Macrophages induce neutrophil apoptosis through membrane TNF, a process amplified by Leishmania major

Allenbach, Cindy; Zufferey, Christel; Perez, Cynthia; Launois, Pascal; Mueller, Christoph; Tacchini-Cottier, Fabienne (2006). Macrophages induce neutrophil apoptosis through membrane TNF, a process amplified by Leishmania major. Journal of immunology, 176(11), pp. 6656-64. Bethesda, Md.: American Association of Immunologists

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Neutrophils are recruited to the site of parasite inoculation within a few hours of infection with the protozoan parasite Leishmania major. In C57BL/6 mice, which are resistant to infection, neutrophils are cleared from the site of s.c. infection within 3 days, whereas they persist for at least 10 days in susceptible BALB/c mice. In the present study, we investigated the role of macrophages (MPhi) in regulating neutrophil number. Inflammatory cells were recruited by i.p. injection of either 2% starch or L. major promastigotes. Neutrophils were isolated and cultured in the presence of increasing numbers of MPhi. Extent of neutrophil apoptosis positively correlated with the number of MPhi added. This process was strictly dependent on TNF because MPhi from TNF-deficient mice failed to induce neutrophil apoptosis. Assays using MPhi derived from membrane TNF knock-in mice or cultures in Transwell chambers revealed that contact with MPhi was necessary to induce neutrophil apoptosis, a process requiring expression of membrane TNF. L. major was shown to exacerbate MPhi-induced apoptosis of neutrophils, but BALB/c MPhi were not as potent as C57BL/6 MPhi in this induction. Our results emphasize the importance of MPhi-induced neutrophil apoptosis, and membrane TNF in the early control of inflammation.

Item Type:

Journal Article (Original Article)


04 Faculty of Medicine > Service Sector > Institute of Pathology

UniBE Contributor:

Zufferey, Christel, Müller, Christoph (C)






American Association of Immunologists




Factscience Import

Date Deposited:

04 Oct 2013 14:48

Last Modified:

29 Mar 2023 23:32

PubMed ID:


Web of Science ID:


URI: (FactScience: 3566)

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