CD4+ and CD8+ T-cell-dependent and -independent host defense mechanisms can operate to control and resolve primary and secondary Francisella tularensis LVS infection in mice.

AUTOR(ES)

Conlan, J W

RESUMO

Immunity to experimental infection with the facultative intracellular bacterium Francisella tularensis is generally considered an example of T-cell-mediated, macrophage-expressed immunity. However, the results of the present study indicate that T-cell-independent mechanisms are also important in anti-Francisella defense. They show that mice selectively depleted of CD4+, CD8+, or both T-cell populations by treatment with T-cell subset-specific monoclonal antibodies remained capable of controlling and partly resolving a primary sublethal Francisella infection. Similarly, it was found that Francisella-immune mice depleted of either or both subsets of T cells retain a high degree of acquired immunity to reinfection. Together, these findings imply that resistance to primary and secondary tularemia can be mediated by cells other than CD4+ and CD8+ T cells.

Documentos Relacionados

• Vesicular stomatitis virus Indiana glycoprotein as a T-cell-dependent and -independent antigen.
• Immunoregulatory mechanisms of T-cell-dependent shock induced by a bacterial superantigen in mice.
• Analysis of T-cell-dependent and -independent antigens of Rickettsia conorii with monoclonal antibodies.
• Neutrophils are critical for host defense against primary infection with the facultative intracellular bacterium Francisella tularensis in mice and participate in defense against reinfection.
• Gamma interferon-dependent temporary resistance to acute Toxoplasma gondii infection independent of CD4+ or CD8+ lymphocytes.