Role of L3T4+ and LyT-2+ cells in experimental visceral leishmaniasis.

Stern, John J.; J, M; Rubin, Berish Y.; Anderson, Shoana; Murray, Henry W.

doi:10.4049/jimmunol.140.11.3971

Cited by 140 publications

(2 citation statements)

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“…Approximately one week after infection, recruited T cells accumulate in granulomas to become the predominant cell type (Stern et al, 1988). Although it was previously assumed that T cells were primed in the spleen and migrated to the liver to combat the infection, recent studies have shown that parasite-specific CD4 + T cells may be primed in other tissues and are sufficient to confer immunity (Engwerda and Kaye, 2000).…”

Section: Murine Models Of Experimental Visceral Leishmaniasismentioning

confidence: 99%

“…Although it was previously assumed that T cells were primed in the spleen and migrated to the liver to combat the infection, recent studies have shown that parasite-specific CD4 + T cells may be primed in other tissues and are sufficient to confer immunity (Engwerda and Kaye, 2000). Both CD4 + and CD8 + T cells are essential for granuloma formation (Stern et al, 1988). Still, whereas CD4 + T cells can be activated by both KCs and granulomaassociated dendritic cells (DCs) (Stanley and Engwerda, 2007), the activation of CD8 + T cells is restricted to KCs (Beattie et al, 2010).…”

Section: Murine Models Of Experimental Visceral Leishmaniasismentioning

confidence: 99%

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The role of CD4+ T cells in visceral leishmaniasis; new and emerging roles for NKG7 and TGFβ

Na,

Engwerda

2024

Front. Cell. Infect. Microbiol.

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Visceral leishmaniasis is a potentially devastating neglected tropical disease caused by the protozoan parasites Leishmania donovani and L. infantum (chagasi). These parasites reside in tissue macrophages and survive by deploying a number of mechanisms aimed at subverting the host immune response. CD4+ T cells play an important role in controlling Leishmania parasites by providing help in the form of pro-inflammatory cytokines to activate microbiocidal pathways in infected macrophages. However, because these cytokines can also cause tissue damage if over-produced, regulatory immune responses develop, and the balance between pro-inflammatory and regulatory CD4+ T cells responses determines the outcomes of infection. Past studies have identified important roles for pro-inflammatory cytokines such as IFNγ and TNF, as well as regulatory co-inhibitory receptors and the potent anti-inflammatory cytokine IL-10. More recently, other immunoregulatory molecules have been identified that play important roles in CD4+ T cell responses during VL. In this review, we will discuss recent findings about two of these molecules; the NK cell granule protein Nkg7 and the anti-inflammatory cytokine TGFβ, and describe how they impact CD4+ T cell functions and immune responses during visceral leishmaniasis.

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Section: Murine Models Of Experimental Visceral Leishmaniasismentioning

confidence: 99%

Section: Murine Models Of Experimental Visceral Leishmaniasismentioning

confidence: 99%

The role of CD4+ T cells in visceral leishmaniasis; new and emerging roles for NKG7 and TGFβ

Na,

Engwerda

2024

Front. Cell. Infect. Microbiol.

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Leishmania donovani infection initiates T cell-independent chemokine responses, which are subsequently amplified in a T cell-dependent manner

1999

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Control of Leishmania donovani infection in immunocompetent mice is associated with hepatic inflammation and granuloma formation, both of which are absent in severe combined immunodeficient (scid) mice. In both BALB/c and scid mice, L. donovani infection induced a rapid hepatic accumulation of mRNA encoding macrophage inflammatory protein-1alpha (MIP-(1alpha), monocyte chemoattractant protein-1 (MCP-1) and interferon-gamma inducible protein-10 (gammaIP-10). This response was not preceded by increased IL-4 production in either strain, unlike that reported in other infectious disease models. Interestingly, only gammaIP-10 mRNA was maintained at elevated levels throughout the first 7 days of infection, by mechanisms involving CD4+ and CD8+ T cells, and CD4+CD8+ cells not activated in scid mice. By in vivo depletion and reconstitution of scid mice it was demonstrated that T cells regulate the expression of all three chemokines studied, while they themselves only produce gammaIP-10 in appreciable quantities.

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CD95 is required for the early control of parasite burden in the liver ofLeishmania donovani-infected mice

2001

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In this study we show an increased incidence of T cell apoptosis in the liver and spleen of mice infected with Leishmania donovani. T cells from L. donovani‐infected mice were found to be increasingly susceptible to CD95‐mediated apoptosis in vitro, compared to controls. To test if suboptimal T cell function resulting from CD95‐mediated apoptosis contributes to sustained parasite burden in L. donovani parasitized mice, B6.gld mice (lacking functional CD95 ligand) were infected with L. donovani. Surprisingly, at four different time points no difference in levels of T cell apoptosis in the spleen and liver was found between these mice and controls following intravenous delivery of L. donovani amastigotes, indicating that the CD95 / CD95L interaction is not essential for T cell apoptosis in the L. donovani‐infected liver and spleen. However, B6.gld mice were increasingly susceptible to L. donovani infection, associated with less efficient granuloma formation in the liver and uncontrolled parasite growth in the spleen. Late in infection (day 56 post‐infection), B6.gld mice had higher numbers of IFN‐γ‐producing CD4+ T cells in the liver and spleen, indicating a role for CD95 signaling in the homeostasis of this subset of cytokine‐producing T cells in L. donovani‐parasitized mice. Adoptive transfer of CD4+ and CD8+ T cells into recombinase activating gene 1 knockout (RAG‐1– / –) recipients, revealed that CD95L expressed on CD4+ T cells contributes to early control of L. donovani infection in the liver via mechanisms that are independent of granuloma formation and induction of apoptosis. These results indicate important roles for CD95 and CD95L that are unrelated to regulation of apoptosis in the early control of L. donovani infection.

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Role of L3T4+ and LyT-2+ cells in experimental visceral leishmaniasis.

Cited by 140 publications

References 0 publications

The role of CD4+ T cells in visceral leishmaniasis; new and emerging roles for NKG7 and TGFβ

The role of CD4+ T cells in visceral leishmaniasis; new and emerging roles for NKG7 and TGFβ

Leishmania donovani infection initiates T cell-independent chemokine responses, which are subsequently amplified in a T cell-dependent manner

CD95 is required for the early control of parasite burden in the liver ofLeishmania donovani-infected mice

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