Pamela L. Dunn

Murine listeriosis as a model of antimicrobial defense

Summary: Murine listeriosis was introduced 35 years ago as a model with which to analyze mechanisms of antibacterial defense that are independent of antibodies. Listeria monocytogenes was shown to be an intramacrophage pathogen with capacity to induce the generation of a state of specific immunity in the form of DTH and a macrophage system with enhanced non‐specific bactericidal activity The demonstration that anti‐Listeria immunity and DTH can be passively transferred with T cells was taken to indicate that the T cells responsible for DTH function upregulate the listericidal function of macrophages. This interpretation is contradicted by recent research showing that CDS T cells, rather than CD4 T cells, are responsible for mediating adoptive immunity. However, T‐cell depletion studies show that primary infection can eventually be resolved in the absence of either CDS or CD4 T cells. On the other hand, infection becomes lethal in the absence of neutrophils or NK cells. It is apparent, therefore, that the most important defense against primary listeriosis resides with the functions of neutrophils and NK cells that are mobilized early in infection. Antigen‐specific T cells function at a later time to infection more efficiently. It is apparent that T cells are much more important in defense against secondary infection.

Effect of advanced aging on ability of mice to cause regression of an immunogenic lymphoma in response to immunotherapy based on depletion of suppressor T cells.

SummaryThis study shows that two therapeutic agents, anti-CD4 mAb and vinblastine, capable of causing T-cellmediated regression of an established L5178Y lymphoma in 3-month-old mice, are incapable of causing regression of this tumor in 20- to 22-month-old mice. It is known that both agents are immunoaugmentative because of their ability to destroy tumor-induced CD4+ suppressor T cells preferentially. Therefore, the results indicate, that aged mice, unlike young mice, are not capable of generating therapeutic numbers of CD8+ effector T cells in the absence of suppressor cells.