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Originally published online as doi:10.1189/jlb.1103572 on August 17, 2004

Published online before print August 17, 2004
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(Journal of Leukocyte Biology. 2004;76:1039-1046.)
© 2004 by Society for Leukocyte Biology

Contribution of CD30/CD153 but not of CD27/CD70, CD134/OX40L, or CD137/4-1BBL to the optimal induction of protective immunity to Mycobacterium avium

Manuela Flórido*, Margarida Borges*, Hideo Yagita{dagger} and Rui Appelberg*,{ddagger},1

* Laboratory of Microbiology and Immunology of Infection, Institute for Molecular and Cell Biology, and
{ddagger} ICBAS, Instituto de Ciências Biomédicas de Abel Salazar, University of Porto, Portugal; and
{dagger} Department of Immunology, Juntendo University School of Medicine, Tokyo, Japan

1 Correspondence: Laboratory of Microbiology and Immunology of Infection, Institute for Molecular and Cell Biology, Rua do Campo Alegre 823, 4150-180 Porto, Portugal. E-mail: rappelb{at}ibmc.up.pt

A panel of monoclonal antibodies specific for CD27 ligand (CD70), CD30 ligand (CD153), CD134 ligand (OX40L), and CD137 ligand (4-1BBL) were screened in vivo for their ability to affect the control of Mycobacterium avium infection in C57Bl/6 mice. Only the blocking of CD153 led to increased mycobacterial burdens. We then used CD30-deficient mice and found an increase in the proliferation of two strains of M. avium in these mice as compared with control animals. The increased mycobacterial growth was associated with decreased T cell expansion and reduced interferon-{gamma} (IFN-{gamma}) responses as a result of reduced polarization of the antigen-specific, IFN-{gamma}-producing T cells. At late times but not early in infection, the lymphoid cuff surrounding granulomas was depleted in the CD30-deficient animals. This report expands our knowledge about tumor necrosis factor superfamily members involved in the immune responses to mycobacterial infection by identifying CD30–CD153 interactions as required for optimal immune control of M. avium infection.

Key Words: mycobacteria • macrophages • cell-mediated immunity




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