell-deficient SCID mice. As early as 1 h after YPM injection, V(38+ T cells were observed in the liver while serum levels of interferon-y were significantly elevated 4h after injection. Co-adminis-tration of anti-interferon-y antibody or anti-YPM monoclonal antibody alleviated the liver injury and protected mice from YPM-induced death. Anti-YPM antibody also suppressed the early migration of V (38 + T cells from the peripheral circulation and the elevation of serum interferon-y. 

Noll T, Hugo-Wisseman D, Littauer A, et al. 1987. The decisive pQ2 levels in haloalkane-mediated liver cell injury. Free Radic Res Commun 3 293-298. 

Liver injury is immune mediated with cytolytic T cells maintaining the primary role in cell destruction. Death of hepatocytes results in viral elimination and eventual resolution of the clinical illness. Viremia begins soon after infection and continues throughout the time liver enzymes are elevated. The host antibody response to HAV initially appears as the viral particles begin to disappear from stool. Like most host antibody responses, antibodies of the IgM class appear first and imply recent infection. IgM anti-HAV usually is detectable 5 to 10 days before symptoms appear. After 2 to 6 months, the IgM antibodies are replaced with IgG antibodies, which usually persist throughout life and confer immunity to HAV. Patients who receive immunoglobulin will have low titers of anti-HAV for several weeks after inoculation. Patients who receive hepatitis A vaccine will also have anti-HAV. ... 

HBV is not directly cytopathic instead liver injury is immune related, and T lymphocytes are important for both the host cellular and humoral responses. Recovery from acute HBV infection depends on both B-cell and T-ceU responses. B-cell-dependent antibodies are produced to presurface and surface antigens. Cytotoxic T lymphocyte response is mounted against multiple epitopes in the HBV envelope, nucleocapsid, and polymerase regions. Cytotoxic T lymphocyte-mediated lysis of infected hepatic cells occurs, resulting in liver injury. Immune clearance of virus is often accompanied by worsening liver disease, known as a flare. An extreme example of this is seen in fulminant hepatitis B, when there is often no evidence... 

Adhikari N, Charles N, Lehmann U, Hall J (2006) Transcription factor and kinase-mediated signaling in atherosclerosis and vascular injury. Curr Atheroscler Rep 8(3) 252-260 Alchera E, Tacchini L, Imarisio C, Dal Ponte C, De Ponti C, Gammella E, Cairo G, Albano E, Carini R (2008) Adenosine-dependent activation of hypoxia-inducible factor-1 induces late preconditioning in liver cells. Hepatology 48(1) 230—239 Bjomheden T, Levin M, Evaldsson M, Wiklund O (1999) Evidence of hypoxic areas within the arterial wall in vivo. Arterioscler Thromb Vase Biol 19(4) 870-876 Blay J, White TD, Hoskin DW (1997) The extracellular fluid of solid carcinomas contains immunosuppressive concentrations of adenosine. Cancer Res 57(13) 2602-2605... 

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