Plasmodium and mononuclear phagocytes

Mac-Daniel, Laura; Ménard, Robert

doi:10.1016/j.micpath.2014.11.011

Cited by 10 publications

(8 citation statements)

References 126 publications

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“…DCs play a central role in the bridge between innate and adaptive immunity by efficiently presenting malaria-related antigens to naive T cells and initiating protective T and B cell-mediated responses . The major function of macrophages is parasite clearance via phagocytosis, although they are also important for the initiation of an anti-inflammatory response to the parasite infection (Chua et al, 2013;Mac-Daniel and Mé nard, 2015). The heterogeneity of the macrophage family, which includes both monocytederived and tissue-resident macrophage subsets (Ginhoux and Jung, 2014;Murray and Wynn, 2011), requires that individual subsets are considered separately to understand their individual roles in disease fully.…”

Section: Discussionmentioning

confidence: 99%

Tissue-Resident CD169 + Macrophages Form a Crucial Front Line against Plasmodium Infection

et al. 2016

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Tissue macrophages exhibit diverse functions, ranging from the maintenance of tissue homeostasis, including clearance of senescent erythrocytes and cell debris, to modulation of inflammation and immunity. Their contribution to the control of blood-stage malaria remains unclear. Here, we show that in the absence of tissue-resident CD169(+) macrophages, Plasmodium berghei ANKA (PbA) infection results in significantly increased parasite sequestration, leading to vascular occlusion and leakage and augmented tissue deposition of the malarial pigment hemozoin. This leads to widespread tissue damage culminating in multiple organ inflammation. Thus, the capacity of CD169(+) macrophages to contain the parasite burden and its sequestration into different tissues and to limit infection-induced inflammation is crucial to mitigating Plasmodium infection and pathogenesis.

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Section: Discussionmentioning

confidence: 99%

Tissue-Resident CD169 + Macrophages Form a Crucial Front Line against Plasmodium Infection

et al. 2016

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“…Activation of phagocytes is mediated by binding of the hemozoin/parasite DNA complex to TLR-9 and the consequent downstream activation of inflammasome signaling [41]. The hemozoin released into circulation during infected RBC lysis is taken up by circulating monocytes and tissue macrophages and activates inflammasome intracellular protein complexes, such as NOD-, LRR-, and pyrin domain-containing (NLRP)3 and NLRP12, resulting in caspase 1 activation and the subsequent release of interleukin (IL)-1β, which is involved in fever during malaria bursts [40,42].…”

Section: Molecular and Cellular Features Of The Malaria-induced Inflamentioning

confidence: 99%

Multiple Organ Dysfunction During Severe Malaria: The Role of the Inflammatory Response

Souza¹,

Pádua²,

Henriques³

2016

Current Topics in Malaria

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Severe malaria is a systemic illness characterized by the dysfunction of one or more peripheral organs, such as the lungs [acute respiratory distress syndrome (ARDS)] and kidneys [acute kidney injury (AKI)]. Several clinical and experimental studies suggest that features of the inflammatory response are related to the multi-organ dysfunction observed in severe malaria. Our group has been dedicated to studying the roles of proand anti-inflammatory mediators in the multi-organ dysfunction observed in experimental severe malaria, especially in the lungs, kidneys, and brain. Herein, we explore severe malaria as a pathology derived from intense inflammatory responses in different organs and further distinguish and compare these organ-specific inflammatory responses. The pathophysiological mechanism of severe malaria is not fully elucidated; however, it is important to study it as a complex inflammatory response assembled by different actors, each one orchestrating a different mechanism.

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“…Coupled with work by Stephens et al [224] and Zander et al [389] describing that Th1 or Th1-like CD4 + effector TEM generated during acute infection arrest Plasmodium proliferation in the local proximity [197], and has also been documented in human P.falciparum malaria [252,412]. replenished), regardless of embryonic or BM ontogeny [71,72,79,[416][417][418].…”

Section: Dcs In Plasmodium Infectionmentioning

confidence: 80%

“…Interestingly, IFNγ-producing NKT cells were found to be the main cell subset responsible for early control of liver-stage parasites [196]. Type I IFN and IFNγ production also promotes monocyte / macrophage involvement, and liver Kupffer cells are known to clear liver-stage parasites [197,198] Sporozoite immunization studies have also largely contributed to elucidating the role of adaptive CD8 + CTLs [199][200][201] and tissue-resident memory Tcells [117] in killing and protection against liver-stage infection, wherein in some circumstances sterile immunity can be achieved [202]. As such, potent anti-Plasmodium immunity and vaccination strategies could be potentiated by targeting the liver stage infection.…”

Section: Animal Models Of Malarial Diseasementioning

confidence: 99%

“…However, with advancing insights In addition to CD4 + Th, the other myeloid cells -monocytes and macrophages, are also crucial to anti-Plasmodium immunity in murine and human malaria. Likewise to CD4 + and CD8 + T-cells, they are activated by IFNγ, produced by the aforementioned cells as well as from NK/NKT and γδT-cell sources [197]. Early Plasmodium infection triggers a rapid, IFNγdependent monocytic egress from the BM followed by infiltration into the spleen, where they exert their effector functions as inflammatory monocytes, or differentiate into effector macrophages [219,247,248], aiding the existing pool of tissue-resident macrophages.…”

Section: The Classical Paradigm Of Anti-plasmodium Immunity Proposed Bymentioning

confidence: 99%

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Modulation of adaptive and innate immune responses by myeloid cells during malaria

Lai¹

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Plasmodium chabaudi chabaudi AS infection 4.2.1. Absence of Clec9A + DCs dysregulates induction of Th1 proinflammatory responses and T effector polyfunctionality in PccAS infection 4.2.2. An intact innate immune compartment compensates for polyfunctional proinflammatory responses in the absence of Clec9A + DCs 4.2.3. Germinal center reactions, B-cell responses and Ig production are not abrogated in absence of Clec9A + DCs 4.2.4. Absence of Clec9A + DCs diminishes Th1-like effector TFH and proinflammatory signals required for class switch recombination to more protective Th1 IgG2 and IgG3 4.2.5. The Th1-TFH relationship conundrum 4.2.6. Clec9A + DC deficiency results in persistent T effector and memory precursor impairment during recrudescent PccAS infection 4.3. Caveats and limitations in the Clec9A-DTR PccAS infection model 4.4. Organ-specific tissue-resident macrophages are replenished with different kinetics during acute Plasmodium yoelii infection 4.4.1. Emptied embryonically-seeded TRMØ niches in spleen and liver are partially replenished by BM-derived monocytic progenitors that differentiate into stable, bona fide TRMØs 4.4.2. Depleted lung alveolar MØs almost exclusively self-renew 8 with negligible input from BM-derived circulatory monocytes during acute Py1.1GFP infection 4.5. Rapidly-responding Ly6C hi inflammatory monocytes and monocyte-derived MØs massively infiltrate afflicted tissues and contribute to Py1.1GFP clearance 4.5.1. Ly6C hi inflammatory monocytes rapidly and massively infiltrate organs upon Py1.1GFP infection 4.5.2. Concerted efforts of FrII inflammatory monocytes and monocyte-derived / other tissue-resident MØs in resolution of Py1.1GFP infection 4.6. BM monocyte-derived MØs are phenotypically and transcriptionally similar to bona fide embryonic tissue-resident MØs 4.7. Plasmodium infection as a new precedent for the general mechanism of beneficial cell suicide 5. Summary 6. Significance of studies on current malaria immunological research 6.1. Clec9A + DCs and their roles in anti-Plasmodium immunity 6.2. Tissue-resident MØ repopulation kinetics during Plasmodium infection 6.3. Concluding remarks 7. Appendix 7.1. Cell phenotype profile 7.2. List of antibody panels 7.3. Supplementary figures 8. References 9. Author's publication(s) 10. Oral and poster presentations 9 Abbreviations ACT Artemisinin-based combination therapy ADCI Antibody-dependent cellular inhibition APC Antigen presenting cells AGM Aorta-gonad-mesonephros AMØ Alveolar macrophage Baf8 Basic leucine zipper ATF-like transcription factor BBB Blood-brain barrier BM Bone marrow BMEM Memory B-cells CD Cluster of differentiation cDC Conventional dendritic cells cKit Tyrosine-protein kinase Kit CSF-1/MCF-1 Colony stimulating factor 1 CCL CC motif chemokine ligand CCR CC chemokine receptor CDP Common dendritic progenitor CLEC9A C-type lectin receptor 9A CMP Common myeloid progenitor CMoP Common monocyte progenitor CTL Cytotoxic T lymphocytes CX3CR1 CX3C chemokine receptor 1 CXCR5 C-X-C chemokine receptor type 5 DNA Deoxyribonucleic ...

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Plasmodium and mononuclear phagocytes

Cited by 10 publications

References 126 publications

Tissue-Resident CD169 + Macrophages Form a Crucial Front Line against Plasmodium Infection

Tissue-Resident CD169 + Macrophages Form a Crucial Front Line against Plasmodium Infection

Multiple Organ Dysfunction During Severe Malaria: The Role of the Inflammatory Response

Modulation of adaptive and innate immune responses by myeloid cells during malaria

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