To ensure an adequate response against pathogens and prevent unwanted self-reactivity, immune cells need to functionally express both activating and inhibitory receptors. CD200R is an inhibitory receptor mainly expressed on myeloid cells that down-modulates cellular activation both in vivo and in vitro. Although previously mainly studied as a regulator of myeloid function, we now show that CD200R is differentially expressed on human and mouse T-cell subsets. In both species, CD4+ T cells express higher amounts of CD200R than CD8+ T cells, and memory cells express higher amounts of CD200R than naïve or effector cells. CD200R expression is up-regulated on both CD4+ and CD8+ T cells after stimulation in vitro. Furthermore, we show CD200R expression on human and mouse B cells. In human tonsils, CD200R is differentially expressed on B cells, with high expression on memory cells and plasmablasts. Mice lacking the ligand for CD200R, CD200-/- mice, do not show abnormal composition of the lymphocyte compartment and have normal B cell responses to antigenic challenge. Although the functional implications remain to be elucidated, the expression of CD200R on lymphocytes suggests a much broader role for CD200R-mediated immune regulation than previously anticipated.
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http://dx.doi.org/10.1016/j.molimm.2007.07.013 | DOI Listing |
Pediatr Pulmonol
May 2018
Translational Research Institute, Princess Alexandra Hospital, Brisbane, Australia.
Aim: Protracted bacterial bronchitis (PBB) is a common cause of prolonged cough in young children, and may be a precursor of bronchiectasis. Bacteria are often present in the lower airways in both PBB and bronchiectasis and may cause persistent infections. However, there is a paucity of information available on the pathogenesis of PBB and the factors associated with persistent bacterial infection and progression to bronchiectasis.
View Article and Find Full Text PDFBrain Behav Immun
May 2018
Department of Psychology and Neuroscience, University of Colorado, Boulder, CO 80309, USA.
Exposure to stressors can enhance neuroinflammatory responses, and both stress and neuroinflammation are predisposing factors in the development of psychiatric disorders. Females suffer disproportionately more from several psychiatric disorders, yet stress-induced changes in neuroinflammation have primarily been studied in males. Here we tested whether exposure to inescapable tail shock sensitizes or 'primes' neuroinflammatory responses in male and female rats.
View Article and Find Full Text PDFPLoS One
December 2017
Department of Psychological and Brain Sciences, Indiana University, Bloomington, IN, United States of America.
Women are more susceptible to numerous stress-linked psychological disorders (e.g., depression) characterized by dysfunction of corticolimbic brain regions critical for emotion regulation and cognitive function.
View Article and Find Full Text PDFData Brief
April 2017
Laboratory of Clinical Cell Therapy, Institut Jules Bordet, Université Libre de Bruxelles (ULB), Campus Erasme, Brussels, Belgium.
In this , we have provided data describing the secretion profile of two main immunoregulatory proteins, heme oxygenase-1 (HO-1) and CD200, from bone marrow (BM), Wharton׳s Jelly (WJ) or adipose tissue (AT) mesenchymal stromal cells (MSCs) being cultivated either in the absence or presence of activated T-cells. Whilst HO-1 is a stress-responsive enzyme displaying diverse cytoprotective effects, CD200 is a membrane glycoprotein delivering immunoregulatory signals following interaction with its receptor (CD200R). Using Enzyme-linked immunosorbent assay (ELISA) techniques, these data are presented to show distinct constitutive secretion of both HO-1 and CD200 depending on MSC types.
View Article and Find Full Text PDFBiomaterials
April 2016
Institute of Pharmacology of Natural Products & Clinical Pharmacology, Ulm University, D-89081 Ulm, Germany. Electronic address:
Macrophages are key regulators of innate and adaptive immune responses. Exposure to microenvironmental stimuli determines their polarization into proinflammatory M1 and anti-inflammatory M2 macrophages. M1 exhibit high expression of proinflammatory TNF-α and IL-1β, and M2 promote tissue repair, but likewise support tumor growth and cause immune suppression by expressing IL-10.
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