Expression of lymphocyte activation markers CD 54 (ICAM-1), CD 5, CD 95 (FAS) and neutrophil activation marker CD15 in the peripheral blood of patients with intermediate uveitis and healthy individuals

ObjectiveNeutrophils contribute to the SLE pathogenesis. Neutrophil to lymphocyte ratio (NLR) is reported to correlate with disease activity in SLE. The aim of the study was to evaluate whether NLR reflects underlying immunopathogenic activity in SLE, as well as to determine the contribution of each component of NLR, neutrophil and lymphocyte count.MethodsData were obtained from a cohort of patients with SLE (n=141) recruited at Lund University, Sweden. NLR levels were compared between patients with SLE and healthy controls (n=79). The relationship between NLR and clinical and immunological markers was examined using Mann-Whitney U test and logistic regression analysis. High NLR was defined as above the 90th percentile of healthy individuals.ResultsPatients with SLE had elevated neutrophil count (p=0.04) and reduced lymphocyte count (p<0.0001), resulting in elevated NLR as compared with healthy controls (p<0.0001). Patients with high NLR had more active disease, and were more frequently on prednisone use and immunosuppressive medicines. High NLR was associated with immune complex (IC)-driven disease with presence of antidouble-stranded DNA antibodies (p=0.006), circulating ICs (p=0.02) and type I interferon (IFN) activity (p=0.009). Further, high NLR was associated with neutrophil abnormalities, including enrichment for low-density granulocytes (LDGs) (p=0.001), and increased levels of the serum neutrophil activation marker, calprotectin (p=0.02). Assessing the individual components within NLR, that is, neutrophil and lymphocyte count, high neutrophil count was associated with neutrophil activation markers (p<0.0001), whereas low lymphocyte count was associated with type I IFN activity and elevated numbers of LDGs (p=0.006 and p=0.001, respectively).ConclusionsNLR is elevated in patients with SLE as compared with healthy individuals, and is associated with key immunopathological events, including type I IFN activity and neutrophil activation. Neutrophil and lymphocyte count reflected different aspects of the pathogenesis of SLE. Further studies are needed to determine the causality of the associations.

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The leukotriene B4 lipid chemoattractant receptor BLT1 defines antigen-primed T cells in humans

Blood ◽

10.1182/blood-2005-06-2362 ◽

2006 ◽

Vol 107 (2) ◽

pp. 444-453 ◽

Cited By ~ 49

Author(s):

Sabina A. Islam ◽

Seddon Y. Thomas ◽

Christoph Hess ◽

Benjamin D. Medoff ◽

Terry K. Means ◽

...

Keyword(s):

T Cells ◽

T Cell ◽

T Cell Activation ◽

Peripheral Blood ◽

Acute Infection ◽

Cell Subset ◽

Leukotriene B4 ◽

Healthy Individuals ◽

Activation Markers ◽

Human T Cell

AbstractWe have recently shown that the leukotriene B4 (LTB4)–BLT1 pathway is important in early effector T-cell recruitment in mouse models of inflammation. Here we characterize the phenotype and function of human peripheral blood BLT1+ T cells in health and illustrate their involvement in asthma and acute infection. In healthy individuals, BLT1+ T cells are a rare peripheral blood T-cell population enriched for the activation markers CD38 and HLA-DR. Compared with BLT1– T cells, a larger proportion of peripheral blood BLT1+ T cells express the effector cytokines IFNγ and IL-4 and inflammatory chemokine receptors, CCR1, CCR2, CCR6, and CXCR1. Consequently, in healthy individuals peripheral blood BLT1+ T cells are a rare antigen-primed T-cell subset with unique phenotypic, migratory, and functional properties. BLT1 expression on T cells is tightly regulated by inflammation and only transiently expressed after naive T-cell activation by dendritic cells. Although rare in the peripheral blood of healthy individuals, BLT1+ T cells are markedly increased in frequency in the peripheral blood in response to acute Epstein-Barr virus (EBV) infection and moderately increased in the airways of asymptomatic allergic asthmatics. Our studies provide novel insights into the LTB4-BLT1 lipid chemoattractant pathway in human T-cell responses, and how it may link innate and adaptive immunity.

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Lymphocyte Activation Markers in Peripheral Blood before and after Natural Exposure to Allergen in Asthmatic Patients

Respiration ◽

10.1159/000196641 ◽

1997 ◽

Vol 64 (1) ◽

pp. 45-49 ◽

Cited By ~ 3

Author(s):

Maria Majori ◽

Laura Piccoli ◽

Roberto Melej ◽

Vincenzo Pileggi ◽

Alberto Pesci

Keyword(s):

Peripheral Blood ◽

Lymphocyte Activation ◽

Activation Markers ◽

Asthmatic Patients ◽

Natural Exposure ◽

Before And After

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CD11b is an activation marker expressed on a large population of sheep peripheral blood B cells

Immunology Letters ◽

10.1016/s0165-2478(97)87225-2 ◽

1997 ◽

Vol 56 (1-3) ◽

pp. 98

Author(s):

N Chevallier

Keyword(s):

B Cells ◽

Peripheral Blood ◽

Large Population ◽

Activation Marker

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XMODULATION IN MICEAND MEN: IL-10 PRODUCING CELLS INBLOOD AND LYMPHOID TISSUE

Clinical & Investigative Medicine ◽

10.25011/cim.v31i4.4789 ◽

2008 ◽

Vol 31 (4) ◽

pp. 3

Author(s):

L Barrett ◽

M Grant ◽

R Liwski ◽

K West

Keyword(s):

Immune System ◽

Peripheral Blood ◽

Lymphoid Tissue ◽

Mononuclear Cells ◽

Ex Vivo ◽

White Blood Cells ◽

Interleukin 10 ◽

Healthy Individuals ◽

Human Immune System ◽

Healthy Humans

Background: The human immune system provides remarkable protection from a plethora of pathogens, but can cause damage when activated for a prolonged time (as inpersistent infections) or against self (autoimmunity). Therefore, mechanisms of immune system downregulation and control are imperative. There is little data on how the immune system is controlled in healthy individuals. We recently described a novel population of white blood cells that constitutively produce the immunomodulatory cytokine interleukin-10 (IL-10). Our objective was to further delineate the distribution of these cells in human and mouse models, as well as potential triggers for interleukin-10 production in vitro. Methods: Human and animal protocols were reviewed and approved by the institutional ethics board and animal care facilities, and informed consent was obtained from all human donors. The ex vivo percentage of peripheral blood CD36^+IL-10^+ mononuclear cells was assessed by intracellular flow cytometry in 10 healthy individuals. IL-10 production after exposure to twoCD36 ligands, thrombospondin and oxidized low density lipoprotein (oxLDL) was measured at 8 hours. Peripheral blood mononuclear cells and splenocytes from BL/6 (n=5) and Balb/c (n=1) micewere assessed for CD36^+IL-10^+ cells ex vivo as well. Results: The percentage of CD36^+IL-10^+ cells in peripheral blood fromhealthy individuals ranges between 0.1% and 0.9%. The percentage was similar in mouse peripheral blood, with a range of 0.4%-1.1%. These cells were also found in mouse spleen at a higher frequency than peripherally (1.1-1.5%). Human CD36^+IL-10^+ cells have more IL-10 when exposed to thrombospondin, oxLDL. Conclusions: Our novel population of IL-10 producing cells is found not only in healthy humans, but also in lymphoid tissue and blood from pathogen free mice. This highlights the evolutionary conservation of the cell across species, and suggests an important homeostatic function. The physiologic ligands for CD36 are ubiquitous in circulation, and ourin vitro data suggests a link between CD36 ligation and IL-10 production. IL-10 is a known immune system modulator, and its production by these cells may help maintain homeostaticcontrol of the immune system.

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Early prolonged neutrophil activation in critically ill patients with sepsis

Innate Immunity ◽

10.1177/1753425920980078 ◽

2021 ◽

Vol 27 (2) ◽

pp. 192-200

Author(s):

Sanna Törnblom ◽

Sara Nisula ◽

Suvi T Vaara ◽

Meri Poukkanen ◽

Sture Andersson ◽

...

Keyword(s):

Intensive Care Unit ◽

Intensive Care ◽

Intensive Care Unit Admission ◽

Plasma Concentrations ◽

Neutrophil Activation ◽

Early Event ◽

Heparin Binding ◽

Activation Markers ◽

Heparin Binding Protein ◽

Pro Inflammatory Cytokines

We hypothesised that plasma concentrations of biomarkers of neutrophil activation and pro-inflammatory cytokines differ according to the phase of rapidly evolving sepsis. In an observational study, we measured heparin-binding protein (HBP), myeloperoxidase (MPO), IL-6 and IL-8 in 167 sepsis patients on intensive care unit admission. We prospectively used the emergence of the first sepsis-associated organ dysfunction (OD) as a surrogate for the sepsis phase. Fifty-five patients (of 167, 33%) developed the first OD > 1 h before, 74 (44%) within ± 1 h, and 38 (23%) > 1 h after intensive care unit admission. HBP and MPO were elevated at a median of 12 h before the first OD, remained high up to 24 h, and were not associated with sepsis phase. IL-6 and IL-8 rose and declined rapidly close to OD emergence. Elevation of neutrophil activation markers HBP and MPO was an early event in the evolution of sepsis, lasting beyond the subsidence of the pro-inflammatory cytokine reaction. Thus, as sepsis biomarkers, HBP and MPO were not as prone as IL-6 and IL-8 to the effect of sample timing.

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Phenotypic and Functional Alterations of Immune Effectors in Periodontitis; A Multifactorial and Complex Oral Disease

Journal of Clinical Medicine ◽

10.3390/jcm10040875 ◽

2021 ◽

Vol 10 (4) ◽

pp. 875

Author(s):

Kawaljit Kaur ◽

Shahram Vaziri ◽

Marcela Romero-Reyes ◽

Avina Paranjpe ◽

Anahid Jewett

Keyword(s):

Periodontal Disease ◽

Peripheral Blood ◽

Mononuclear Cells ◽

Oral Disease ◽

Healthy Controls ◽

Healthy Individuals ◽

Tnf Α ◽

Blood Mononuclear Cells ◽

Ifn Γ ◽

And Function

Survival and function of immune subsets in the oral blood, peripheral blood and gingival tissues of patients with periodontal disease and healthy controls were assessed. NK and CD8 + T cells within the oral blood mononuclear cells (OBMCs) expressed significantly higher levels of CD69 in patients with periodontal disease compared to those from healthy controls. Similarly, TNF-α release was higher from oral blood of patients with periodontal disease when compared to healthy controls. Increased activation induced cell death of peripheral blood mononuclear cells (PBMCs) but not OBMCs from patients with periodontal disease was observed when compared to those from healthy individuals. Unlike those from healthy individuals, OBMC-derived supernatants from periodontitis patients exhibited decreased ability to induce secretion of IFN-γ by allogeneic healthy PBMCs treated with IL-2, while they triggered significant levels of TNF-α, IL-1β and IL-6 by untreated PBMCs. Interaction of PBMCs, or NK cells with intact or NFκB knock down oral epithelial cells in the presence of a periodontal pathogen, F. nucleatum, significantly induced a number of pro-inflammatory cytokines including IFN-γ. These studies indicated that the relative numbers of immune subsets obtained from peripheral blood may not represent the composition of the immune cells in the oral environment, and that orally-derived immune effectors may differ in survival and function from those of peripheral blood.

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