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1.
Immunology ; 164(2): 348-357, 2021 10.
Article in English | MEDLINE | ID: mdl-34037988

ABSTRACT

Granulocytes mediate broad immunoprotection through phagocytosis, extracellular traps, release of cytotoxic granules, antibody effector functions and recruitment of other immune cells against pathogens. However, descriptions of granulocytes in HIV infection and mucosal tissues are limited. Our goal was to characterize granulocyte subsets in systemic, mucosal and lymphoid tissues during lentiviral infection using the rhesus macaque (RM) model. Mononuclear cells from jejunum, colon, cervix, vagina, lymph nodes, spleen, liver and whole blood from experimentally naïve and chronically SHIVsf162p3-infected RM were analysed by microscopy and polychromatic flow cytometry. Granulocytes were identified using phenotypes designed specifically for RM: eosinophils-CD45+  CD66+  CD49d+ ; neutrophils-CD45+  CD66+  CD14+ ; and basophils-CD45+  CD123+  FcRε+ . Nuclear visualization with DAPI staining and surface marker images by ImageStream (cytometry/microscopy) further confirmed granulocytic phenotypes. Flow cytometric data showed that all RM granulocytes expressed CD32 (FcRγII) but did not express CD16 (FcRγIII). Additionally, constitutive expression of CD64 (FcRγI) on neutrophils and FcRε on basophils indicates the differential expression of Fc receptors on granulocyte subsets. Granulocytic subsets in naïve whole blood ranged from 25·4% to 81·5% neutrophils, 0·59% to 13·3% eosinophils and 0·059% to 1·8% basophils. Interestingly, elevated frequencies of circulating neutrophils, colorectal neutrophils and colorectal eosinophils were all observed in chronic lentiviral disease. Conversely, circulating basophils, jejunal eosinophils, vaginal neutrophils and vaginal eosinophils of SHIVsf162p3-infected RM declined in frequency. Overall, our data suggest modulation of granulocytes in chronic lentiviral infection, most notably in the gastrointestinal mucosae where a significant inflammation and disruption occurs in lentivirus-induced disease. Furthermore, granulocytes may migrate to inflamed tissues during infection and could serve as targets of immunotherapeutic intervention.


Subject(s)
Granulocytes/immunology , Lentivirus Infections/immunology , Macaca mulatta/immunology , Mucous Membrane/immunology , Animals , Basophils/immunology , Basophils/virology , Eosinophils/immunology , Eosinophils/virology , Flow Cytometry/methods , Granulocytes/virology , HIV Infections/immunology , HIV Infections/virology , Leukocyte Count/methods , Mucous Membrane/virology , Neutrophils/immunology , Neutrophils/virology , Receptors, IgG/immunology
2.
Front Immunol ; 11: 601504, 2020.
Article in English | MEDLINE | ID: mdl-33154758

ABSTRACT

Ticks are blood-sucking arthropods of great importance in the medical and veterinary fields worldwide. They are considered second only to mosquitos as vectors of pathogenic microorganisms that can cause serious infectious disorders, such as Lyme borreliosis and tick-borne encephalitis. Hard (Ixodid) ticks feed on host animals for several days and inject saliva together with pathogens to hosts during blood feeding. Some animal species can acquire resistance to blood-feeding by ticks after a single or repeated tick infestation, resulting in decreased weights and numbers of engorged ticks or the death of ticks in subsequent infestations. Importantly, this acquired tick resistance (ATR) can reduce the risk of pathogen transmission from pathogen-infected ticks to hosts. This is the basis for the development of tick antigen-targeted vaccines to forestall tick infestation and tick-borne diseases. Accumulation of basophils is detected in the tick re-infested skin lesion of animals showing ATR, and the ablation of basophils abolishes ATR in mice and guinea pigs, illustrating the critical role for basophils in the expression of ATR. In this review article, we provide a comprehensive overview of recent advances in our understanding of the cellular and molecular mechanisms responsible for the development and manifestation of ATR, with a particular focus on the role of basophils.


Subject(s)
Basophils/immunology , Immunologic Memory , Insect Bites and Stings/immunology , Saliva/immunology , Skin/immunology , Tick-Borne Diseases/prevention & control , Ticks/immunology , Animals , Basophils/microbiology , Basophils/parasitology , Basophils/virology , Histamine/immunology , Histamine Release , Host-Pathogen Interactions , Humans , Immunoglobulin E/immunology , Insect Bites and Stings/microbiology , Insect Bites and Stings/parasitology , Insect Bites and Stings/virology , Saliva/microbiology , Saliva/parasitology , Saliva/virology , Skin/microbiology , Skin/parasitology , Skin/virology , Tick-Borne Diseases/etiology , Tick-Borne Diseases/immunology , Tick-Borne Diseases/transmission , Ticks/microbiology , Ticks/parasitology , Ticks/virology , Vaccination , Vaccines/therapeutic use
3.
Int Arch Allergy Immunol ; 171(3-4): 158-165, 2016.
Article in English | MEDLINE | ID: mdl-27960171

ABSTRACT

The World Health Organization AIDS epidemic update estimates that more than 37 million people are living with HIV infection. Despite the unprecedented success of antiretroviral treatments, significant challenges remain in the fight against HIV. In particular, how uninfected cells capture HIV and transmit virions to target cells remains an unanswered question. Tissue mast cells and peripheral blood basophils can be exposed to virions or HIV products during infection. Several HIV proteins (i.e., envelope glycoproteins gp120 and gp41, Tat, and Nef) can interact with distinct surface receptors expressed by human basophils and mast cells and modulate their functional responses at different levels. Additionally, several groups have provided evidence that human mast cells can be infected in vitro, as well as in vivo, by certain strains of HIV. Recently, it has been demonstrated that basophils purified from healthy donors and intestinal mast cells can efficiently capture HIV on their cell surface and, cocultured with CD4+ T cells, they can transfer the virus to the cocultured cells leading to infection. Direct contact between human basophils or intestinal mast cells and CD4+ T cells can mediate viral trans-infection of T cells through the formation of viral synapses. Thus, basophils and mast cells can provide a cellular basis for capturing and then spreading viruses throughout the body. Collectively, these findings suggest that human basophils and mast cells play a complex and possibly distinct role in HIV infection, warranting further investigations.


Subject(s)
Basophils/immunology , Basophils/metabolism , HIV Infections/etiology , HIV Infections/metabolism , HIV-1/physiology , Mast Cells/immunology , Mast Cells/metabolism , Basophils/virology , Human Immunodeficiency Virus Proteins/immunology , Human Immunodeficiency Virus Proteins/metabolism , Humans , Immune System/cytology , Immune System/immunology , Immune System/metabolism , Mast Cells/virology
4.
J Virol ; 89(15): 8050-62, 2015 Aug.
Article in English | MEDLINE | ID: mdl-26018157

ABSTRACT

UNLABELLED: Cell-associated HIV-1 infection has been proposed to play a pivotal role in the spread of HIV-1 infection. Granulocytes are a category of white blood cells, comprising mainly basophils, neutrophils, and eosinophils, and participate in various inflammatory reactions and defense against pathogens. Here, we investigated the role of human blood granulocytes in the dissemination of HIV-1. These cells were found to express a variety of HIV-1 attachment factors (HAFs). Basophils expressed HAFs dendritic cell (DC)-specific intercellular adhesion molecule 3 (ICAM3)-grabbing nonintegrin (DC-SIGN), DC immunoreceptor (DCIR), heparan sulfate proteoglycan (HSPG), and α4ß7 integrin and mediated the most efficient capture of HIV-1 on the cell surface. Neutrophils were found to express DCIR and demonstrated limited efficiency of viral capture. Eosinophils expressed α4ß7 integrin but exhibited little or no virus-binding capacity. Intriguingly, following direct contact with CD4+ T cells, viruses harbored on the surface of basophils were transferred to T cells. The contact between basophils and CD4+ T cells and formation of infectious synapses appeared necessary for efficient HIV-1 spread. In HIV-1-infected individuals, the frequency of basophils remained fairly stable over the course of disease, regardless of CD4+ T depletion or the emergence of AIDS-associated opportunistic infections. Collectively, our results provide novel insights into the roles of granulocytes, particularly basophils, in HIV-1 dissemination. Thus, strategies designed to prevent basophil-mediated viral capture and transfer may be developed into a new form of therapy. IMPORTANCE: Cell-associated HIV-1 infection has been proposed to play a pivotal role in the spread of HIV-1 infection. Here, we demonstrated that human blood-circulating granulocytes, particularly basophils, can capture HIV-1 and mediate viral trans-infection of CD4+ T cells. The expression of a variety of HIV-1 attachment factors, such as the C-type lectins, etc., facilitates viral capture and transfer. Intriguingly, the frequency of basophils in patients with different levels of CD4+ T counts remains fairly stable during the course of disease. Our results provide novel insights into the roles of granulocytes, particularly basophils, in HIV-1 dissemination. We suggest that strategies designed to prevent basophil-mediated viral capture and transfer may be a new direction for the development of anti-HIV therapy.


Subject(s)
Basophils/virology , CD4-Positive T-Lymphocytes/virology , HIV Infections/virology , HIV-1/physiology , Basophils/metabolism , CD4-Positive T-Lymphocytes/metabolism , Cells, Cultured , HIV Envelope Protein gp120/genetics , HIV Envelope Protein gp120/metabolism , HIV Infections/genetics , HIV Infections/metabolism , HIV-1/genetics , Humans , Receptors, Virus/genetics , Receptors, Virus/metabolism
5.
J Allergy Clin Immunol ; 130(2): 489-95, 2012 Aug.
Article in English | MEDLINE | ID: mdl-22766097

ABSTRACT

BACKGROUND: Children with allergic asthma have more frequent and severe human rhinovirus (HRV)-induced wheezing and asthma exacerbations through unclear mechanisms. OBJECTIVE: We sought to determine whether increased high-affinity IgE receptor (FcεRI) expression and cross-linking impairs innate immune responses to HRV, particularly in allergic asthmatic children. METHODS: PBMCs were obtained from 44 children, and surface expression of FcεRI on plasmacytoid dendritic cells (pDCs), myeloid dendritic cells, monocytes, and basophils was assessed by using flow cytometry. Cells were also incubated with rabbit anti-human IgE to cross-link FcεRI, followed by stimulation with HRV-16, and IFN-α and IFN-λ1 production was measured by Luminex. The relationships among FcεRI expression and cross-linking, HRV-induced IFN-α and IFN-λ1 production, and childhood allergy and asthma were subsequently analyzed. RESULTS: FcεRIα expression on pDCs was inversely associated with HRV-induced IFN-α and IFN-λ1 production. Cross-linking FcεRI before HRV stimulation further reduced PBMC IFN-α (47% relative reduction; 95% CI, 32% to 62%; P< .0001) and IFN-λ1 (81% relative reduction; 95% CI, 69% to 93%; P< .0001) secretion. Allergic asthmatic children had higher surface expression of FcεRIα on pDCs and myeloid dendritic cells when compared with that seen in nonallergic nonasthmatic children. Furthermore, after FcεRI cross-linking, allergic asthmatic children had significantly lower HRV-induced IFN responses than allergic nonasthmatic children (IFN-α, P= .004; IFN-λ1, P= .02) and nonallergic nonasthmatic children (IFN-α, P= .002; IFN-λ1, P= .01). CONCLUSIONS: Allergic asthmatic children have impaired innate immune responses to HRV that correlate with increased FcεRI expression on pDCs and are reduced by FcεRI cross-linking. These effects likely increase susceptibility to HRV-induced wheezing and asthma exacerbations.


Subject(s)
Asthma/immunology , Immunity, Innate/genetics , Picornaviridae Infections/immunology , Receptors, IgE/immunology , Respiratory Sounds/immunology , Antibodies, Anti-Idiotypic/immunology , Antibodies, Anti-Idiotypic/pharmacology , Antibodies, Neutralizing/immunology , Antibodies, Neutralizing/pharmacology , Asthma/genetics , Asthma/virology , Basophils/metabolism , Basophils/pathology , Basophils/virology , Child , Dendritic Cells/metabolism , Dendritic Cells/pathology , Dendritic Cells/virology , Female , Flow Cytometry , Gene Expression , Humans , Interferon-alpha/biosynthesis , Interferon-alpha/immunology , Interferons , Interleukins/biosynthesis , Interleukins/immunology , Male , Monocytes/metabolism , Monocytes/pathology , Monocytes/virology , Picornaviridae Infections/genetics , Picornaviridae Infections/virology , Receptors, IgE/genetics , Respiratory Sounds/genetics , Rhinovirus/immunology
6.
J Immunol ; 183(3): 2016-26, 2009 Aug 01.
Article in English | MEDLINE | ID: mdl-19587017

ABSTRACT

IL-4 contributes to immunopathology induced in mice by primary respiratory syncytial virus (RSV) infection. However, the cellular source of IL-4 in RSV infection is unknown. We identified CD3(-)CD49b(+) cells as the predominant source of IL-4 in the lungs of RSV-infected BALB/c mice. We ruled out T cells, NK cells, NKT cells, mast cells, and eosinophils as IL-4 expressors in RSV infection by flow cytometry. Using IL4 GFP reporter mice (4get) mice, we identified the IL-4-expressing cells in RSV infection as basophils (CD3(-)CD49b(+)FcepsilonRI(+)c-kit(-)). Because STAT1(-/-) mice have an enhanced Th2-type response to RSV infection, we also sought to determine the cellular source and role of IL-4 in RSV-infected STAT1(-/-) mice. RSV infection resulted in significantly more IL-4-expressing CD3(-)CD49b(+) cells in the lungs of STAT1(-/-) mice than in BALB/c mice. CD49b(+)IL-4(+) cells sorted from the lungs of RSV-infected STAT1(-/-) mice and stained with Wright-Giemsa had basophil characteristics. As in wild-type BALB/c mice, IL-4 contributed to lung histopathology in RSV-infected STAT1(-/-) mice. Depletion of basophils in RSV-infected STAT1(-/-) mice reduced lung IL-4 expression. Thus, we show for the first time that a respiratory virus (RSV) induced basophil accumulation in vivo. Basophils were the primary source of IL-4 in the lung in RSV infection, and STAT1 was a negative regulator of virus-induced basophil IL-4 expression.


Subject(s)
Basophils/virology , Gene Expression Regulation , Interleukin-4/genetics , Lung/metabolism , Respiratory Syncytial Virus Infections/immunology , STAT1 Transcription Factor/physiology , Animals , Basophils/metabolism , Basophils/pathology , Flow Cytometry , Immunophenotyping , Lung/pathology , Mice , Mice, Inbred BALB C
7.
J Immunol ; 175(7): 4441-9, 2005 Oct 01.
Article in English | MEDLINE | ID: mdl-16177086

ABSTRACT

Human and rodent CD200 are recognized by the inhibitory CD200R, and these molecules play an important role in the regulation of the immune system. Several viruses, such as human herpesvirus-6 (HHV-6), HHV-7, and HHV-8, possess a CD200 homologue, suggesting that these viruses regulate the immune response via CD200R. In this study, we analyzed the effect of human CD200 and the viral CD200 homologues on human CD200R-expressing cells. We found that human CD200R is predominantly expressed on basophils in amounts higher than on other human peripheral blood leukocytes. Furthermore, the viral CD200 homologues as well as human CD200 were recognized by human CD200R, and the activation of basophils was down-regulated by these CD200 proteins. These results suggested that CD200R is an important regulatory molecule of basophil activation. In addition, the presence of CD200 homologues on several viruses suggests a potentially unique relationship between basophil function and viral infection.


Subject(s)
Antigens, CD/physiology , Antigens, Surface/physiology , Basophils/immunology , Basophils/virology , Down-Regulation/immunology , Herpesvirus 8, Human/immunology , Molecular Mimicry/immunology , Receptors, Cell Surface/physiology , Viral Proteins/physiology , Animals , Antigens, CD/genetics , Basophils/metabolism , Cell Line , Cell Line, Tumor , Herpesvirus 6, Human/immunology , Herpesvirus 7, Human/immunology , Humans , Killer Cells, Natural/physiology , Lymphocyte Activation/immunology , Membrane Glycoproteins/genetics , Membrane Glycoproteins/physiology , Mice , Orexin Receptors , Transfection , Viral Proteins/genetics
8.
J Immunol ; 168(8): 4127-34, 2002 Apr 15.
Article in English | MEDLINE | ID: mdl-11937573

ABSTRACT

AIDS patients often contain HIV-1-infected mast cells (MCs)/basophils in their peripheral blood, and in vivo-differentiated MCs/basophils have been isolated from the blood of asthma patients that are HIV-1 susceptible ex vivo due to their surface expression of CD4 and varied chemokine receptors. Because IL-16 is a ligand for CD4 and/or an undefined CD4-associated protein, the ability of this multifunctional cytokine to regulate the development of human MCs/basophils from nongranulated progenitors residing in cord or peripheral blood was evaluated. After 3 wk of culture in the presence of c-kit ligand, IL-16 induced the progenitors residing in the blood of normal individuals to increase their expression of chymase and tryptase about 20-fold. As assessed immunohistochemically, >80% of these tryptase(+) and/or chymase(+) cells expressed CD4. The resulting cells responded to IL-16 in an in vitro chemotaxis assay, and this biologic response could be blocked by anti-IL-16 and anti-CD4 Abs as well as by a competitive peptide inhibitor corresponding to a sequence in the C-terminal domain of IL-16. The additional finding that IL-16 induces calcium mobilization in the HMC-1 cell line indicates that IL-16 acts directly on MCs and their committed progenitors. IL-16-treated MCs/basophils also are less susceptible to infection by an M/R5-tropic strain of HIV-1. Thus, IL-16 regulates MCs/basophils at a number of levels, including their vulnerability to retroviral infection.


Subject(s)
Basophils/immunology , Basophils/virology , HIV-1/immunology , Interleukin-16/physiology , Mast Cells/immunology , Mast Cells/virology , Antiviral Agents/physiology , Basophils/cytology , Calcium/metabolism , Calcium Signaling/immunology , Cell Differentiation/immunology , Cells, Cultured , Chemotaxis, Leukocyte/immunology , Fetal Blood/cytology , Fetal Blood/immunology , HIV Infections/immunology , HIV Infections/prevention & control , HIV-1/growth & development , Humans , Immunity, Innate/immunology , Interleukin-16/blood , Mast Cells/cytology , Stem Cells/cytology , Stem Cells/immunology , Tumor Cells, Cultured , Virus Replication/immunology
9.
Int Arch Allergy Immunol ; 125(2): 89-95, 2001 Jun.
Article in English | MEDLINE | ID: mdl-11435725

ABSTRACT

HIV-1 gp120 interacts with IgE V(H)3(+) on the surface of human basophils and mast cells (Fc epsilon RI(+) cells), acting as a viral immunoglobulin superantigen. gp120 from different clades induces mediator release from Fc epsilon RI(+) cells. gp120 also induces IL-4 and IL-13 synthesis in human basophils. The chemokine receptors CCR3 and CXCR4, which are coreceptors of HIV-1 infection, are expressed by human Fc epsilon RI(+) cells. HIV-1 Tat protein is a potent chemoattractant for basophils and lung mast cells, interacting with CCR3. Incubation of basophils with Tat protein upregulates the surface expression of the CCR3 receptor. There is evidence that human Fc epsilon RI(+) cells could be infected in vitro by M-tropic HIV-1 strains.


Subject(s)
Basophils/virology , HIV Envelope Protein gp120/physiology , HIV Infections/immunology , HIV-1/physiology , Mast Cells/virology , Receptors, Chemokine/physiology , Receptors, IgE/physiology , Basophils/metabolism , Chemotaxis , Gene Expression Regulation, Viral , Gene Products, tat/pharmacology , Gene Products, tat/physiology , HIV Envelope Protein gp120/immunology , HIV Infections/virology , HIV-1/immunology , Histamine Release , Humans , Immunoglobulin E/biosynthesis , Immunoglobulin E/genetics , Interleukin-13/biosynthesis , Interleukin-4/biosynthesis , Macromolecular Substances , Mast Cells/metabolism , Receptors, CCR3 , Receptors, CXCR4/biosynthesis , Receptors, CXCR4/genetics , Receptors, CXCR4/physiology , Receptors, Chemokine/biosynthesis , Receptors, Chemokine/genetics , Superantigens/immunology , Th1 Cells/immunology , Th2 Cells/immunology , Virus Replication , tat Gene Products, Human Immunodeficiency Virus
10.
Blood ; 97(11): 3484-90, 2001 Jun 01.
Article in English | MEDLINE | ID: mdl-11369641

ABSTRACT

A population of metachromatic cells with mast cell (MC) and basophil features was identified recently in the peripheral blood of patients with several allergic disorders. This study now shows that these metachromatic cells express on their surface the high-affinity IgE receptor (FcepsilonRI), CD4, and the chemokine receptors CCR3, CCR5, and CXCR4, but not the T-cell surface protein CD3 and the monocyte/macrophage surface protein CD68. This population of MCs/basophils can be maintained ex vivo for at least 2 weeks, and a comparable population of cells can be generated in vitro from nongranulated hematopoietic CD3(-)/CD4(+)/CD117(-) progenitors. Both populations of MCs/basophils are susceptible to an M-tropic strain of human immunodeficiency virus 1 (HIV-1). Finally, many patients with acquired immunodeficiency syndrome have HIV-1-infected MCs/basophils in their peripheral blood. Although it is well known that HIV-1 can infect CD4(+) T cells and monocytes, this finding is the first example of a human MC or basophil shown to be susceptible to the retrovirus. (Blood. 2001;97:3484-3490)


Subject(s)
Basophils/virology , CD4 Antigens/analysis , HIV-1/physiology , Hypersensitivity/virology , Mast Cells/virology , Receptors, Chemokine/analysis , Acquired Immunodeficiency Syndrome/immunology , Animals , Asthma/blood , Asthma/immunology , Asthma/virology , Basophils/immunology , Cells, Cultured , Disease Susceptibility , Humans , Hypersensitivity/blood , Hypersensitivity/immunology , Mast Cells/immunology , Mice , Receptors, CCR3 , Receptors, CCR5/analysis , Receptors, CXCR4/analysis
11.
Immunol Rev ; 179: 128-38, 2001 Feb.
Article in English | MEDLINE | ID: mdl-11292016

ABSTRACT

Enhanced serum IgE levels in adults and children with HIV-1 infection could be a marker of poor prognosis. HIV-1 infection is believed to involve a switch toward a "TH2-like" cytokine pattern. HIV-1 gp120 from different clades is a potent stimulus for histamine release from human basophils and mast cells. Gp120 also induces IL-4 and IL-13 synthesis from basophils. It functions as a viral superantigen by interacting with the VH3 region of IgE to induce mediator release from human FcepsilonRI+ cells. The chemokine receptor CCR3, which binds the chemokines eotaxin and RANTES, is expressed by basophils and lung mast cells. By interacting with the CCR3 receptor on FcepsilonRI+ cells, HIV-1 Tat protein is a potent chemoattractant for basophils and lung mast cells. Tat protein also induces IL-4 and IL-13 release from basophils. Incubation of basophils with Tat protein upregulates the surface expression of the CCR3 receptor, a co-receptor of HIV-1 infection. Extracellular Tat affects the directional migration of human FcepsilonRI+ cells, CCR3 expression and TH2 cytokines release. We have shown that HIV-1 proteins gp120 and Tat trigger the release of cytokines critical for TH2 polarization from FcepsilonRI+ cells through two distinct mechanisms. In addition, Tat upregulates the beta-chemokine receptor CCR3, making FcepsilonRI+ cells more susceptible to infection with CCR3 tropic HIV-1 isolates.


Subject(s)
Basophils/immunology , Chemokines, CC , HIV Infections/immunology , Mast Cells/immunology , Receptors, IgE/immunology , Antibodies, Monoclonal/pharmacology , Antigen-Antibody Reactions , B-Lymphocytes/immunology , Basophils/metabolism , Basophils/virology , Binding Sites , Cells, Cultured , Chemokine CCL11 , Chemotaxis , Cytokines/metabolism , Cytokines/pharmacology , Gene Products, tat/physiology , HIV Antibodies/pharmacology , HIV Envelope Protein gp120/chemistry , HIV Envelope Protein gp120/physiology , HIV-1/genetics , HIV-1/isolation & purification , HIV-1/physiology , Humans , Immunoglobulin M/pharmacology , Interleukin-13/metabolism , Interleukin-3/pharmacology , Interleukin-4/metabolism , Mast Cells/drug effects , Mast Cells/metabolism , Mast Cells/virology , Th1 Cells/immunology , Th1 Cells/metabolism , Th2 Cells/immunology , Th2 Cells/metabolism , tat Gene Products, Human Immunodeficiency Virus
12.
J Virol ; 74(15): 7146-50, 2000 Aug.
Article in English | MEDLINE | ID: mdl-10888655

ABSTRACT

We report here the first demonstration of dengue virus infection and vasoactive cytokine response of a cell of the mast cell/basophil lineage. Infection of KU812 cells was dependent on dengue-specific antibody and gave rise to infectious virions. This antibody-enhanced dengue virus infection triggered a four- to fivefold increase in the release of interleukin-1beta (IL-1beta) and a modest increase for IL-6 but not for an alternate cytokine, granulocyte-macrophage colony-stimulating factor. The results suggest a potential role for mast cells/basophils in the pathogenesis of dengue virus-induced disease.


Subject(s)
Antibodies, Viral/immunology , Basophils/virology , Dengue Virus/pathogenicity , Interleukin-1/metabolism , Interleukin-6/metabolism , Mast Cells/virology , Animals , Basophils/immunology , Cell Line , Chlorocebus aethiops , Dengue Virus/immunology , Humans , Mast Cells/immunology , Vero Cells , Virion/physiology
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