About: Diminished production of type-I interferons and interleukin-2 in patients with multiple sclerosis

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An Entity of Type : schema:ScholarlyArticle, within Data Space : covidontheweb.inria.fr associated with source document(s)

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type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Diminished production of type-I interferons and interleukin-2 in patients with multiple sclerosis
Creator	Kirchner, Holger Neustock, Petra Siekhaus, Aja Wandinger, Klaus-Peter Wessel, Karl
Source	Elsevier; Medline; PMC
abstract	Abstract Several lines of evidence have supported the role of immunological mechanisms in the pathogenesis of multiple sclerosis (MS) and new immunomodulatory strategies for its treatment, e.g. subcutaneous application of interferon (IFN)-β, have emerged. We investigated the ability of peripheral blood mononuclear cells (PBMC) in 21 consecutive patients with clinically definite MS to produce interferons and lymphokines in response to viral or mitogenic stimulation. Ten patients showed clinical signs of disease activity (acute relapse) and 11 patients were in a stable condition. Additionally, white blood count, leukocyte differentiation and lymphocyte subtyping were performed. A group of age-related healthy blood donors served as control (n=20). There was no difference between patients and controls in the production of IFN-γ, tumor necrosis factor (TNF)-α and soluble interleukin (IL)-2 receptor. IFN-α and IFN-β responsiveness, however, was significantly lower in patients with stable disease than in patients with active disease and controls (p<0.001). Furthermore, secretion of IL-2 after stimulation was significantly diminished in both patient groups as compared to the control group (p<0.01). Analysis of T-cell subsets revealed a significantly lower amount of CD8+ T-cells in patients with stable disease, leading to a significantly higher CD4/CD8 ratio in this group as compared to patients with active disease. Our study depicted an IL-2 deficiency in MS patients which is shared with other autoimmune diseases. In addition, our findings suggest that the ability to produce type-I IFNs, IFN-α and IFN-β, is primarily impaired in MS patients and changes in correlation to the course of disease activity.
has issue date	1997-07-01(xsd:dateTime)
bibo:doi	10.1016/s0022-510x(97)05383-5
bibo:pmid	9168171
has license	els-covid
sha1sum (hex)	44221b95d7931c51f83060d114e9c7fb43007971
schema:url	https://doi.org/10.1016/s0022-510x%2897%2905383-5
resource representing a document's title	Diminished production of type-I interferons and interleukin-2 in patients with multiple sclerosis
has PubMed Central identifier	PMC7127026
has PubMed identifier	9168171
schema:publication	Journal of the Neurological Sciences
resource representing a document's body	covid:44221b95d7931c51f83060d114e9c7fb43007971#body_text
is schema:about of	named entity 'INTERLEUKIN-2 ' named entity 'INTERFERONS' named entity 'leukocyte' named entity 'control' named entity 'patients' named entity 'patients' named entity 'emerged' named entity 'blood donors' named entity 'interferons' named entity 'interleukin' named entity 'production' named entity 'MULTIPLE SCLEROSIS' named entity 'PATIENTS' named entity 'PRODUCTION' named entity 'BLOOD COUNT' named entity 'LOWER' named entity 'A GROUP' named entity 'CONDITION' named entity 'RESPONSIVENESS' named entity 'PATIENT' named entity 'HAVE' named entity 'SOLUBLE' named entity 'PATHOGENESIS' named entity 'RELAPSE' named entity 'AGE' named entity 'APPLICATION' named entity 'COMPARED' named entity 'IL-2' named entity 'INTERLEUKIN ' named entity 'TUMOR NECROSIS FACTOR ' named entity 'LINES' named entity 'MITOGENIC' named entity 'ABILITY' named entity 'PERFORMED' named entity 'ACTIVE' named entity 'SUPPORTED' named entity 'CLINICALLY DEFINITE MS' named entity 'TYPE' named entity 'CONTROL GROUP' named entity 'ROLE' named entity 'CONTROL' named entity 'CONSECUTIVE' named entity 'HEALTHY' named entity 'LEUKOCYTE DIFFERENTIATION' named entity 'INTERFERONS' named entity 'TREATMENT' named entity 'NO DIFFERENCE' named entity 'DIMINISHED' named entity 'DIMINISHED' named entity 'PERIPHERAL BLOOD MONONUCLEAR CELLS' named entity 'RESPONSE TO' named entity 'GROUPS' named entity 'IMMUNOLOGICAL' named entity 'LYMPHOKINES' named entity 'PRODUCTION' named entity 'IFN' named entity 'DISEASE ACTIVITY' named entity 'INVESTIGATED' named entity 'MULTIPLE SCLEROSIS' named entity 'STABLE DISEASE' named entity 'VIRAL' named entity 'IMMUNOMODULATORY' named entity 'IFN-G' named entity 'SECRETION' named entity 'TO PRODUCE' named entity 'RECEPTOR' named entity 'SUBCUTANEOUS' named entity 'BLOOD DONORS' named entity 'OF EVIDENCE' named entity 'ITS' named entity 'RELATED' named entity 'STRATEGIES' named entity 'MECHANISMS' named entity 'LYMPHOCYTE' named entity 'NEW' named entity 'STIMULATION' named entity 'DISEASE'

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