Immunology of Leishmaniasis

Novais, Fernanda O.; Scott, Phillip

doi:10.1016/b978-0-12-374279-7.13011-5

Cited by 6 publications

(3 citation statements)

References 124 publications

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“…This suggests that CD8 T cells are important in skewing towards T H 1 response through the production of IFNγ and in eliminating the majority of parasites before lesion development. The role that CD8 + T cells play in infection may be associated with their location in the host [106]. When located in the draining lymph node, CD8 + T cells produce IFNγ and are protective [107].…”

Section: Cd8 + T Cellsmentioning

confidence: 99%

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Protective and Pathogenic Immune Responses to Cutaneous Leishmaniasis

Panahi¹,

Stanisic²,

Peacock³

et al. 2022

Leishmaniasis - General Aspects of a Stigmatized Disease

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Leishmania (Kinetoplastida: Trypanosomatidae) parasites are known to cause a broad spectrum of clinical diseases in humans, collectively known as the leishmaniases. Cutaneous leishmaniasis is the most common clinical presentation with varying degrees of severity largely driven by host immune responses, specifically the interplay between innate and adaptive immune response. The establishment of a T lymphocyte driven cell-mediated immune response, leading to activated phagocytic cells, leading to Leishmania parasite killing and control of infection. Alternatively, the Leishmania parasite manipulates the host immune system, enabling parasite proliferation and clinical disease. Here we review how the cumulative interactions of different aspects of the host immune response determines disease outcome, severity, and immunity to re-infection.

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Section: Cd8 + T Cellsmentioning

confidence: 99%

“…In CL patients a link between CD8 + T cell mediated cytotoxicity and IL-1β inflammasome activation was observed [111]. This activation of NLRP3 inflammasome pathway and its promotion of disease inflammation is currently targeted for host-directed therapy [88,106].…”

Section: Cd8 + T Cellsmentioning

confidence: 99%

Protective and Pathogenic Immune Responses to Cutaneous Leishmaniasis

Panahi¹,

Stanisic²,

Peacock³

et al. 2022

Leishmaniasis - General Aspects of a Stigmatized Disease

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“…IL4 and IL10 cytokines alternatively activate the macrophages in such a way that the parasite survives inside the macrophages and the resultant phenotype is called M2 phenotype [ 5 ]. The outcome of the infection or the disease manifestation depends upon the balance between Th1/Th2 response [ 6 , 7 ].…”

Section: Introductionmentioning

confidence: 99%

Synthetic Perturbations in IL6 Biological Circuit Induces Dynamical Cellular Response

Soni

Singh

2021

Molecules

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Macrophage phenotype plays a crucial role in the pathogenesis of Leishmanial infection. Pro-inflammatory cytokines signals through the Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway that functions in parasite killing. Suppression of cytokine signaling (SOCS) is a well-known negative feedback regulator of the JAK/STAT pathway. However, change in the expression levels of SOCSs in correlation with the establishment of infection is not well understood. IL6 is a pleotropic cytokine that induces SOCS1 and SOCS3 expression through JAK-STAT signaling. Mathematical modeling of the TLR2 and IL6 signaling pathway has established the immune axis of SOCS1 and SOCS3 functioning in macrophage polarization during the early stage of Leishmania major infection. The ratio has been quantified both in silico and in vitro as 3:2 which is required to establish infection during the early stage. Furthermore, phosphorylated STAT1 and STAT3 have been established as an immunological cross talk between TLR2 and IL6 signaling pathways. Using synthetic biology approaches, peptide based immuno-regulatory circuits have been designed to target the activity of SOCS1 which can restore pro-inflammatory cytokine expression during infection. In a nutshell, we explored the potential of synthetic biology to address and rewire the immune response from Th2 to Th1 type during the early stage of leishmanial infection governed by SOCS1/SOCS3 immune axis.

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