Effective protection against Listeria monocytogenes and delayed-type hypersensitivity to listerial antigens depend on cooperation between specific L3T4+ and Lyt 2+ T cells

Kaufmann, Stefan H. E.; Hug, E.; Väth, Ulla; Müller, Ingrid

doi:10.1128/iai.48.1.263-266.1985

Cited by 110 publications

(48 citation statements)

References 21 publications

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“…Antigen-specific T lymphocytes mediate recovery from primary listerial infections and protective immunity to subsequent infections (16,17). Both CD4 + (helper, MHC class IIrestricted) and CD8 + (cytotoxic/suppressor, MHC class Irestricted) T-cell subpopulations have been implicated (11,18). Recent experimental evidence indicates, however, that CD8 + T cells play the predominant role.…”

Section: Mhc Class I-restricted Cd8 + T-cell-response To Listeriamentioning

confidence: 99%

CD8+ T-cell-mediated response to Listeria monocytogenes taken up in the liver and replicating within hepatocytes

Gregory

Liu

2000

Immunological Reviews

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Like most other organisms that enter the bloodstream, the bulk of Listeria monocytogenes injected i.v. into mice is taken up by the liver. Listeriae not killed rapidly by infiltrating neutrophils are internalized by hepatocytes which constitute the principal site of intracellular replication in the liver. CD8+ T cells play a critical role in eliminating infected hepatocytes and resolving listerial infections of the liver; the specific mechanisms involved are not understood fully. Here, we review recent data implicating the cytolytic activities expressed by MHC class Ia- and class Ib-restricted CD8+ T cells in host resistance to Listeria. Evidence demonstrating the perforin- and/or Fas ligand-dependent induction of caspase activity and the resultant apoptosis of Listeria-infected hepatocytes is discussed.

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Section: Mhc Class I-restricted Cd8 + T-cell-response To Listeriamentioning

confidence: 99%

CD8+ T-cell-mediated response to Listeria monocytogenes taken up in the liver and replicating within hepatocytes

Gregory

Liu

2000

Immunological Reviews

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“…The immune response to L. monocytogenes is considered a paradigm of T cell-mediated immunity, as both the CD4 + and CD8 + T cell subsets contribute to the resolution of infection, whereas antibody plays no measurable role (2). Adoptive transfer studies have implicated CD8 + cells as the most critical effector T cell subset (5,6) that secretes cytokines (7,8) and actively lyses infected cells in vitro (9,10). The induction of protective immunity to L. monocytogenes requires administration of live hemolytic bacteria (11,12).…”

Section: From the Department Of Microbiology University Of Pennsylvamentioning

confidence: 99%

Delivery of a viral antigen to the class I processing and presentation pathway by Listeria monocytogenes.

Ikonomidis

Paterson

Kos

et al. 1994

The Journal of Experimental Medicine

116

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SummaryListeria monocytogenes is a facultative intracellular pathogen that grows in the cytoplasm of infected host cells. We examined the capacity of L. monocytogenes to introduce influenza nucleoprotein (NP) into the class I pathway of antigen presentation both in vitro and in vivo. Recombinant L. monocTtogenes secreting a fusion of listeriolysin O and NP (LLO-NP) targeted infected cells for lysis by NP-specific class I-restricted cytotoxic T cells. Antigen presentation occurred in the context of three different class I haplotypes in vitro. A hemolysin-negative L. monocytogenes strain expressing LLO-NP was able to present in a class II-restricted manner. However, it failed to target infected cells for lysis by CD8 + T cells, indicating that hemolysin-dependent bacterial escape from the vacuole is necessary for class I presentation in vitro. Immunization of mice with a recombinant L. monocytogenes strain that stably expressed and secreted LLO-NP induced NPspecific CD8 + cytotoxic T lymphocytes. These studies have implications for the use of L. monocytogenes to deliver potentially any antigen to the class I pathway in vivo.

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“…Thus, the observation that CD8 T cells (Ly! 23* T cells at that time) rather than CD4 T cells were essential for protective immunity against L. monocytogenes was contrary to the dogma that the control of microbial or viral infections was partitioned between CD4 and CD8 Tcells, respectively (9,10). Moreover, the observation that apparently MHC-unrestricted CD8 T cells were capable of transferring antiiisterial resistance questioned the importance of MHC restriction in listeriosis altogether (11).…”

Section: Introductionmentioning

confidence: 97%

Interleukin‐4 and listeriosis

Kaufmann

Emoto

Szalay

et al. 1997

Immunological Reviews

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Experimental infection of mice with Listeria monocytogenes (L. monocytogenes) has served as an appropriate model for analyzing Th1-cell-driven immune responses. Generally, Th2 responses are absent and IL-4 is not detectable. Here, we describe experimental settings under which IL-4 is detectable in listeriosis. Our data suggest that IL-4 is rapidly produced after infection. This prompt IL-4 burst seems to stimulate chemokine responses and, therefore, may participate in the regulation of the early antilisterial host response. Soon thereafter, IL-4 production wanes. At least partially this seems to be caused by downregulation of IL-4-producing CD4+ NK1+ TCR alpha beta int lymphocytes by IL-12. In the absence of IFN-gamma responsiveness, IL-4 production is demonstrable during acquired immunity against L monocytogenes, and this elevated IL-4 production apparently contributes to disease exacerbation. In conclusion, the data are consistent with a detrimental role of IL-4 in listeriosis and active control of IL-4 synthesis by the antilisterial immune response. The rapid, but transient, IL-4 burst in listeriosis probably contributes to host defense without impairing development of the acquired T-cell response because of its shortness.

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Effective protection against Listeria monocytogenes and delayed-type hypersensitivity to listerial antigens depend on cooperation between specific L3T4+ and Lyt 2+ T cells

Cited by 110 publications

References 21 publications

CD8+ T-cell-mediated response to Listeria monocytogenes taken up in the liver and replicating within hepatocytes

CD8+ T-cell-mediated response to Listeria monocytogenes taken up in the liver and replicating within hepatocytes

Delivery of a viral antigen to the class I processing and presentation pathway by Listeria monocytogenes.

Interleukin‐4 and listeriosis

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