Human Pharmacological Investigation of a Human Recombinant Tumor Necrosis Factor Preparation

Tanneberger, S; Lenk, H; Müller, U; Ebert, Juliane; Shiga, Taro

doi:10.1159/000415895

Cited by 1 publication

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“…All recovered without residual neurological deficit, which is reminiscent of cerebral malaria. Even the labial herpes often seen in malaria may be reproduced by infusing TNF into tumor patients (119,397), implying a role for TNF in malarial immunosuppression. We subsequently attributed this to its ability to induce inducible nitric oxide synthase (iNOS) (331).…”

Section: Cytokine Theory Of Disease the Pre-rtnf Eramentioning

confidence: 99%

Pathogenesis of Malaria and Clinically Similar Conditions

et al. 2004

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There is now wide acceptance of the concept that the similarity between many acute infectious diseases, be they viral, bacterial, or parasitic in origin, is caused by the overproduction of inflammatory cytokines initiated when the organism interacts with the innate immune system. This is also true of certain noninfectious states, such as the tissue injury syndromes. This review discusses the historical origins of these ideas, which began with tumor necrosis factor (TNF) and spread from their origins in malaria research to other fields. As well the more established proinflammatory mediators, such as TNF, interleukin-1, and lymphotoxin, the roles of nitric oxide and carbon monoxide, which are chiefly inhibitory, are discussed. The established and potential roles of two more recently recognized contributors, overactivity of the enzyme poly(ADP-ribose) polymerase 1 (PARP-1) and the escape of high-mobility-group box 1 (HMGB1) protein from its normal location into the circulation, are also put in context. The pathogenesis of the disease caused by falciparum malaria is then considered in the light of what has been learned about the roles of these mediators in these other diseases, as well as in malaria itself

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Section: Cytokine Theory Of Disease the Pre-rtnf Eramentioning

confidence: 99%