Tumor necrosis factor-α promoter polymorphisms and the risk of rejection after liver transplantation: A case control analysis of 210 donor-recipient pairs

Jazrawi, S.; Zaman, Atif; Muhammad, Zafaruddin; Rabkin, John M.; Corless, Christopher L.; Olyaei, Ali J.; Biggs, Amy; Ham, J. M.; Chou, Sunwen; Rosen, Hugo R.

doi:10.1053/jlts.2003.50064

Cited by 22 publications

(21 citation statements)

References 34 publications

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“…Tumor necrosis factor (TNF-␣) and interleukin-1 (IL-1) are the two most important proinflammatory cytokines in the pathogenesis of I-R injury. Both induce the synthesis of IL-8 [22] and up-regulate the expression of adhesion molecules such as selectin and ␤-integrin, giving rise to increased leukocyte-sinusoidal-endothelial cell interactions [23], which result in further cytokine production and activation of additional Kupffer cells [7][8][9][10]. In rats, ischemic preconditioning of the liver, before transplantation, resulted in improved survival and decreased release of serum transaminases and TNF-␣ [24].…”

Section: Discussionmentioning

confidence: 99%

Effect of Ischemic Preconditioning on Rat Liver Microcirculation Monitored with Laser Doppler Flowmetry

Szíjártó

Hahn

Lotz

et al. 2006

Journal of Surgical Research

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Section: Discussionmentioning

confidence: 99%

Effect of Ischemic Preconditioning on Rat Liver Microcirculation Monitored with Laser Doppler Flowmetry

Szíjártó

Hahn

Lotz

et al. 2006

Journal of Surgical Research

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“…54 However, a study from Newcastle, UK did not confirm this alleged association. 15 Similarly, in the data obtained from Scottish, Brazilian, and Chinese series of patients with PBC, 43,55,56 and from a small population of patients undergoing liver transplantation for end-stage PBC, 57 no association of TNF genotypes with disease susceptibility or onset was observed.…”

Section: Mhc and Pbcmentioning

confidence: 98%

Genes and (auto)immunity in primary biliary cirrhosis

et al. 2005

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Primary biliary cirrhosis (PBC) is a chronic autoimmune cholestatic liver disease most commonly encountered in postmenopausal women; it is characterized by high-titer serum autoantibodies to mitochondrial antigens, elevated serum IgM, progressive destruction of intrahepatic bile ducts, and ultimately liver cirrhosis and failure. The cytopathic mechanisms leading to the selective destruction of intrahepatic cholangiocytes are still largely unknown. The current theory on the pathogenesis of PBC indicated that environmental factors might trigger autoimmunity in genetically susceptible individuals. In fact, genetic predisposition is critical to disease onset and progression, yet peculiar among autoimmune diseases, as indicated by the lack of a strong association with major histocompatibility complex haplotypes. Further, the recently reported concordance rate among monozygotic twins strenghtens the importance of genetic factors, while also indicating that additional factors, possibly infectious agents or xenobiotics, intervene to trigger the disease. In this review, the available data regarding the genetic factors associated with PBC susceptibility and progression, as well as the available evidence regarding the immunomediated pathogenesis of PBC, will be critically illustrated and discussed.

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“…33 In liver transplant recipients, the TNF-a high genotype was associated with acute rejection in some studies [51][52][53] but not in others. [54][55][56] The TNF-a high genotype correlates with acute rejection in multiple adult kidney transplant studies from various demographic populations. 23,[45][46][47]57 Interleukin-6.…”

Section: Interleukinmentioning

confidence: 99%