Activated peripheral lymphocytes with increased expression of cell adhesion molecules and cytotoxic markers are associated with dengue fever disease

Azeredo, Elzinandes Leal de; Zagne, S.M.O.; Alvarenga, Allan R.; Nogueira, Rita Maria Ribeiro; Kubelka, Claire Fernandes; Oliveira-Pinto, Luzia Maria de

doi:10.1590/s0074-02762006000400016

Cited by 44 publications

(51 citation statements)

References 44 publications

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“…The absolute CD4+ T-lymphocyte count differed significantly among days of fever (p<0.05). Unlike our study, Azeredo et al 7 reported that the mean percentage of CD4+ T-cells was reduced during acute phase of dengue infection and its absolute cell counts decreased when compared to controls. This did not return to normal level until the convalesence period.…”

Section: Discussioncontrasting

confidence: 99%

Kinetics of CD4+ T-Lymphocyte in Dengue Virus Infection

Laksono¹,

Intansari²

2014

mkb

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Cellular immunity plays an important role in viral infection. The activation of effector T-lymphocytes and the release of cytokines define the course of dengue viral infection. CD4+ T-lymphocyte induces the immunopathology via various mechanisms; however, its kinetics in different onset of fever and disease severity are not fully understood. This study was conducted to observe the kinetics of CD4 + T-lymphocyte level among dengue infected patients and to obtain the absolute cell count and relative percentage of CD4 + T-lymphocyte. This was a descriptive study on thirty six patients who met the WHO-1997 criteria of dengue infection, hospitalized in Dr. Sardjito Hospital in the period of March to May 2009. The CD4 + T-lymphocytes were examined using the flow cytometer. The significance of median CD4 + T-lymphocytes among days were assessed using Kruskal-Wallis and Mann-Whitney SPSS 11 for Window. The absolute CD4 + T-lymphocyte was significantly different among days (p<0.05) between DF and DHF patients, while the relative CD4 + percentage count was not different (p>0.05). The absolute CD4 + T-lymphocytes count was low in the beginning of the disease course and increased from the 2nd day of fever to the normal level on the 7th day. In conclusion, DF and DHF do not differ in the absolute CD4 + T-lymphocytes count as well as in the relative CD4+ T-lymphocytes percentage. [MKB. 2014;46(4)

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Section: Discussioncontrasting

confidence: 99%

Kinetics of CD4+ T-Lymphocyte in Dengue Virus Infection

Laksono¹,

Intansari²

2014

mkb

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“…Herein we showed that endogenously activated PF-derived NK cells express increased amounts of ICAM-1 and LFA-1 molecules, as has been observed in peripheral lymphocytes from other inflammatory diseases [32][33][34]. Furthermore, we observed differential expression of ICAM-1 and LFA-1, which is consistent with the functional divergent activities of CD56 bright and CD56 dim subsets [7].…”

Section: Discussionsupporting

confidence: 85%

“…The role of ICAM-1 has been widely studied in APC and endothelial cells, however, little is known about its expression and function on human lymphocytes in an inflammatory context [31][32][33][34]. To address this, we evaluated ICAM-1 expression on lymphocyte subpopulations in PBMC and PF mononuclear cells (PFMC) from patients with tuberculous pleurisy (TB-PF).…”

Section: Nk Cells From Tuberculous Pleural Fluid Express High Icam-1 mentioning

confidence: 99%

NK cells from tuberculous pleurisy express high ICAM‐1 levels and exert stimulatory effect on local T cells

et al. 2009

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Tuberculous pleurisy, one of the most common manifestations of extrapulmonary tuberculosis, is characterized by a T-cell-mediated hypersensitivity reaction along with a Th1 immune profile. In this study, we investigated functional cross-talk among T and NK cells in human tuberculous pleurisy. We found that endogenously activated pleural fluidderived NK cells express high ICAM-1 levels and induce T-cell activation ex vivo through ICAM-1. Besides, upon in vitro stimulation with monokines and PAMP, resting peripheral blood NK cells increased ICAM-1 expression leading to cellular activation and Th1 polarization of autologous T cells. Furthermore, these effects were abolished by anti-ICAM-1 Ab. Hence, NK cells may contribute to the adaptive immune response by a direct cellcontact-dependent mechanism in the context of Mycobacterium tuberculosis infection.Key words: ICAM-1 . NK cells . Pleurisy . Th1 . Tuberculosis Supporting Information available online IntroductionPleuritis is the most frequent clinical manifestation of extrapulmonary tuberculosis (TB) among young adults, and is normally considered a relatively benign form of disease since it may resolve without chemotherapy [1]. Tuberculous pleurisy is caused by a severe delayed-type hypersensitivity reaction in response to the rupture of a subpleural focus of Mycobacterium tuberculosis (Mtb) infection, but it may also be developed as a complication of primary pulmonary TB [2,3]. This pleural effusion is characterized by a strong granulomatous inflammatory response to Mtb together with high levels of . NK cells are CD56 1 CD16 1/À /CD3 À CD19 À lymphocytes of the innate immune system whose function is controlled by an array of germline-encoded activator/inhibitory receptors [5,6]. Two subsets of NK cells have been identified in humans according to CD56 expression differing in phenotype and function, and also in terms of chemokine receptors and adhesion molecules expression [7,8,9]. Functionally, CD56 bright cells are effective cytokine producers, whereas CD56 dim cells are efficient effectors of natural and Ab-dependent target cell lysis. Recently, we have described that an endogenously activated pleural fluid NK (PF-NK) population is a major source of IFN-g in response to Mtb [10,11]. Consistently, PF-NK are enriched in CD56 bright cells, as has been observed in other chronic inflammatory sites [12,13] or in tumor-affected tissues [14]. Together with the classical NK functions (i.e. cytotoxicity and cytokine production), novel skills have recently been described in niche-specific and in vitro-activated human NK cells. These unconventional capabilities include [16,17,18] and direct pathogen recognition [19,20]. In this regard, a novel innate immune cell population called Interferon-producing killer dendritic cells has been recently described in mice [21,22].ICAM-1/CD54 is the major ligand of costimulatory a L b 2 integrin (CD11a/CD18), commonly known as lymphocyte function-associated antigen (LFA-1) [23,24]. The surface enhancement of ICAM-1 on endothelial, APC and...

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“…in CD8 positive T-lymphocytes from dengue patients, which presented low levels of Bcl-2 (Azeredo et al 2006). The present data suggest that other anti-apoptotic proteins, such as Bcl-xL, might be negatively regulated during infection in monocytes.…”

Section: Discussionmentioning

confidence: 99%

Dengue-2 infection and the induction of apoptosis in human primary monocytes

Torrentes-Carvalho

Azeredo

Reis

et al. 2009

Mem. Inst. Oswaldo Cruz

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Monocytes/macrophages are important targets for dengue virus (DENV) replication; they induce inflammatory mediators and are sources of viral dissemination in the initial phase of the disease. Apoptosis is an active process of cellular destruction genetically regulated, in which a complex enzymatic pathway is activated and may be trigged by many viral infections. Since the mechanisms of apoptotic induction in DENV-infected target cells are not yet defined, we investigated the virus-cell interaction using a model of primary human monocyte infection with DENV-2 with the aim of identifying apoptotic markers. Cultures analyzed by flow cytometry and confocal microscopy yielded DENV antigen positive cells with rates that peaked at the second day post infection (p.i.), decayed afterwards and produced the apoptosis-related cytokines TNF-α and IL-10. Phosphatidylserine, an early marker for apoptosis, was increased at the cell surface and the Fas death receptor was upregulated at the second day p.i. at significantly higher rates in DENV infected cell cultures than controls. However, no detectable changes were observed in the expression of the anti-apoptotic protein Bcl-2 in infected cultures. Our data support virus modulation of extrinsic apoptotic factors in the in vitro model of human monocyte DENV-2 infection. DENV may be interfering in activation and death mechanisms by inducing apoptosis in target cells.Key words: dengue -apoptosis -monocytes -human The dengue fever emergency has become one of the most dramatic public health issues in Latin America. Epidemics are presenting increased severity and frequency and are continuously expanding geographically (Gubler 2002). In Brazil, the disease is endemic and during the last five years the region has accounted for 70% reported cases in the Americas (Nogueira et al. 2007). Infection with the Dengue virus (DENV) causes a disease spectrum ranging from asymptomatic to shock and hemorrhages, with a risk of lethality. Acute vascular permeability may be followed by abnormal vascular homeostasis. Clinical manifestations include plasmatic leakage, bleeding tendency and liver commitment followed by mild seric transaminase elevation. The physiopathology of the disease may be explained as result of infected monocyte activation by the production of factors that act to increase the vascular permeability and disturb the coagulation system. Pleural effusion, ascites and hemoconcentration are signs of intravascular volume loss. Such factors promote rapid progression to shock (Gibbons & Vaughn 2002).Mononuclear phagocytes are considered the main targets for viral replication (Jessie et al. 2004, NevesSouza et al. 2005). Cells such as B lymphocytes, monocytes, hepatocytes and dendritic cells are described as potential virus targets and may undergo programmed cell death when infected in culture. Reports show apoptotic induction in DENV infected endothelial cells elevates IL-8 and RANTES production, which are chemokines related to inflammatory processes during cell migration (Avirutnan et al. 1...

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Activated peripheral lymphocytes with increased expression of cell adhesion molecules and cytotoxic markers are associated with dengue fever disease

Abstract: The immune mechanisms involved in dengue fever and dengue hemorrhagic/dengue shock syndrome are not well understood. The

Cited by 44 publications

References 44 publications

Kinetics of CD4+ T-Lymphocyte in Dengue Virus Infection

Kinetics of CD4+ T-Lymphocyte in Dengue Virus Infection

NK cells from tuberculous pleurisy express high ICAM‐1 levels and exert stimulatory effect on local T cells

Dengue-2 infection and the induction of apoptosis in human primary monocytes

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