Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021345 (infectious mononucleosis)
 3,358 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Biological and clinical effects of i.v. administration of gamma-globulin (0.9-1.5 g/kg) to 9 patients with infectious mononucleosis have been compared with the effects observed in 4 untreated patients. An increase of OKT4/OKT8 ratio has been measured in treated cases whereas this ratio remains low in untreated patients. Interleukin-2 secretion by stimulated lymphocytes increases also in treated patients but not in untreated ones. On the other hand gamma-globulin inhibits in vitro the cytotoxic activity of lymphocytes from immune subjects. Clinically gamma-globulin i.v. had a beneficial effect on the course of the disease and on adenopathies. As infectious mononucleosis has usually a favourable outcome, this treatment should be restrained to severe or chronic cases.
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PMID:[Effect of i.v. gamma-globulin on T lymphocytes and on interleukin-2 secretion in infectious mononucleosis]. 245 37

Interleukin-2 (IL-2) activated killer (LAK) cells, generated in vitro by treating peripheral blood lymphocytes (PBL) with human IL-2, are able to lyse a wide variety of target cells without restriction by major histocompatibility complex (MHC) molecules. Earlier observations from this and other laboratories indicated that patients with Epstein-Barr virus (EBV) induced infectious mononucleosis, a self-limiting viral disease, have high EBV-non-specific natural killer (NK) cell activity. Since the effect of LAK cells on EBV-immortalized B lymphocytes has not yet been studied, we decided to investigate LAK cell activity against autologous and heterologous B lymphocytes immortalized in vitro by EBV and other EBV genome-positive and -negative targets of malignant origin. LAK activity was determined by 51Chromium release assay. The results obtained show that LAK activity was not specific for EBV and was not MHC-restricted. Results of experiments using NK cell reactive monoclonal antibodies suggest that the cytotoxicity is due predominantly to activated NK cells. Our observations suggest that LAK cells may be very effective for immunotherapy in patients with chronic or progressive EBV infections and EBV-induced lymphoproliferative diseases.
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PMID:Interleukin-2 induced killer cell activity against Epstein-Barr virus-immortalized human B cells. 254 Oct 81

Interleukin-2 (IL-2) enhances the proliferation of in vivo Epstein-Barr virus-(EBV)-transformed B-cells from patients with a present or past history of infectious mononucleosis. In contrast, there is less expression of functional IL-2 receptors on EBV-transformed B-cells from patients with rheumatoid arthritis. These results suggest differences in the involvement of B-cells in EBV-associated diseases.
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PMID:[Expression of interleukin 2 receptors in in vivo Epstein-Barr virus transformed B lymphocytes]. 283 87

Somatic cell hybridization was utilized to produce hybrids with surface receptors that would pertain directly to those expressed in vivo during Epstein-Barr virus (EBV) infection. Lymphocytes were obtained during acute infectious mononucleosis (IM) and fused to a double mutant of the JM human T-lymphoma cell lines. Hybrid cells that reacted with autologous EBV-infected lymphoblasts were detected by the release of Interleukin-2 into the culture medium. Reactive hybridomas also released IL-2 following coculture with allogeneic EBV-infected cells when those cells shared HLA-DR antigens of the primary parental cells. In contrast, stimulator cells with no shared HLA-DR or without evidence of EBV infection never induced IL-2 release. These results suggest the existence of a population of T cells that arise during acute IM and could account for the known proliferative phase of the disease. The requirements of IL-2 stimulation are currently under study using this system.
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PMID:Characterization of Epstein-Barr virus-specific T-cell hybridomas derived from infectious mononucleosis. 299 57

Interleukin-2 (IL-2) has been implicated as being necessary for the optimal formation of primary CD8(+) T cell responses against various pathogens. Here we have examined the role that IL-2 signaling plays in several aspects of a CD8(+) T cell response against murine gammaherpesvirus 68 (MHV-68). Exposure to MHV-68 causes a persistent infection, along with infectious mononucleosis, providing a model for studying these processes in mice. Our study indicates that CD25 is necessary for optimal expansion of the antigen-specific CD8(+) T cell response but not for the long-term memory response. Contrastingly, IL-2 signaling through CD25 is absolutely required for CD8(+) T cell mononucleosis.
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PMID:Mononucleosis and antigen-driven T cell responses have different requirements for interleukin-2 signaling in murine gammaherpesvirus infection. 2068 22

In patients with underlying immunodeficiency, Epstein-Barr virus (EBV) may lead to severe immune dysregulation manifesting as fatal mononucleosis, lymphoma, lymphoproliferative disease (LPD), lymphomatoid granulomatosis, hemophagocytic lymphohistiocytosis (HLH) and dysgammaglobulinemia. Several newly discovered primary immunodeficiencies (STK4, CD27, MAGT1, CORO1A) have been described in recent years; our group and collaborators were able to reveal the pathogenicity of mutations in the Interleukin-2-inducible T-cell Kinase (ITK) in a cohort of nine patients with most patients presenting with massive EBV B-cell lymphoproliferation. This review summarizes the clinical and immunological findings in these patients. Moreover, we describe the functional consequences of the mutations and draw comparisons with the extensively investigated function of ITK in vitro and in the murine model.
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PMID:Interleukin-2-inducible T-cell kinase (ITK) deficiency - clinical and molecular aspects. 2533 95