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)

Investigations of HLA and blood-groups were carried out in 68 patients with infectious mononucleosis comprising all known cases diagnosed within one year in a restricted geographical area of Denmark. The HLA distribution of these patients did not differ significantly from that of controls. Combining the results of the present investigation with two previous studies did not show any significantly different distribution from that of combined control groups. The ABO and Rhesus typing was in accordance with that found in a major Danish control group. However, available studies do not exclude the possibility that HLA-D/DR or still unknown HLA factors may be involved in the susceptibility to mononucleosis.
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PMID:HLA types and ABO blood groups in patients with infectious mononucleosis. 10 11

Peripheral T-lymphocytes from patients with infectious mononucleosis are cytotoxic towards target cells from Epstein-Barr virus-genome carrying human lumphoblastoid lines. Thus, these T-cells appear to be sensitized to viral coded determinants. Daudi cells, that carry EBV-genome, but lack HLA antigens are resistant to specific cytolysis in this model. These results suggest direct HLA involvement in the target structure recognized by birus-sensitized cytolytic T-lymphocytes in human.
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PMID:[Cytotoxicity of human T-lymphocytes sensitized by Epstein-Barr virus. Role of HLA antigens at the surface of target cells infected by the virus]. 19 80

The beta2-microglobulin/HLA deficient Burkitt lymphoma line Daudi was tested for sensitivity to EBV-specific cytotoxicity mediated by natural killer (NK)-depleted T-cells from acute mononucleosis patients. While the Daudi line was not as sensitive as the reference EBV-genome-positive target line, it was clearly sensitive in the majority of cases. This would speak against a major role of syngeneic restriction in this system.
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PMID:The EBV-carrying, beta2M/HLA deficient Burkitt lymphoma line Daudi is sensitive to EBV-specific killer T-cells of mononucleosis patients. 22 36

Peripheral T lymphocytes from patients with infectious mononucleosis (IM) are sensitized in vivo against the Epstein-Barr virus (EBV). The expression of HLA-A, B, or C molecules at the target cell surface is necessary for the cytotoxic reaction because (a) EBV-positive Daudi cells lacking HLA-A, B, and C determinants are resistant to anti-EBV T-cell lysis, (b) cytolysis of EBV-positive target cells can be consistently inhibited by anti-HLA-A, B, and C and anti-beta 2 microglobulin antibodies. However, no evidence for allogeneic restriction in this system was apparent as (a) cytotoxic T lymphocytes (CTL) from one given individual could exert a cytotoxicity of a similar magnitude on different EBV-positive target cells, regardless of the number of HLA-A or B specificities shared by the effectors and targets; (b) CTL from IM patients were able to kill target cells without any HLA-A or B antigen in common; and (c) T5-1 variants lacking one or two HLA antigens at the A, B, or D locus are killed to the same extent as the parental cells. 7 of the 9 IM patients with detectable circulating anti-EBV CTL carried the HLA-A1 antigen, whereas none of the 16 IM patients lacking detectable peripheral CTL were HLA-A1 positive (mean specific lysis of T5-1 target cells by T cells from HLA-A1 positive patients: 29.3 vs. 0.6% in HLA-A1-negative patients) (P less than 10(-9)). These data suggest an HLA-A1-linked gene control of the magnitude of the anti-EBV CTL response. Thus, the HLA region appears to act at two different level sin the T-cell-mediated lysis of EBV-infected cells by controlling first, the development of anti-EBV and second, the expression of HLA-A, B, and C molecules involved as recognition structures at the target cell surface.
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PMID:Absence of allogeneic restriction in human T-cell-mediated cytotoxicity to Epstein-Barr virus-infected target cells. Demonstration of an HLA-linked control at the effector level. 22 86

Following an attack of infectious mononucleosis, the red cells of HLA B7 patients may show a greatly increased reactivity with anti-Bga antibodies. This occurs from about the 3rd week of the disease, the reactivity then slowly decreasing over a period of months or years. Both specific and nonspecific reactions to other HLA antisera may also occur. Five patients were followed in detail and the reason for the increase in antigen strength was investigated without a conclusive result.
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PMID:Increase in strength of red cell Bga antigen following infectious mononucleosis. 32 Jul 65

Neutrophil antigens may be classified into two major categories: antigens shared with other cells and antigens specific for neutrophils. The first category includes the ABH, I, i, 5a,b and HLA determinants. Additional antigens with special characteristics in this category are the blood-group U, Kx, JkaJkb, and Ge determinants which apparently neutrophils share only with erythrocytes. Neutrophil-specific antigens include the NA1, NA2, NB1 and 9a. These specificities are detected by the agglutination test and have been shown to be present on mature neutrophils. Independent allospecificities, detectable by the granulocytotoxicity test, may also exist. In addition, neutrophil antigens, which are species-specific, have been identified by the use of xenogeneic antibodies. The EDTA-dependent agglutination test remains a most reliable assay for the study of neutrophil-specific antigens. The lack of reproducibility known in the leukoagglutination reaction does not pertain to the modification used in the assay of neutrophil-specific antibodies. It does apply, however, to those tests that were performed in the absence of EDTA, and in connection to the study of HLA-related antigens. For every pathophysiological state involving the erythrocyte antigens a neutrophil analogue is observed, the difference being in symptomatology which is related to the structural and functional characteristics of the cells: febrile and pulmonary transfusion reactions result from incompatibility neutrophils. It is found that similarity in the HLA antigens and nonreactivity in the MLC test do not preclude immunization against neutrophil-specific antigens. Therefore, it is probable that febrile and pulmonary reactions will occur in the recipients of multiple granulocyte transfusions, even though donors and recipients may be considered "histocompatible" by the HLA assays. It has been shown that fetal-maternal incompatibility can cause neonatal neutropenia, and several forms of autoimmune neutropenia are described: in "idiopathic" neutropenia of infancy, autoantibodies have been found to have specificity against NA1 and NA2 and in one adult, autoimmune neutropenia due to anti-NA1 antibody has been observed. Neutropenia also occurs due to idiopathic, cold-reacting antileukocyte antibodies, and with cold agglutinins associated with lymphoma, infectious mononucleosis, and Mycoplasma pneumonia. Although the role of neutrophil antigens in bone marrow transplantation has not as yet been determined, these antigens are undoubtedly immunogenic and potentially play an important role in neutrophil compatibility. It is obvious that neutrophils cannot survive in the presence of antineutrophil antibodies.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Neutrophil antigens: immunology and clinical implications. 40 Jul 55

The human herpes virus 6 (HHV 6) may induce not only the wellknown condition of exanthem subitum, but also a number of more common (cf. Part 1) or rare, even previously unknown, clinical manifestations. Part 2 of this paper deals with the more rarely observed manifestations. These include complications of ARD (sinusitis, otitis media, bronchial pneumonia) hepatitis, encephalitis or Pfeiffer's disease (mononucleosis-like syndrome). In individuals with a relevant disposition (genetic HLA/DR type?) initiation or (re-)activation of rheumatoid arthritis (JCA = juvenile chronic arthritis) or chronic iridocyclitis may occur. Although, on account of the high prevalence of vaccination in our population (approximately 95%), prenatal infections are extremely rare, they may manifest in a severe "septic" form (fatalities have occurred) or may lead to neurological deficits (comparable with cytomegalovirus infection). To date, no specific therapy (e.g. gammaglobulin, virostatics) or reliable preventive measures (e.g. vaccination) are available.
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PMID:[Infections with herpesvirus 6--really only "exanthema subitum"? Part 2: Rare or unknown disease pictures]. 133 53

Cytotoxic T lymphocytes (CTL) with the CD4+ phenotype that recognize major histocompatibility complex (MHC) class II antigens are detectable very frequently in cultures of human alloreactive or virus-specific T cells. The significance of these CD4+ CTL for an immune reaction in vivo is not clear. Since Epstein-Barr virus (EBV) transformed B cells express HLA-class I and class II antigens equally well both CD8+ and CD4+ CTL should be stimulated during an acute EBV infection. We analysed the MHC specificity and the phenotype of EBV-specific CTL from patients with infectious mononucleosis (IM). When tested directly without any previous culture, T cells from patients in the acute phase of IM showed specific MHC-restricted cytotoxicity against the autologous B cell line. Addition of a HLA class I specific monoclonal antibody (MoAb) but not of a HLA class II specific MoAb resulted in a complete blocking of the lytic activity. Cell sorting revealed that the entire cytotoxic activity was present in the CD8+ fraction whereas no specific CTL were detectable in the CD4+ fraction. The absence of cytotoxicity in CD4+ cells was not due to a lack of activation of these cells since both CD8+ and CD4+ cells were activated in situ, showing spontaneous growth in interleukin-2 (IL-2) and expressing the activation marker TP103. Frequency estimation revealed that 1/300-1/600 CD8+ but only 1/2000-1/4000 CD4+ T cells gave rise to a specific CTL colony after 10 days. If CD4+ colonies were tested repeatedly for cytotoxicity we found that CD4+ CTL acquired their cytotoxicity during in vitro culture. In addition, we isolated EBV-specific CD4+ T cell clones able to lyse their stimulator cells in the presence but not in the absence of lectin, even after a long period of culture. Taken together our results show that cytotoxicity mediated by CD4+ T cells does not play a role in an anti-viral immune response.
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PMID:Absence of Epstein-Barr virus-specific, HLA class II-restricted CD4+ cytotoxic T lymphocytes in infectious mononucleosis. 169 Jun 17

The levels of soluble CD4 (sCD4) and sCD8 in serum correlate with the T cell subset activation and may be important in monitoring and characterizing disease processes during immunological diseases. We compared acute Kawasaki disease (KD) with anaphylactoid purpura (AP) and acute febrile viral infections, such as measles and infectious mononucleosis (IM), in terms of serum sCD4 and sCD8 levels. The levels of serum sCD4 and sCD8 were measured by a sandwich enzyme immunoassay. In addition, peripheral blood mononuclear cell subsets were analysed by single and two-colour flow-cytometric analyses in KD and IM patients. The levels of serum sCD4 and sCD8 were significantly elevated in patients during acute stages of KD, measles and IM, but not AP. Peripheral blood CD4+, CD8+ and also HLA-DR+ T cells count did not increase during the acute stage of KD; however, peripheral blood CD8+ and HLA-DR+ T cell counts were increased during the acute stage of IM. Our results suggest that there is a low level of activation of peripheral blood T cells during acute KD, or that infiltrated T cells in some local tissues of KD patients contribute to the elevated levels of serum sCD4 and sCD8.
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PMID:Serum soluble CD4 and CD8 levels in Kawasaki disease. 191 26

Mononuclear peripheral blood lymphocytes (PBL) from patient with infectious mononucleosis (IM) were tested in a 51Cr-release assay for cytotoxicity against autologous and allogeneic lymphoblastoid cell line (LCL), or Epstein-Barr virus (EBV)-genome positive and negative cell line. In acute phase, PBL lyse an autologous LCL as well as allogeneic LCL (Wa cells). High levels of cytotoxicity were observed in the combinations between effector and target cells sharing HLA-Class 1 product. EBV-genome positive Daudi and Raji cells which lack HLA-Class 1 antigen and have mismactched HLA-Class 1 antigen, respectively showed resistance to killing. EBV-genome negative tumor cells except NK sensitive K562 cells were not killed by IM lymphocytes. However, the IM lymphocytes without atypical form in convalescent phase failed to show killing activity against autologous and allogeneic LCL. These findings suggest that cell surface membrane antigen structure on EBV-infected LCL may be able to explain the recognition and triggering of lysis of target cells by HLA-Class 1 restricted cytotoxic T cells (CTL) from acute IM. Phenotypic analysis of PBL with atypical form from IM was made by two-color flow cytometry. The data demonstrate that CD8+ T cells quantitatively represent the major population of lymphocytes expanded during acute IM. Furthermore, approximately 70% of these CD8+ T cells express HLA-DR on these surface, suggesting that they have undergone activation. However, IL 2R (CD25 antigen) expression was not significantly elevated on activated T cells. The salient profile on cytofluorographs of an acute IM was the increased number of CD3+CD19-, CD8+CD11b-, CD8+CD28+ and CD8+S6F1+ cells. However, CD3-CD19+, CD8+CD11b+, CD8+S6F1-, CD4+Leu8- and CD25+HLA-DR+ antigens were little expressed. Increased number of CD8+CD11b-, CD8+CD28+ and CD8+S6F1+ cells, which are regarded as CTL were reduced according to the improvement of the clinical symptoms and laboratory findings. These results together with HLA typing analysis suggested a possibility HLA-Class 1 restriction of the CTL with surface phenotype of CD8+CD11b-, CD8+CD28+, and CD8+S6F1+.
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PMID:CD8+ T cell subsets of cytotoxic T lymphocytes induced by Epstein-Barr virus infection in infectious mononucleosis. 196 52


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