The immunopathology of experimental visceral leishmaniasis

Paul M Kaye; Mattias Svensson; Manabu Ato; Asher Maroof; Rosalind Polley; Simona Stager; Soombul Zubairi; Christian R Engwerda

doi:10.1111/j.0105-2896.2004.00188.x

The immunopathology of experimental visceral leishmaniasis

Paul M Kaye, Mattias Svensson, Manabu Ato, Asher Maroof, Rosalind Polley, Simona Stager, Soombul Zubairi, Christian R Engwerda

Research output: Contribution to journal › Article › peer-review

Abstract

Experimental murine infection with the parasites that cause human visceral leishmaniasis (VL) results in the establishment of infection in the liver, spleen, and bone marrow. In most strains of mice, parasites are eventually cleared from the liver, and hepatic resistance to infection results from a coordinated host response involving a broad range of effector and regulatory pathways targeted within defined tissue structures called granulomas. In contrast, parasites persist in the spleen and bone marrow by mechanisms that are less well understood. Parasite persistence is accompanied by the failure of granuloma formation and by a variety of pathologic changes, including splenomegaly, disruption of lymphoid tissue microarchitecture, and enhanced hematopoietic activity. Here, we review the salient features of these distinct tissue responses and highlight the varied roles that cytokines of the tumor necrosis factor family play in immunity to this infection. In addition, we also discuss recent studies aimed at understanding how splenomegaly affects the survival and function of memory cells specific for heterologous antigens, an issue of considerable importance for our understanding of the disease-associated increase in secondary infections characteristic of human VL.

Original language	English
Pages (from-to)	239-53
Number of pages	15
Journal	Immunological Reviews
Volume	201
DOIs	https://doi.org/10.1111/j.0105-2896.2004.00188.x
Publication status	Published - Oct 2004

Keywords

Animals
Disease Models, Animal
Humans
Leishmania donovani
Leishmaniasis, Visceral
Mice
Mice, Inbred Strains

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10.1111/j.0105-2896.2004.00188.x

Cite this

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title = "The immunopathology of experimental visceral leishmaniasis",

abstract = "Experimental murine infection with the parasites that cause human visceral leishmaniasis (VL) results in the establishment of infection in the liver, spleen, and bone marrow. In most strains of mice, parasites are eventually cleared from the liver, and hepatic resistance to infection results from a coordinated host response involving a broad range of effector and regulatory pathways targeted within defined tissue structures called granulomas. In contrast, parasites persist in the spleen and bone marrow by mechanisms that are less well understood. Parasite persistence is accompanied by the failure of granuloma formation and by a variety of pathologic changes, including splenomegaly, disruption of lymphoid tissue microarchitecture, and enhanced hematopoietic activity. Here, we review the salient features of these distinct tissue responses and highlight the varied roles that cytokines of the tumor necrosis factor family play in immunity to this infection. In addition, we also discuss recent studies aimed at understanding how splenomegaly affects the survival and function of memory cells specific for heterologous antigens, an issue of considerable importance for our understanding of the disease-associated increase in secondary infections characteristic of human VL.",

keywords = "Animals, Disease Models, Animal, Humans, Leishmania donovani, Leishmaniasis, Visceral, Mice, Mice, Inbred Strains",

author = "Kaye, {Paul M} and Mattias Svensson and Manabu Ato and Asher Maroof and Rosalind Polley and Simona Stager and Soombul Zubairi and Engwerda, {Christian R}",

year = "2004",

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doi = "10.1111/j.0105-2896.2004.00188.x",

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T1 - The immunopathology of experimental visceral leishmaniasis

AU - Kaye, Paul M

AU - Svensson, Mattias

AU - Ato, Manabu

AU - Maroof, Asher

AU - Polley, Rosalind

AU - Stager, Simona

AU - Zubairi, Soombul

AU - Engwerda, Christian R

PY - 2004/10

Y1 - 2004/10

N2 - Experimental murine infection with the parasites that cause human visceral leishmaniasis (VL) results in the establishment of infection in the liver, spleen, and bone marrow. In most strains of mice, parasites are eventually cleared from the liver, and hepatic resistance to infection results from a coordinated host response involving a broad range of effector and regulatory pathways targeted within defined tissue structures called granulomas. In contrast, parasites persist in the spleen and bone marrow by mechanisms that are less well understood. Parasite persistence is accompanied by the failure of granuloma formation and by a variety of pathologic changes, including splenomegaly, disruption of lymphoid tissue microarchitecture, and enhanced hematopoietic activity. Here, we review the salient features of these distinct tissue responses and highlight the varied roles that cytokines of the tumor necrosis factor family play in immunity to this infection. In addition, we also discuss recent studies aimed at understanding how splenomegaly affects the survival and function of memory cells specific for heterologous antigens, an issue of considerable importance for our understanding of the disease-associated increase in secondary infections characteristic of human VL.

AB - Experimental murine infection with the parasites that cause human visceral leishmaniasis (VL) results in the establishment of infection in the liver, spleen, and bone marrow. In most strains of mice, parasites are eventually cleared from the liver, and hepatic resistance to infection results from a coordinated host response involving a broad range of effector and regulatory pathways targeted within defined tissue structures called granulomas. In contrast, parasites persist in the spleen and bone marrow by mechanisms that are less well understood. Parasite persistence is accompanied by the failure of granuloma formation and by a variety of pathologic changes, including splenomegaly, disruption of lymphoid tissue microarchitecture, and enhanced hematopoietic activity. Here, we review the salient features of these distinct tissue responses and highlight the varied roles that cytokines of the tumor necrosis factor family play in immunity to this infection. In addition, we also discuss recent studies aimed at understanding how splenomegaly affects the survival and function of memory cells specific for heterologous antigens, an issue of considerable importance for our understanding of the disease-associated increase in secondary infections characteristic of human VL.

KW - Animals

KW - Disease Models, Animal

KW - Humans

KW - Leishmania donovani

KW - Leishmaniasis, Visceral

KW - Mice

KW - Mice, Inbred Strains

U2 - 10.1111/j.0105-2896.2004.00188.x

DO - 10.1111/j.0105-2896.2004.00188.x

M3 - Article

C2 - 15361245

SN - 0105-2896

VL - 201

SP - 239

EP - 253

JO - Immunological Reviews

JF - Immunological Reviews

ER -