Publications by authors named "Véronique Olislagers"

6 Publications

  • Page 1 of 1

Predictive factors of smell recovery in a clinical series of 288 coronavirus disease 2019 patients with olfactory dysfunction.

Eur J Neurol 2021 Jun 22. Epub 2021 Jun 22.

Institute for Medical Immunology, Université libre de Bruxelles, Charleroi, Belgium.

Background And Purpose: The aim was to evaluate potential predictive factors of smell recovery in a clinical series of 288 patients presenting olfactory dysfunction (OD) related to coronavirus disease 2019 (COVID-19). Potential correlations were sought between epidemiological, clinical and immunological characteristics of patients and the persistence of OD at 60 days.

Methods: COVID-19 positive patients presenting OD were prospectively recruited from three European hospitals. Baseline clinical and olfactory evaluations were performed within the first 2 weeks after OD onset and repeated at 30 and 60 days. In a subgroup of patients, anti-severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) antibodies were measured in serum, saliva and nasal secretions at 60 days.

Results: A total of 288 COVID-19 patients with OD were included in the study. Two weeks after the onset of the loss of smell, 52.4% of patients had OD on psychophysical tests, including 113 cases (39.2%) of anosmia and 38 cases (13.2%) of hyposmia. At 60-day follow-up, 25.4% of the patients presented persistent OD. There was no significant correlation between sex, age, viral load on nasopharyngeal swab or COVID-19 severity and poor olfactory outcome. In a subgroup of 63 patients, it was demonstrated that patients with poor olfactory outcomes at 60 days had lower levels of salivary and nasal immunoglobulin G (IgG) and IgG1, but similar levels of antibodies in the serum.

Conclusions: No clinical markers predicted the evolution of OD at 60 days. Patients with poor olfactory outcome at 60 days had lower saliva and nasal antibodies, suggesting a role for local immune responses in the persistence of COVID-19 related OD.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1111/ene.14994DOI Listing
June 2021

Functional Exhaustion Limits CD4+ and CD8+ T-Cell Responses to Congenital Cytomegalovirus Infection.

J Infect Dis 2015 Aug 5;212(3):484-94. Epub 2015 Feb 5.

Institute for Medical Immunology, Université Libre de Bruxelles, Charleroi ImmuneHealth, Gosselies, Belgium.

Background: Cytomegalovirus (CMV) infection during fetal life causes severe symptoms and is associated with prolonged viral excretion. Previous studies reported low CD4(+) T-cell responses to CMV infection in early life, contrasting with large responses of effector CD8(+) T cells. The mechanisms underlying the defective CD4(+) T-cell responses and the possible dissociation with CD8(+) T-cell responses have not been clarified.

Methods: The magnitude and the quality of the fetal CD8(+) and CD4(+) T-cell responses to CMV infection were compared to those of adults with primary or chronic infection.

Results: In utero CMV infection induced oligoclonal expansions of fetal CD4(+) and CD8(+) T lymphocytes expressing a T-helper type 1 or Tc1 effector phenotype similar to that of adult CMV-specific cells. However, the effector cytokine responses and the polyfunctionality of newborn CD4(+) and CD8(+) T cells were markedly lower than those of adult cells. This reduced functionality was associated with a higher expression of the programmed death 1 inhibitory receptor, and blockade of this receptor increased newborn T-cell responses.

Conclusions: Functional exhaustion limits effector CD4(+) and CD8(+) T-lymphocyte responses to CMV during fetal life.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1093/infdis/jiv071DOI Listing
August 2015

Functional exhaustion of CD4+ T lymphocytes during primary cytomegalovirus infection.

J Immunol 2012 Sep 3;189(5):2665-72. Epub 2012 Aug 3.

Institute for Medical Immunology, Université Libre de Bruxelles, 6041 Charleroi, Belgium.

Human CMV establishes lifelong persistence after primary infection. Chronic CMV infection is associated with intermittent viral reactivation inducing high frequencies of CD4+ T lymphocytes with potent antiviral and helper properties. Primary CMV infection is characterized by an intense viral replication lasting for several months. The impact of this prolonged exposure to high Ag loads on the functionality of CD4+ T cells remains incompletely understood. In pregnant women with primary CMV infection, we observed that CMV-specific CD4+ T lymphocytes had a decreased capacity to proliferate and to produce IL-2. A very large proportion of CMV-specific CD4+ T cells had downregulated the expression of CD28, a costimulatory molecule centrally involved in the production of IL-2. Unexpectedly, both CD28+ and CD28+ CD4+ T cells produced low levels of IL-2. This defective production of IL-2 was part of a larger downregulation of cytokine production. Indeed, CMV-specific CD4+ T cells produced lower amounts of IFN-γ and TNF-α and showed lower functional avidity during primary as compared with chronic infection. Increased programmed death-1 expression was observed in CD28+ CMV-specific CD4+ T cells, and programmed death-1 inhibition increased proliferative responses. These results indicate that primary CMV infection is associated with the exhaustion of CMV-specific CD4+ T cells displaying low functional avidity for viral Ags.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.4049/jimmunol.1101165DOI Listing
September 2012

Impaired responses to toll-like receptor 4 and toll-like receptor 3 ligands in human cord blood.

J Autoimmun 2003 Nov;21(3):277-81

Laboratory of Experimental Immunology, Université Libre de Bruxelles, 808, Route de Lennik, B-1070, Brussels, Belgium.

Toll-like receptor (TLR)-4 signaling pathway plays an essential role in host defense against gram-negative bacteria while TLR-3-mediated signaling is critically involved in anti-viral immunity. To gain insight into the defects responsible for impaired Th1 responses in human newborns, we investigated the responses of human cord blood cells to lipopolysaccharide, LPS, and to polyinosinic-polycytidylic acid, Poly (I:C), ligands of TLR-4 and TLR-3, respectively. Measurement of cytokine levels revealed a profound defect in IL-12 (p70) synthesis and an increased release of IL-10 in cord blood exposed to LPS or Poly (I:C), as compared to adult blood. Moreover, Poly (I:C)-induced IFN-alpha production was found to be significantly impaired in cord blood. Phenotypic maturation of myeloid DC in response to LPS or Poly (I:C) was next compared in cord and adult blood. We observed that neonatal myeloid DC displayed decreased upregulation of CD40, CD80 whereas CD86 and HLA-DR upregulation did not differ significantly between adults and neonates. Taken together, these findings might be relevant to the increased vulnerability of human newborns to intracellular pathogens and to their inability to develop efficient Th1-type responses.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.jaut.2003.08.003DOI Listing
November 2003

Blood plasmacytoid dendritic cell responses to CpG oligodeoxynucleotides are impaired in human newborns.

Blood 2004 Feb 22;103(3):1030-2. Epub 2003 Sep 22.

Hôpital Erasme-Department of Immunology, 808, Route de Lennik, B-1070 Brussels, Belgium.

Plasmacytoid dendritic cells (pDCs) respond to unmethylated cytosine-phosphate-guanosine (CpG) motifs present in bacterial DNA or unmethylated synthetic oligodeoxynucleotides (CpG). In order to assess the function of pDCs in human newborns, interferon-alpha (IFN-alpha) production induced by CpG 2216 and phenotypic maturation of pDCs in response to CpG 2006 were compared in cord blood and adult blood. We first observed that neonatal pDCs displayed decreased up-regulation of CD80, CD83, CD86, and CD40, whereas HLA-DR and CD54 up-regulation did not differ significantly between adults and neonates. We then found that the production of IFN-alpha in response to CpG was dramatically impaired in cord blood. This neonatal defect was detected both at protein and mRNA levels and was still present in blood of 4-day-old babies. Further experiments on enriched pDCs confirmed that these cells are intrinsically deficient in CpG-induced IFN-alpha production at birth. These findings might be relevant to the increased susceptibility of human newborns to infections as well as to the use of CpG oligodeoxynucleotides as vaccine adjuvants in the neonatal period.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1182/blood-2003-04-1216DOI Listing
February 2004

Human gamma delta T cells induce dendritic cell maturation.

Clin Immunol 2002 Jun;103(3 Pt 1):296-302

Laboratoire d'Immunologie Expérimentale, Université Libre de Bruxelles, Brussels, Belgium.

gamma delta T cells are known to be involved in the innate immune defenses against infectious microorganisms. Herein, we considered that gamma delta T cells could also influence adaptative immunity by interacting with dendritic cells (DC) in the early phase of the immune response. To investigate this hypothesis, gamma delta T cells isolated from the peripheral blood of healthy volunteers were cocultured with autologous monocyte-derived dendritic cells, which were subsequently analyzed for their expression of key surface molecules and for their production of IL-12. First, we found that gamma delta T cells induced the upregulation of HLA-DR, CD86, and CD83 on DC. This effect did not require cell to cell contact and could be blocked by a neutralizing anti-TNF antibody. We then observed that gamma delta T cells activated by the synthetic phosphoantigen bromohydrin pyrophosphate (BrHPP) induced the production of IL-12 (p40) and IL-12 (p70) by DC, an effect that involved IFN-gamma production. The relevance of this finding to DC function was demonstrated by the increased production of IFN-gamma by alloreactive T cells when stimulated in a mixed leucocyte reaction with DC preincubated with activated gamma delta T cells. We conclude that gamma delta T cell activation might result in DC maturation and thereby in enhanced alpha beta T cell responses.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1006/clim.2002.5218DOI Listing
June 2002
-->