Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P14784 (IL-2 receptor)
 3,849 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The lymphocytosis manifested in infectious mononucleosis (IM) during acute phase is ascribed to a reactive expansion of CD8+ T lymphocytes caused by Epstein-Barr virus (EBV)-infected B lymphocytes. Expression of HLA-DR antigen on IM lymphocytes suggests that these T lymphocytes are somehow activated in vivo. In the present study, we analyzed the interleukin-2 (IL-2) receptor expression on lymphocytes from six patients with acute IM. Radiolabeled IL-2 binding assay revealed that IM lymphocytes from all patients examined had a considerable number of IL-2 binding sites with an intermediate affinity, although they did not express the IL-2 receptor recognized by anti-Tac antibody (p55). The number of binding sites (1,070 to 4,600 sites per cell) was larger than that of a normal, resting T lymphocyte-enriched population (650 sites per cell). Furthermore, IM lymphocytes showed marked proliferative responses to higher concentrations of IL-2, which were almost completely blocked by an anti-p70 IL-2 receptor antibody, indicating that their IL-2 receptor is a functional receptor. The results of an affinity cross-linking study seem to indicate that the IL-2 receptor expressed on IM lymphocytes is p70, the second chain of the IL-2 receptor distinct from p55. Flow cytometric analysis following immunofluorescent staining with anti-p70 IL-2 receptor antibody confirmed p70 expression on CD8+ HLA-DR+ lymphocytes. These data suggest that p70 IL-2 receptor expression is involved in the immune response triggered by EBV infection.
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PMID:Selective expression of the p70 subunit of the interleukin-2 receptor on lymphocytes from patients with infectious mononucleosis. 229

Epstein-Barr virus (EBV) readily immortalizes human peripheral blood lymphocytes (PBL) in vitro. However, during the past several years, we found that PBL from two exceptional EBV-seropositive healthy adult individuals were refractory to immortalization by EBV. We report here a study aimed at learning about the immunobiological features which differentiate these EBV-resistant (R) PBL from others which are susceptible (S) to EBV immortalization. Results of this investigation indicate that: (a) Following EBV infection, R-PBL produced significantly higher amounts of interferon gamma (IFN-gamma) than S-PBL. There were however no differences in regard to interferon alpha production between these two types (R and S) of EBV-infected cultures. (b) R-PBL had a maximal interleukin-2 (IL-2) production by S-PBL occurred at least 48 hr later, i.e., at Day 7. (c) The percentage of non-B cells expressing the IL-2 receptor was also higher in EBV-infected R-PBL than S-PBL. (d) In contrast, expression of IL-2 receptors after EBV infection was higher on B cells from S-PBL than on B cells from R-PBL. Interestingly, no differences were noted in regard to IL-2 receptor expression between R-PBL and S-PBL treated with mitogens (i.e., phytohemagglutinin and pokeweed mitogen). (e) Finally, using anti-IL-2 and anti-IFN-gamma antibodies in EBV-infected R-PBL cultures, we were able to obtain EBV-induced immortalization of these cultures. Taken together, these results suggest that an early IL-2 synthesis and high IFN-gamma production by EBV-infected PBL play an important role against lymphocyte immortalization by EBV.
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PMID:Differential interleukin-2 and interferon-gamma production by human lymphocyte cultures exceptionally resistant to Epstein-Barr virus immortalization. 254 40

Serum cytokine profiles, T-cell subsets, and general parameters of immune activation were evaluated in 15 patients with acute primary HIV-1 infection, and compared with those obtained from 18 patients with acute primary Epstein-Barr virus (EBV) infection and from 18 control subjects in order to elucidate possible defects of immune response to HIV in early phases of virus-host interaction. Mean CD4+ cell count, serum concentrations of interleukin (IL)-2, IL-4, soluble IL-2 receptor (sIL-2R), tumor necrosis factor (TNF)-alpha, 5'-neopterin, and beta 2-microglobulin were significantly lower in acute HIV-1 infection than in EBV infection. Both acute HIV-1 and EBV infections were characterized by significantly higher mean CD8+ cell count and soluble CD8 antigen (sCD8) levels compared to control subjects, while acute HIV-1 infection was accompanied by the highest interferon (IFN)-gamma serum concentrations. In primary HIV-1 infection, significant impairment of CD4+- mediated T-helper function may lead to viral escape and persistence of infection despite an early and vigorous CD8+ T-lymphocyte activation.
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PMID:Serum cytokine profiles in acute primary HIV-1 infection and in infectious mononucleosis. 859 86

CD56 (NCAM)-positive lymphoma frequently involves the skin and nasal area. This study shows it is likely that the clinicopathologic features of this lymphoma are distinctive to each of the primarily involved sites. Sixteen cutaneous and 11 nasal cases of CD56-positive lymphoma were examined. In 10 cutaneous cases, the lesions consisted of pleomorphic large-cell lymphoma that expressed CD3epsilon (CD3), CD2 (LFA2), CD4, CD122 (IL-2B receptor), TIA1, perforin, and granzyme B and displayed angiocentric/angiodestructive features. Lobular panniculitis was found in 8 of these cases, and 6 cases showed other organ involvement. The remaining 6 cutaneous cases consisted mostly of CD3epsilon- and CD4-positive, CD2-, CD122-, and TIA1-negative large blastic lymphoma, having less angiodestruction and panniculitis. Bone marrow invasion and leukemic changes were found in 4 of these cases during the clinical course. All 11 nasal cases showed pleomorphic small and medium-size lymphoma cells with angiodestructive features and were positive for CD3epsilon, CD2, CD122, TIA1, perforin, and granzyme B. CD4-positive lymphoma was found in 4 of these cases. Only 3 nasal cases showed other organ involvement. Genotypically, 2 of the 4 cases examined in the first cutaneous group, 3 of the 4 cases examined in the second cutaneous group, and only 1 of the 11 nasal cases showed rearrangement of the TcRCbeta gene by the Southern blot method. Only 2 cutaneous cases with panniculitis and all 11 nasal cases showed a positive nuclear signal for EBV-encoded RNA (EBERs) by in situ hybridization. Thus, two types of cutaneous CD56-positive lymphoma were found, each having a unique cell characteristic, genotype, and EBV infection pattern that differed from that of nasal-type lymphoma.
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PMID:Cases of cutaneous and nasal CD56 (NCAM)-positive lymphoma in Japan have differences in immunohistology, genotype, and etiology. 1049 36

The clinical picture of infectious mononucleosis and the consequences of EBV infection are due to immune response mechanisms. The level of soluble form of IL-2 receptor (sIL-2R) is thought to be a marker of T-cell activity, especially CD8+. Intercellular adhesion molecule (ICAM-1, CD 54) plays an important role in the process of antigen presentation. The aim of this study was to assess the serum concentration of sIL-2R, ICAM-1 and anti-VCA IgM in patients with infectious mononucleosis. The study group comprised 42 persons: 20 healthy subjects as a control group and 22 individuals with infectious mononucleosis. The highest anti-VCA IgM serum level in all patients was during the 1st day of hospitalization, and decreased in the 8th day of hospitalization. The lowest antibody concentration was observed when the symptoms and sings ceased. The level of sIL-2R was significantly increased and during farther hospitalization we observed lower, but still elevated concentrations. Our study has demonstrated statistically significant elevation of sICAM-1 level during the entire period of hospitalization. This data indicates the importance of antigen presentation process. Although the serum concentration of immune response mediators does not reflect their contents in organism, but is a useful method for in vivo examination.
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PMID:[Levels of soluble intracellular adhesion molecules 1 (sICAM-1) , soluble receptors for interleukin 2 (sIL-2R) and anti-Epstein-Barr viral capsid antigen (anti-VCA IgM) in blood serum during the course of infectious mononucleosis]. 1143 83

Murine gammaherpesvirus 68 (MHV68) establishes long-term latency in memory B cells similar to the human gammaherpesvirus Epstein Barr Virus (EBV). EBV encodes an interleukin-10 (IL-10) homolog and modulates cellular IL-10 expression; however, the role of IL-10 in the establishment and/or maintenance of chronic EBV infection remains unclear. Notably, MHV68 does not encode an IL-10 homolog, but virus infection has been shown to result in elevated serum IL-10 levels in wild-type mice, and IL-10 deficiency results in decreased establishment of virus latency. Here we show that a unique MHV68 latency-associated gene product, the M2 protein, is required for the elevated serum IL-10 levels observed at 2 weeks post-infection. Furthermore, M2 protein expression in primary murine B cells drives high level IL-10 expression along with increased secretion of IL-2, IL-6, and MIP-1alpha. M2 expression was also shown to significantly augment LPS driven survival and proliferation of primary murine B cells. The latter was dependent on IL-10 expression as demonstrated by the failure of IL10-/- B cells to proliferate in response to M2 protein expression and rescue of M2-associated proliferation by addition of recombinant murine IL-10. M2 protein expression in primary B cells also led to upregulated surface expression of the high affinity IL-2 receptor (CD25) and the activation marker GL7, along with down-regulated surface expression of B220, MHC II, and sIgD. The cells retained CD19 and sIgG expression, suggesting differentiation to a pre-plasma memory B cell phenotype. These observations are consistent with previous analyses of M2-null MHV68 mutants that have suggested a role for the M2 protein in expansion and differentiation of MHV68 latently infected B cells-perhaps facilitating the establishment of virus latency in memory B cells. Thus, while the M2 protein is unique to MHV68, analysis of M2 function has revealed an important role for IL-10 in MHV68 pathogenesis-identifying a strategy that appears to be conserved between at least EBV and MHV68.
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PMID:The MHV68 M2 protein drives IL-10 dependent B cell proliferation and differentiation. 1838 62