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Article ; Online: Control of complement-induced inflammatory responses to SARS-CoV-2 infection by anti-SARS-CoV-2 antibodies.

Bermejo-Jambrina, Marta / van der Donk, Lieve Eh / van Hamme, John L / Wilflingseder, Doris / de Bree, Godelieve / Prins, Maria / de Jong, Menno / Nieuwkerk, Pythia / van Gils, Marit J / Kootstra, Neeltje A / Geijtenbeek, Teunis Bh

The EMBO journal

2024 Volume 43, Issue 7, Page(s) 1135–1163

Abstract: Dysregulated immune responses contribute to the excessive and uncontrolled inflammation observed in severe COVID-19. However, how immunity to SARS-CoV-2 is induced and regulated remains unclear. Here, we uncover the role of the complement system in the ... ...

Abstract	Dysregulated immune responses contribute to the excessive and uncontrolled inflammation observed in severe COVID-19. However, how immunity to SARS-CoV-2 is induced and regulated remains unclear. Here, we uncover the role of the complement system in the induction of innate and adaptive immunity to SARS-CoV-2. Complement rapidly opsonizes SARS-CoV-2 particles via the lectin pathway. Complement-opsonized SARS-CoV-2 efficiently induces type-I interferon and pro-inflammatory cytokine responses via activation of dendritic cells, which are inhibited by antibodies against the complement receptors (CR) 3 and 4. Serum from COVID-19 patients, or monoclonal antibodies against SARS-CoV-2, attenuate innate and adaptive immunity induced by complement-opsonized SARS-CoV-2. Blocking of CD32, the FcγRII antibody receptor of dendritic cells, restores complement-induced immunity. These results suggest that opsonization of SARS-CoV-2 by complement is involved in the induction of innate and adaptive immunity to SARS-CoV-2 in the acute phase of infection. Subsequent antibody responses limit inflammation and restore immune homeostasis. These findings suggest that dysregulation of the complement system and FcγRII signaling may contribute to severe COVID-19.
MeSH term(s)	Humans ; COVID-19 ; SARS-CoV-2 ; Antibodies, Viral ; Complement System Proteins ; Inflammation ; Immunity, Innate
Chemical Substances	Antibodies, Viral ; Complement System Proteins (9007-36-7)
Language	English
Publishing date	2024-02-28
Publishing country	England
Document type	Journal Article
ZDB-ID	586044-1
ISSN	1460-2075 ; 0261-4189
ISSN (online)	1460-2075
ISSN	0261-4189
DOI	10.1038/s44318-024-00061-0
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Article ; Online: Role of Complement Receptors (CRs) on DCs in Anti-HIV-1 Immunity.

Posch, Wilfried / Bermejo-Jambrina, Marta / Lass-Flörl, Cornelia / Wilflingseder, Doris

Frontiers in immunology

2020 Volume 11, Page(s) 572114

Abstract: Upon entry of human immunodeficiency virus 1 (HIV-1) into the host, innate immune mechanisms are acting as a first line of defense, that considerably also modify adaptive immunity by the provision of specific signals. Innate and adaptive immune responses ...

Abstract	Upon entry of human immunodeficiency virus 1 (HIV-1) into the host, innate immune mechanisms are acting as a first line of defense, that considerably also modify adaptive immunity by the provision of specific signals. Innate and adaptive immune responses are intimately linked and dendritic cells (DCs) together with complement (C) play an important role in regulation of adaptive immunity. Initially, the role of complement was considered to primarily support - or COMPLEMENT - cytolytic actions of antibodies or antibody-complexed antigens (immune complexes, ICs) or directly kill the pathogens by complement-mediated lysis. Recently, the role of complement was revised and found to significantly augmenting and modulating adaptive immunity, in particular against viruses. Complement and DCs are therefore predestined to open novel avenues for antiviral research and potential therapeutic interventions. Recent studies on interactions of complement-opsonized HIV-1 with DCs demonstrated a high potential of such primed DCs to initiate efficient antiviral and cytotoxic anti-HIV-1 immunity and complement-coated viral particles shift DCs functions
MeSH term(s)	Animals ; Antigen Presentation ; Antigens, Viral/immunology ; Complement System Proteins/metabolism ; Cytotoxicity, Immunologic ; Dendritic Cells/immunology ; HIV Infections/immunology ; HIV Infections/metabolism ; HIV-1/physiology ; Humans ; Immunity ; Integrin alphaXbeta2 ; Macrophage-1 Antigen/metabolism ; Signal Transduction ; Virus Internalization
Chemical Substances	Antigens, Viral ; Integrin alphaXbeta2 ; Macrophage-1 Antigen ; Complement System Proteins (9007-36-7)
Language	English
Publishing date	2020-11-03
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2020.572114
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: SARS-CoV-2 suppresses TLR4-induced immunity by dendritic cells via C-type lectin receptor DC-SIGN.

van der Donk, Lieve E H / Bermejo-Jambrina, Marta / van Hamme, John L / Volkers, Mette M W / van Nuenen, Ad C / Kootstra, Neeltje A / Geijtenbeek, Teunis B H

PLoS pathogens

2023 Volume 19, Issue 10, Page(s) e1011735

Abstract: SARS-CoV-2 causes COVID-19, an infectious disease with symptoms ranging from a mild cold to severe pneumonia, inflammation, and even death. Although strong inflammatory responses are a major factor in causing morbidity and mortality, superinfections with ...

Abstract	SARS-CoV-2 causes COVID-19, an infectious disease with symptoms ranging from a mild cold to severe pneumonia, inflammation, and even death. Although strong inflammatory responses are a major factor in causing morbidity and mortality, superinfections with bacteria during severe COVID-19 often cause pneumonia, bacteremia and sepsis. Aberrant immune responses might underlie increased sensitivity to bacteria during COVID-19 but the mechanisms remain unclear. Here we investigated whether SARS-CoV-2 directly suppresses immune responses to bacteria. We studied the functionality of human dendritic cells (DCs) towards a variety of bacterial triggers after exposure to SARS-CoV-2 Spike (S) protein and SARS-CoV-2 primary isolate (hCoV-19/Italy). Notably, pre-exposure of DCs to either SARS-CoV-2 S protein or a SARS-CoV-2 isolate led to reduced type I interferon (IFN) and cytokine responses in response to Toll-like receptor (TLR)4 agonist lipopolysaccharide (LPS), whereas other TLR agonists were not affected. SARS-CoV-2 S protein interacted with the C-type lectin receptor DC-SIGN and, notably, blocking DC-SIGN with antibodies restored type I IFN and cytokine responses to LPS. Moreover, blocking the kinase Raf-1 by a small molecule inhibitor restored immune responses to LPS. These results suggest that SARS-CoV-2 modulates DC function upon TLR4 triggering via DC-SIGN-induced Raf-1 pathway. These data imply that SARS-CoV-2 actively suppresses DC function via DC-SIGN, which might account for the higher mortality rates observed in patients with COVID-19 and bacterial superinfections.
MeSH term(s)	Humans ; SARS-CoV-2/metabolism ; Toll-Like Receptor 4/metabolism ; Lipopolysaccharides/pharmacology ; Lipopolysaccharides/metabolism ; Superinfection ; COVID-19/metabolism ; Lectins, C-Type/metabolism ; Cytokines/metabolism ; Dendritic Cells
Chemical Substances	DC-specific ICAM-3 grabbing nonintegrin ; spike protein, SARS-CoV-2 ; Toll-Like Receptor 4 ; Lipopolysaccharides ; Lectins, C-Type ; Cytokines ; TLR4 protein, human
Language	English
Publishing date	2023-10-16
Publishing country	United States
Document type	Journal Article
ZDB-ID	2205412-1
ISSN	1553-7374 ; 1553-7374
ISSN (online)	1553-7374
ISSN	1553-7374
DOI	10.1371/journal.ppat.1011735
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: HIV-1 subverts the complement system in semen to enhance viral transmission.

Nijmeijer, Bernadien M / Bermejo-Jambrina, Marta / Kaptein, Tanja M / Ribeiro, Carla M S / Wilflingseder, Doris / Geijtenbeek, Teunis B H

Mucosal immunology

2021 Volume 14, Issue 3, Page(s) 743–750

Abstract: Semen is important in determining HIV-1 susceptibility but it is unclear how it affects virus transmission during sexual contact. Mucosal Langerhans cells (LCs) are the first immune cells to encounter HIV-1 during sexual contact and have a barrier ... ...

Abstract	Semen is important in determining HIV-1 susceptibility but it is unclear how it affects virus transmission during sexual contact. Mucosal Langerhans cells (LCs) are the first immune cells to encounter HIV-1 during sexual contact and have a barrier function as LCs are restrictive to HIV-1. As semen from people living with HIV-1 contains complement-opsonized HIV-1, we investigated the effect of complement on HIV-1 dissemination by human LCs in vitro and ex vivo. Notably, pre-treatment of HIV-1 with semen enhanced LC infection compared to untreated HIV-1 in the ex vivo explant model. Infection of LCs and transmission to target cells by opsonized HIV-1 was efficiently inhibited by blocking complement receptors CR3 and CR4. Complement opsonization of HIV-1 enhanced uptake, fusion, and integration by LCs leading to an increased transmission of HIV-1 to target cells. However, in the absence of both CR3 and CR4, C-type lectin receptor langerin was able to restrict infection of complement-opsonized HIV-1. These data suggest that complement enhances HIV-1 infection of LCs by binding CR3 and CR4, thereby bypassing langerin and changing the restrictive nature of LCs into virus-disseminating cells. Targeting complement factors might be effective in preventing HIV-1 transmission.
MeSH term(s)	Antibodies, Blocking/metabolism ; Antigens, CD/metabolism ; Cell Line ; Complement Activation ; Disease Transmission, Infectious ; HIV Infections/immunology ; HIV Infections/transmission ; HIV-1/pathogenicity ; HIV-1/physiology ; Host-Parasite Interactions ; Humans ; Immune Evasion ; Integrin alphaXbeta2/metabolism ; Langerhans Cells/immunology ; Lectins, C-Type/metabolism ; Macrophage-1 Antigen/metabolism ; Mannose-Binding Lectins/metabolism ; Opsonization ; Semen/immunology ; Semen/virology
Chemical Substances	Antibodies, Blocking ; Antigens, CD ; CD207 protein, human ; Integrin alphaXbeta2 ; Lectins, C-Type ; Macrophage-1 Antigen ; Mannose-Binding Lectins
Language	English
Publishing date	2021-02-10
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2411370-0
ISSN	1935-3456 ; 1933-0219
ISSN (online)	1935-3456
ISSN	1933-0219
DOI	10.1038/s41385-021-00376-9
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Inhalation of Low Molecular Weight Heparins as Prophylaxis against SARS-CoV-2.

Eder, Julia / Bermejo-Jambrina, Marta / Vlaming, Killian E / Kaptein, Tanja M / Zaderer, Viktoria / Kemper, E Marleen / Wilflingseder, Doris / Reitsma, Sietze / de Bree, Godelieve J / Cohn, Danny M / Geijtenbeek, Teunis B H

mBio

2022 Volume 13, Issue 6, Page(s) e0255822

Abstract: New SARS-CoV-2 variants of concern and waning immunity demonstrate the need for a quick and simple prophylactic agent to prevent infection. Low molecular weight heparins (LMWH) are potent inhibitors of SARS-CoV-2 binding and infection in vitro. The ... ...

Abstract	New SARS-CoV-2 variants of concern and waning immunity demonstrate the need for a quick and simple prophylactic agent to prevent infection. Low molecular weight heparins (LMWH) are potent inhibitors of SARS-CoV-2 binding and infection in vitro. The airways are a major route for infection and therefore inhaled LMWH could be a prophylactic treatment against SARS-CoV-2. We investigated the efficacy of in vivo inhalation of LMWH in humans to prevent SARS-CoV-2 attachment to nasal epithelial cells in a single-center, open-label intervention study. Volunteers received enoxaparin in the right and a placebo (NaCl 0.9%) in the left nostril using a nebulizer. After application, nasal epithelial cells were retrieved with a brush for
MeSH term(s)	Humans ; Heparin, Low-Molecular-Weight/adverse effects ; SARS-CoV-2 ; Enoxaparin/therapeutic use ; COVID-19
Chemical Substances	Heparin, Low-Molecular-Weight ; Enoxaparin
Language	English
Publishing date	2022-11-03
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2557172-2
ISSN	2150-7511 ; 2161-2129
ISSN (online)	2150-7511
ISSN	2161-2129
DOI	10.1128/mbio.02558-22
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Article ; Online: SARS-CoV-2 suppresses TLR4-induced immunity by dendritic cells via C-type lectin receptor DC-SIGN.

Lieve E H van der Donk / Marta Bermejo-Jambrina / John L van Hamme / Mette M W Volkers / Ad C van Nuenen / Neeltje A Kootstra / Teunis B H Geijtenbeek

PLoS Pathogens, Vol 19, Iss 10, p e

2023 Volume 1011735

Abstract	SARS-CoV-2 causes COVID-19, an infectious disease with symptoms ranging from a mild cold to severe pneumonia, inflammation, and even death. Although strong inflammatory responses are a major factor in causing morbidity and mortality, superinfections with bacteria during severe COVID-19 often cause pneumonia, bacteremia and sepsis. Aberrant immune responses might underlie increased sensitivity to bacteria during COVID-19 but the mechanisms remain unclear. Here we investigated whether SARS-CoV-2 directly suppresses immune responses to bacteria. We studied the functionality of human dendritic cells (DCs) towards a variety of bacterial triggers after exposure to SARS-CoV-2 Spike (S) protein and SARS-CoV-2 primary isolate (hCoV-19/Italy). Notably, pre-exposure of DCs to either SARS-CoV-2 S protein or a SARS-CoV-2 isolate led to reduced type I interferon (IFN) and cytokine responses in response to Toll-like receptor (TLR)4 agonist lipopolysaccharide (LPS), whereas other TLR agonists were not affected. SARS-CoV-2 S protein interacted with the C-type lectin receptor DC-SIGN and, notably, blocking DC-SIGN with antibodies restored type I IFN and cytokine responses to LPS. Moreover, blocking the kinase Raf-1 by a small molecule inhibitor restored immune responses to LPS. These results suggest that SARS-CoV-2 modulates DC function upon TLR4 triggering via DC-SIGN-induced Raf-1 pathway. These data imply that SARS-CoV-2 actively suppresses DC function via DC-SIGN, which might account for the higher mortality rates observed in patients with COVID-19 and bacterial superinfections.
Keywords	Immunologic diseases. Allergy ; RC581-607 ; Biology (General) ; QH301-705.5
Subject code	572 ; 616
Language	English
Publishing date	2023-10-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: SARS-CoV-2 infection activates dendritic cells via cytosolic receptors rather than extracellular TLRs.

van der Donk, Lieve E H / Eder, Julia / van Hamme, John L / Brouwer, Philip J M / Brinkkemper, Mitch / van Nuenen, Ad C / van Gils, Marit J / Sanders, Rogier W / Kootstra, Neeltje A / Bermejo-Jambrina, Marta / Geijtenbeek, Teunis B H

European journal of immunology

2022 Volume 52, Issue 4, Page(s) 646–655

Abstract: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes coronavirus disease 2019 (COVID-19), an infectious disease characterized by strong induction of inflammatory cytokines, progressive lung inflammation, and potentially multiorgan ... ...

Abstract	Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes coronavirus disease 2019 (COVID-19), an infectious disease characterized by strong induction of inflammatory cytokines, progressive lung inflammation, and potentially multiorgan dysfunction. It remains unclear how SARS-CoV-2 infection leads to immune activation. The Spike (S) protein of SARS-CoV-2 has been suggested to trigger TLR4 and thereby activate immunity. Here, we have investigated the role of TLR4 in SARS-CoV-2 infection and immunity. Neither exposure of isolated S protein, SARS-CoV-2 pseudovirus nor primary SARS-CoV-2 isolate induced TLR4 activation in a TLR4-expressing cell line. Human monocyte-derived DCs express TLR4 but not angiotensin converting enzyme 2 (ACE2), and DCs were not infected by SARS-CoV-2. Notably, neither S protein nor SARS-CoV-2 induced DC maturation or cytokines, indicating that both S protein and SARS-CoV-2 virus particles do not trigger extracellular TLRs including TLR4. Ectopic expression of ACE2 in DCs led to efficient infection by SARS-CoV-2 and, strikingly, efficient type I IFN and cytokine responses. These data strongly suggest that not extracellular TLRs but intracellular viral sensors are key players in sensing SARS-CoV-2. These data imply that SARS-CoV-2 escapes direct sensing by TLRs, which might underlie the lack of efficient immunity to SARS-CoV-2 early during infection.
MeSH term(s)	COVID-19/immunology ; Cell Line ; Dendritic Cells/immunology ; Humans ; SARS-CoV-2 ; Spike Glycoprotein, Coronavirus/immunology ; Toll-Like Receptor 4/immunology
Chemical Substances	Spike Glycoprotein, Coronavirus ; TLR4 protein, human ; Toll-Like Receptor 4 ; spike protein, SARS-CoV-2
Language	English
Publishing date	2022-02-16
Publishing country	Germany
Document type	Journal Article
ZDB-ID	120108-6
ISSN	1521-4141 ; 0014-2980
ISSN (online)	1521-4141
ISSN	0014-2980
DOI	10.1002/eji.202149656
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Article ; Online: Complement Potentiates Immune Sensing of HIV-1 and Early Type I Interferon Responses.

Posch, Wilfried / Bermejo-Jambrina, Marta / Steger, Marion / Witting, Christina / Diem, Gabriel / Hörtnagl, Paul / Hackl, Hubert / Lass-Flörl, Cornelia / Huber, Lukas A / Geijtenbeek, Teunis B H / Wilflingseder, Doris

mBio

2021 Volume 12, Issue 5, Page(s) e0240821

Abstract: Complement-opsonized HIV-1 triggers efficient antiviral type I interferon (IFN) responses in dendritic cells (DCs), which play an important role in protective responses at the earliest stages in retroviral infection. In contrast, HIV-1 suppresses or ... ...

Abstract	Complement-opsonized HIV-1 triggers efficient antiviral type I interferon (IFN) responses in dendritic cells (DCs), which play an important role in protective responses at the earliest stages in retroviral infection. In contrast, HIV-1 suppresses or escapes sensing by STING- and MAVS-associated sensors. Here, we identified a complement receptor-mediated sensing pathway, where DCs are activated in CCR5/RLR (RIG-I/MDA5)/MAVS/TBK1-dependent fashion. Increased fusion of complement-opsonized HIV-1 via complement receptor 4 and CCR5 leads to increased incoming HIV-1 RNA in the cytoplasm, sensed by a nonredundant cooperative effect of RIG-I and MDA5. Moreover, complement-opsonized HIV-1 down-modulated the MAVS-suppressive Raf-1/PLK1 pathway, thereby opening the antiviral recognition pathway via MAVS. This in turn was followed by MAVS aggregation and subsequent TBK1/IRF3/NF-κB activation in DCs exposed to complement- but not non-opsonized HIV-1. Our data strongly suggest that complement is important in the induction of efficient antiviral immune responses by preventing HIV-1 suppressive mechanisms as well as inducing specific cytosolic sensors.
MeSH term(s)	Adaptor Proteins, Signal Transducing/genetics ; Adaptor Proteins, Signal Transducing/immunology ; Complement System Proteins/immunology ; Dendritic Cells/immunology ; Dendritic Cells/virology ; HIV Infections/genetics ; HIV Infections/immunology ; HIV Infections/virology ; HIV-1/genetics ; HIV-1/immunology ; Humans ; Integrin alphaXbeta2/genetics ; Integrin alphaXbeta2/immunology ; Interferon Type I/genetics ; Interferon Type I/immunology ; Interferon-Induced Helicase, IFIH1/genetics ; Interferon-Induced Helicase, IFIH1/immunology ; Receptors, CCR5/genetics ; Receptors, CCR5/immunology
Chemical Substances	Adaptor Proteins, Signal Transducing ; CCR5 protein, human ; Integrin alphaXbeta2 ; Interferon Type I ; MAVS protein, human ; Receptors, CCR5 ; Complement System Proteins (9007-36-7) ; IFIH1 protein, human (EC 3.6.1.-) ; Interferon-Induced Helicase, IFIH1 (EC 3.6.4.13)
Language	English
Publishing date	2021-10-12
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2557172-2
ISSN	2150-7511 ; 2161-2129
ISSN (online)	2150-7511
ISSN	2161-2129
DOI	10.1128/mBio.02408-21
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Article ; Online: Antibodies against SARS-CoV-2 control complement-induced inflammatory responses to SARS-CoV-2

Bermejo-Jambrina, Marta / van der Donk, Lieve E.H. / van Hamme, John L. / Wilflingseder, Doris / de Bree, Godelieve / Prins, Maria / de Jong, Menno / Nieuwkerk, Pythia / van Gils, Marit J. / Kootstra, Neeltje A. / Geijtenbeek, Teunis B.H.

bioRxiv

Abstract: Dysregulated immune responses contribute to pathogenesis of COVID-19 leading to uncontrolled and exaggerated inflammation observed during severe COVID-19. However, it remains unclear how immunity to SARS-CoV-2 is induced and subsequently controlled. ... ...

Abstract	Dysregulated immune responses contribute to pathogenesis of COVID-19 leading to uncontrolled and exaggerated inflammation observed during severe COVID-19. However, it remains unclear how immunity to SARS-CoV-2 is induced and subsequently controlled. Notably, here we have uncovered an important role for complement in the induction of innate and adaptive immunity to SARS-CoV-2. Complement rapidly opsonized SARS-CoV-2 via the lectin pathway. Complement-opsonized SARS-CoV-2 efficiently interacted with dendritic cells (DCs), inducing type I IFN and pro-inflammatory cytokine responses, which were inhibited by antibodies against the complement receptors (CR)3 and CR4. These data suggest that complement is important in inducing immunity via DCs in the acute phase against SARS-CoV-2. Strikingly, serum from COVID-19 patients as well as monoclonal antibodies against SARS-CoV-2 attenuated innate and adaptive immunity induced by complement-opsonized SARS-CoV-2. Blocking the FcyRII, CD32, restored complement-induced immunity. These data strongly suggest that complement opsonization of SARS-CoV-2 is important for inducing innate and adaptive immunity to SARS-CoV-2. Subsequent induction of antibody responses is important to limit the immune responses and restore immune homeostasis. These data suggest that dysregulation in complement and FcyRII signalling might underlie mechanisms causing severe COVID-19.
Keywords	covid19
Language	English
Publishing date	2023-05-30
Publisher	Cold Spring Harbor Laboratory
Document type	Article ; Online
DOI	10.1101/2023.05.29.542735
Database	COVID19

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Article: C-Type Lectin Receptors in Antiviral Immunity and Viral Escape.

Bermejo-Jambrina, Marta / Eder, Julia / Helgers, Leanne C / Hertoghs, Nina / Nijmeijer, Bernadien M / Stunnenberg, Melissa / Geijtenbeek, Teunis B H

Frontiers in immunology

2018 Volume 9, Page(s) 590

Abstract: C-type lectin receptors (CLRs) are important pattern recognition receptors involved in recognition and induction of adaptive immunity to pathogens. Certain CLRs play an important role in viral infections as they efficiently interact with viruses. However, ...

Abstract	C-type lectin receptors (CLRs) are important pattern recognition receptors involved in recognition and induction of adaptive immunity to pathogens. Certain CLRs play an important role in viral infections as they efficiently interact with viruses. However, it has become clear that deadly viruses subvert the function of CLRs to escape antiviral immunity and promote infection. In particular, viruses target CLRs to suppress or modulate type I interferons that play a central role in the innate and adaptive defense against viruses. In this review, we discuss the function of CLRs in binding to enveloped viruses like HIV-1 and Dengue virus, and how uptake and signaling cascades have decisive effects on the outcome of infection.
MeSH term(s)	Adaptive Immunity ; Animals ; Antigen Presentation/immunology ; Cell Communication/immunology ; Host-Pathogen Interactions/immunology ; Humans ; Immunity, Innate ; Lectins, C-Type/metabolism ; Lymphocyte Activation/immunology ; Lysosomes/immunology ; Lysosomes/metabolism ; Receptors, Complement/metabolism ; Receptors, Pattern Recognition/metabolism ; T-Lymphocyte Subsets/immunology ; T-Lymphocyte Subsets/metabolism ; Virus Diseases/immunology ; Virus Diseases/metabolism ; Virus Diseases/transmission ; Virus Diseases/virology ; Viruses/immunology
Chemical Substances	Lectins, C-Type ; Receptors, Complement ; Receptors, Pattern Recognition
Keywords	covid19
Language	English
Publishing date	2018-03-26
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2606827-8
ISSN	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2018.00590
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