Disease relevance of CD8-Positive T-Lymphocytes

• The mechanism of suppression by PWM-activated T8+ cells of T4+ cell proliferation, not only to PWM, but also to tetanus toxoid, was pursued by measuring decreased interleukin 2 (IL2) recovery from cultures containing suppressors [1].
• Interferon-alpha modulates the immune response enhancing B7-1 and B7-2 costimulatory molecules and T8 lymphocytes in chronic myeloid leukemia [2].
• Immunohistochemical experiments showed that in AIDS lymphomas intratumoral CD8-positive T lymphocytes accumulated and expressed the TIA-1 antigen, a marker of cytotoxic cells [3].
• OBJECTIVES: We investigated the shifts of T4/T8 lymphocytes from BAL fluid (BALF) and peripheral blood by the clinical grade of pulmonary tuberculosis (TB), which is determined by factors such as extent of pulmonary involvement, fever, and loss of body weight [4].
• Since in HIV-infected persons, the increased number of HLA-DR+ CD38+T (T8) cells is associated with a fall in CD4-level and with development of AIDS, we are looking for the elimination of these HLA-DR+ targets by our novel technique in two AIDS-simulating (FIV/FeLV and SIV) animal models [5].

Psychiatry related information on CD8-Positive T-Lymphocytes

• The significance of LCA, T4 and T8 cells in Alzheimer's disease is unknown but may be indicative of a cell mediated immune response in the disease [6].

High impact information on CD8-Positive T-Lymphocytes

• During the course of investigating the regulation of IL-2-dependent T cell proliferation, we found that the subset of human T cells expressing the T4 surface glycoprotein become refractory to IL-2 growth promotion earlier than T8+ cells [7].
• Moreover, a detailed comparison of IL-2-R expression by T4+ vs. T8+ cells revealed no differences in the number, affinity, rate of expression, or functional activity of high-affinity IL-2-R expressed by the two subsets [7].
• Both T4 and T8 lymphocytes were found to make mRNA for TGF-beta upon activation [8].
• In contrast, the clusters in RA SF cultures have a T4/T8 ratio of less than 1 and a majority of the T8 cells coexpress the Leu 7 marker [9].
• In this study, we demonstrate that both highly purified T4+ and T8+ lymphocytes can produce substantial amounts of Interleukin 2(IL 2) when stimulated with the combination of concanavalin A (Con A) and phorbol myristate acetate [10].

Chemical compound and disease context of CD8-Positive T-Lymphocytes

• After cyclosporin withdrawal T4 and T8 cells as well as lymphadenopathy returned to pretreatment status [11].
• Chlorambucil treatment was responsible for a decrease in circulating T4+ and T8+ cells; nevertheless, T lymphocyte function was slightly improved during relapses [12].

Biological context of CD8-Positive T-Lymphocytes

• No characteristic alterations in CSF phenotypes could be related to changes in circulating T8 cells or to disease activity [13].
• In a group of 75 patients, CSF cell count was higher in patients with low numbers of circulating T8 cells than in those with normal T8 cells [13].
• This suppressive effect was also seen in IL-2-driven cell growth of CD8-positive lymphocytes purified from 7-day PHA-blasts, indicating that CD4 molecules were not required for the suppression [14].
• The stimulation of angiotensin-converting enzyme induction in cultured monocytes by T4+ and T8+ lymphocytes [15].
• Laboratory analysis of tumor samples revealed the presence of IL-2 plasmid DNA in six of eight patients posttreatment, increased IL-2 expression in tumor cells in four of eight patients posttreatment, and increased tumor infiltration by CD8-positive lymphocytes in five of eight patients posttreatment [16].

Anatomical context of CD8-Positive T-Lymphocytes

• Finally, whereas TsGF in the absence of IL-2 could not support the proliferation of T suppressor cells, it did cause T8+ cells to become strongly IL-2 receptor-positive [17].
• In the majority of sera, cytotoxicity for T4+ cells was greater than that for T8+ cells regardless of cellular activation status [18].
• By performing reconstitution experiments involving E+, T4+, or T8+ cells derived from either MS patients or controls, and normal allogeneic macrophages or E- cells, we sought to define the cellular basis for this suppressor defect [19].
• To see if PAGF was a T-dependent polyclonal activator of B cells, T and non-T populations were obtained by SRBC rosettes and negatively selected T4 and T8 cells by complement-mediated lysis of SRBC+(T) cells [20].
• In this context, the rejection of TSA-IL4 seems to involve a variety of reactive cells and rests on a continuous cross-talk between basophils, mast cells, macrophages, CD8-positive lymphocytes, and granulocyte subsets, mostly neutrophils [21].

Associations of CD8-Positive T-Lymphocytes with chemical compounds

• Treatment of the same cells with hydroxyurea, an inhibitor of DNA synthesis, failed to induce T4 on T8+ cells [22].
• Furthermore, T8+ cell-depleted T lymphocyte cultures, incubated for 24 hr with LTB4, showed a significant increase in the proportion of T8+ cells [23].
• Substantial levels of IL-2 responsiveness were induced in T8+ cells by lectin, Con A, mAb directed against the CD3 Ag, OKT3, Ca2+ ionophore, ionomycin or phorbol ester, PMA [24].
• Using either approach we found that both T4 and T8 lymphocytes expressed the 1,25-(OH)2D3 receptor protein upon activation [25].
• The selective activation of T8+ cells by neuraminidase and galactose oxidase is mediated by activated T4+ cells [26].

Gene context of CD8-Positive T-Lymphocytes

• Moreover, an Mab directed at the CD4 molecule (66.1) inhibited OKT3-induced T4 but not T8 cell proliferation, whereas an Mab directed at the CD8 molecule (OKT8) inhibited T8 but not T4 cell responses [27].
• Splenic CD8-positive lymphocytes expressed increased levels of IFN-gamma and IL-10 but the latter decreased sharply when diabetes occurred [28].
• Moreover, addition of mAb to the p55 component of IL2 receptor (anti-Tac) inhibited the generation of suppressor activity from CD45RA+ and CD45RA- T8 cells [29].
• After exposure to HCV E2 markedly fewer CD8-positive lymphocytes were attracted by RANTES when compared with CD8+ cells that were studied in the absence of HCV E2 [30].
• Furthermore, IL-1 beta was negatively correlated with the number of T8 lymphocytes [31].

Analytical, diagnostic and therapeutic context of CD8-Positive T-Lymphocytes

• No differences were noted in [3H]thymidine uptake by the OKT3-stimulated T8+ cell lines of MS and control groups [32].
• Using indirect immunofluorescence and flow cytometry, we determined the proportion and number of T3+, T4+, and T8+ cells in the peripheral blood of patients with systemic lupus erythematosus whose sera were positive for cold-reactive antilymphocyte antibodies versus values in patients whose sera were negative for these antibodies [33].
• Comparison to seronegative prostitutes and minor surgery control patients were made and significant elevations were seen in T8 lymphocytes (p = .03), IgG (p = .0001), and beta 2-microglobulin (p = .03) [34].
• In so-called nonresponder cultures as well as in monocyte-depleted cell cultures addition of IL-2 increased the CD3-induced activation and proliferation of T4 and T8 cell subsets [35].
• Vaccination required activities of both CD4 and CD8 positive lymphocytes, and likely involved the augmentation by GM-CSF of host professional antigen-presenting cell function [36].

References