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1
*
Department of Pathology, University of Geneva, Geneva, Switzerland;
Department of Pathology, University of Bern, Bern, Switzerland;
Department of Internal Medicine, University Hospital, Zurich, Switzerland; and
Laboratoire du Bacillus Calmette-Guérin and Unité de Physiopathologie de l’Infection, Institut Pasteur, Paris, France
The contribution of a transmembrane (Tm) form of TNF to protective
immunity against Mycobacterium bovis bacillus
Calmette-Guérin (BCG) was studied in transgenic (tg) mice
expressing a noncleavable Tm TNF but lacking the
TNF/lymphotoxin-
(LT-) locus (Tm TNF tg
mice). These mice were as resistant to BCG infection as wild-type mice,
whereas TNF/LT--/-, TNF-/-, and
LT--/- mice succumbed. Tm TNF tg mice developed
granulomas of smaller size but at 2- to 4-fold increased frequencies
compared with wild-type mice. Granulomas were mainly formed by
monocytes and activated macrophages expressing Tm TNF mRNA and
accumulating acid phosphatase. NO synthase 2 activation as a key
macrophage bactericidal mechanism was low during the acute phase of
infection in Tm TNF tg mice but was still sufficient to limit bacterial
growth and increased in late infection. While infection with virulent
Mycobacterium tuberculosis resulted in very rapid
death of TNF/LT--/- mice, it also resulted in survival
of Tm TNF tg mice which presented an increase in the number of CFU in
spleen (5-fold) and lungs (10-fold) as compared with bacterial load of
wild-type mice. In conclusion, the Tm form of TNF induces an efficient
cell-mediated immunity and total resistance against BCG even in the
absence of LT- and secreted TNF. However, Tm TNF-mediated protection
against virulent M. tuberculosis infection can also be
efficient but not as strong as in BCG infection, in which cognate
cellular interactions may play a more predominant role in providing
long-term surveillance and containment of BCG-infected
macrophages.
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