TY  - JOUR
A1  - Bogdan, Christian
A1  - Moll, Heidrun
A1  - Solbach, Werner
A1  - Röllinghoff, Martin
T1  - Tumor necrosis factor-\(\alpha\) in combination with interferon-\(\gamma\), but not with  interleukin 4 activates murine macrophages for elimination of Leishmania major amastigotes
N2  - We have previously shown that during an infection with Leishmania major, susceptible BALB/c mice, as opposed to mice of a resistant strain (C57BLl6), are primed by lipopolysaccharide for the production of high levels of tumor necrosis factor-\(\alpha\) (TNF-\(\alpha\)) which is known to be a potent maerophage M\(\Phi\) stimulator in other parasitic diseases. In the present study we investigated whether TNF-\(\alpha\) activates M\(\Phi\) for killing of L. major parasites. In the absence of interferon-y (IFN-\(\gamma\)) or lipopolysaccharide, TNF-\(\alpha\) (0.025-25000 U/ml) failed to activate peritoneal exudate M\(\Phi\) from BALB/c mice for killling of L. major amastigotes. In the presence of suboptimal doses of IFN-\(\gamma\) (5 or 10 Vlml), however, TNF-\(\alpha\) mediated a rapid elimination of intracellular parasites, which was highly significant compared to IFN-\(\gamma\) alone. Tbe combination of TNF with interleukin 4, in contrast, was inactive in this respect and allowed survival of intracellular parasites. From these data we conelude that the presence of IFN-\(\gamma\) is crucial for TNF-\(\alpha\)-mediated killing of L. major parasites by M\(\Phi\). Disease progression in susceptible mice therefore seems to be a consequence of a deficiency of IFN-\(\gamma\) and a predominance of interleukin 4 rather than the result of an excess amount of TNF-\(\alpha\).
KW  - Infektionsbiologie
Y1  - 1990
UR  - https://opus.bibliothek.uni-wuerzburg.de/frontdoor/index/index/docId/4792
UR  - https://nbn-resolving.org/urn:nbn:de:bvb:20-opus-31614
VL  - 20
SP  - 1131
EP  - 1135
ER  -