Gamma interferon-mediated increase in the number of Ia-bearing macrophages during infection with Listeria monocytogenes

Abstract

The role of gamma interferon (IFN-gamma) in an increase in Ia-bearing macrophages during Listeria monocytogenes infection was studied. The peritoneal macrophages from L. monocytogenes-infected mice contained a high proportion of Ia. Intraperitoneal injection of the supernatant from a culture of spleen cells from L. monocytogenes-infected mice induced Ia-rich exudates in normal mice. The Ia-inducing activity in the culture supernatant was abrogated by the pretreatment of spleen cells with anti-Thy-1.2 antibody plus complement. Immunoadsorption of the culture supernatant with anti-recombinant IFN-gamma antibody and protein A-Sepharose CL-4B completely abrogated its Ia-inducing activity. These results suggested that an increase in Ia-bearing macrophages during L. monocytogenes infection was attributable to T-cell-derived IFN-gamma.

Persistent production of interferon-gamma (IFN-γ) and IL-12 is essential for the generation of protective immunity against Listeria monocytogenes

“…This form of immunity is dependent on the ability of the host to withstand the intracellular replication of bacteria, and is mediated by immune T lymphocytes, which function to activate macrophages to increased bactericidal levels [5][6][7]. Macrophage activation is apparently mediated by cytokines, especially IFN-g, released following the recognition of Listerial antigens in the context of MHC molecules on antigen-presenting cells [8].…”

Pathogenicity and immunogenicity of Listeria monocytogenes small-plaque mutants defective for intracellular growth and cell-to-cell spread

“…This form of immunity is dependent on the ability of the host to withstand the intracellular replication of bacteria and is mediated by immune T lymphocytes, which function to activate macrophages to increased bactericidal levels (2,33,35,36,38,42). This activation apparently is mediated by lymphokines, especially gamma interferon, released following the recognition of listerial antigens associated with restrictive major histocompatibility complex molecules on antigen-presenting cells (26,27,32).…”

The Host Response to Listeria monocytogenes Mutants Defective in Genes Encoding Phospholipases C (plcA, plcB) and Actin Assembly (actA)

“…The involvement of virulence determinants in the interaction of L. monocytogenes bacteria with host cells of the immune system is still poorly understood. In general, three defensive mechanisms appear to control the growth of L. monocytogenes in vivo: a) listericidal capacity of neutrophils (6) and macrophages (24); b) the synthesis of IL-12, which induces in NK cells and T cells the production of IFN-y which in turn, activates macrophage microbicidal systems (4,23,32); and c) development of Listeria-specific cellular immunity (1,12,13,34) resulting from the activation of CD8+ T cytotoxic cells to kill Listeria-infected host cells (11,30) and CD4+ T helper cells releasing mediators to increase the bactericidal capacity of macrophages (15,(18)(19)(20).…”