Function and specificity of human V gamma 9/V delta 2 T lymphocytes.
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Clone Cells↗
Biomedical subjects
M Malkovsky
Publications and source records attributed to M Malkovsky.
Recognition by human V gamma 9/V delta 2 T cells of a GroEL homolog on Daudi Burkitt's lymphoma cells.
All human gamma delta T cells coexpressing the products of the variable (V) region T cell receptor (TCR) gene segments V gamma 9 and V delta 2 recognize antigens from mycobacterial extracts and Daudi cells. Exogenous and endogenous ligands on the cell surface, homologous to the groEL heat shock family, induced reactivities that resembled superantigen responses in this major subset of human peripheral blood gamma delta T cells. Stimulation of human V gamma 9/V delta 2 T cells is not restricted by human leukocyte antigens (HLA), including nonpolymorphic beta 2-microglobulin (beta 2M)-associated class Ib molecules. These data may be important for understanding the role of gamma delta T cells in autoimmunity and in responses to microorganisms and tumors.
Antigen-Presenting Cells↗
Gamma/delta T cell clones and natural killer cell clones mediate distinct patterns of non-major histocompatibility complex-restricted cytolysis.
Non-MHC-restricted killer cells are cytotoxic lymphocytes that can mediate cytolysis of most tumor targets without apparent selectivity and restriction by the MHC, particularly when activated with IL-2. These effector cells include predominantly NK cells and T cells expressing the TCR-gamma/delta. We found that TCR-gamma/delta-1+, delta TSC1-, BB3+, Ti gamma A+ T cell clones mediate a characteristic cytolytic pattern of non-MHC-restricted cytolysis that is markedly different from NK clones and alpha/beta T cell clones derived from the peripheral blood of the same normal individuals. The characteristic finding is that all BB3/Ti gamma A+ gamma/delta clones mediate strong cytolysis of Daudi cells but they do not lyse Raji cells. In contrast, NK clones from the same donors mediate strong cytolysis of both Daudi and Raji targets. Cytotoxicity by the gamma/delta clones on certain target cells such as Daudi and Molt 4 can be specifically inhibited by mAbs reactive against the TCR-gamma/delta. Therefore, the TCR-gamma/delta on these clones either directly recognizes target epitopes on some tumor targets or it is involved in the regulation of their cytotoxic function. The expression of TCR-gamma/delta products reacting with the BB3 and Ti gamma A mAbs reflects the usage of identical TCR-gamma/delta V region genes that appear to be associated with the characteristic pattern of non-MHC-restricted cytotoxicity displayed by this major subset of human peripheral blood gamma/delta cells.
Antibodies, Monoclonal↗
Endogenous release of interferon-gamma and diminished response of peripheral blood mononuclear cells to antigenic stimulation.
The capacity of T lymphocytes to proliferate in response to stimulation and the amount of representative lymphokines produced in vitro often correlate with the immunocompetence of patients. However, direct and indirect measurement of endogenous interferon-gamma (IFN-gamma) brings some evidence that decreased in vitro production of IFN-gamma by T lymphocytes is associated with increased concentrations in vivo. The data indicate that both a functional inhibition of IFN-gamma and its continuous presence at high levels may result in hyporesponsiveness or unresponsiveness of immune cells. A possible role of IFN-gamma in the induction of tolerance is discussed.
Animals↗
A kinetic analysis of lymphocyte 5'-nucleotidase in B-cell clones from control subjects and patients with primary hypogammaglobulinaemia.
The affinity of lymphocyte 5'-nucleotidase (5NT) for its substrate adenosine monophosphate (AMP) was studied in Epstein-Barr virus immortalized B-lymphocyte clones from healthy controls and patients with primary hypogammaglobulinaemia. Km values for AMP for 5NT in most of the patient clones were found to be significantly increased compared to B-cell clones from normal subjects, whereas Vmax values were within the normal range.
5'-Nucleotidase↗
Inactivation of HIV by nonoxynol-9.
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Acquired Immunodeficiency Syndrome↗
Surgical gloves as a mechanical barrier against human immunodeficiency viruses.
A wide variety of surgical gloves are presently available. Seven different types of gloves were investigated for the ability to prevent transmission of the human immunodeficiency virus (HIV), the causative agent of AIDS. Six types of gloves withstood severe compression tests and also exhibited direct antiviral properties. No penetration of HIV through the intact glove was detected.
Acquired Immunodeficiency Syndrome↗
A search for retrovirus infection in systemic lupus erythematosus and rheumatoid arthritis.
Evidence for retroviral infection in general and human immunodeficiency virus (HIV) infection in particular was sought in freshly isolated peripheral blood T cells, B cells, and monocyte-macrophages from patients with rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) and also in T cell and B cell lines established from the same source. Similar cells isolated from rheumatoid synovial membrane were also examined. The strategy used for the detection of virus was cocultivation with susceptible cell lines looking for syncytia formation, reverse transcriptase production, and nucleic acid hybridisation with HIV cDNA probes. No evidence for infection was obtained.
Acquired Immunodeficiency Syndrome↗
Antigen test versus reverse transcriptase assay for detecting HIV.
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Acquired Immunodeficiency Syndrome↗
Neutralisation of HIV isolates by anti-idiotypic antibodies which mimic the T4 (CD4) epitope: a potential AIDS vaccine.
Polyclonal anti-idiotypic antibodies were raised in mice against anti-Leu3a, a mouse monoclonal anti-human T4 (CD4) antibody that blocks the in-vitro binding of human immunodeficiency virus (HIV) to the CD4 molecule. The anti-idiotypes recognized anti-Leu3a but not OKT4, an anti-human T4 antibody that does not inhibit HIV binding to CD4. The anti-idiotypes specifically reacted with the HIV envelope glycoprotein in solid-phase immunoassays. More importantly, the anti-idiotypes neutralised three distinct isolates of HIV-1 and one isolate of HIV-2 in a syncytial inhibition assay. These results have implications for a potential AIDS vaccine of anti-CD4 preparations to induce an anti-idiotypic response with the capacity to bind HIV at its receptor site.
Acquired Immunodeficiency Syndrome↗
Inhibition of HIV replication in vitro by fusidic acid.
A 58-year-old man with AIDS improved clinically after the introduction of fusidic acid, 500 mg three times a day orally, to his therapeutic regimen. Fusidic acid may have had a direct effect against HIV. Fusidic acid has anti-HIV activity in vitro at levels readily attainable in vivo. The drug does not appear to be a reverse transcriptase inhibitor and its mode of action against HIV is unknown. Fusidic acid can be given orally and has few side-effects. These results justify fuller evaluation of fusidic acid as therapy against AIDS and HIV infection.
Acquired Immunodeficiency Syndrome↗
Nonrestricted cytotoxicity mediated by interleukin 2-expanded leukocytes is inhibited by anti-LFA-1 monoclonal antibodies (MoAb) but potentiated by anti-CD3 MoAb.
Previous results have shown that in addition to their ability to kill tumor cell lines, peripheral blood leukocytes (PBL) expanded in interleukin 2 (IL-2) can also destroy normal PBL targets. Cold target competition results show that PBL and tumor cells can be destroyed by the same population of IL-2-expanded leukocytes (IEL), with better killing observed for tumor cell targets. Since cytolytic activity of IEL is nonspecific, differential binding of target cells by IEL could determine how well each target cell type can be killed. The binding affinity of IEL, in turn, could be influenced by the accessory molecules expressed on effector and target cells. We tested the effect of MoAb to LFA-1, CD2, CD3, CD4, CD8, and HLA molecules on killing mediated by IEL. Anti-LFA-1 inhibited strongly the killing of normal PBL and to a lesser extent the killing of tumor cells. Anti-CD2, CD3, CD4, CD8, and HLA class I molecules did not inhibit the nonspecific killing; rather, anti-CD3 potentiated the killing of PBL, K562, and Daudi cells. These results support the notion that qualitative and quantitative variations in LFA-1-mediated binding of target cells by IEL could result in differential killing of targets. The possibility of using anti-CD3 to selectively potentiate the killing of tumor cells is discussed.
Antibodies, Monoclonal↗
Increased lymphokine activated killer (LAK) activity in the regional lymph nodes of mice following immunization with contact sensitizing agents.
The regional lymph nodes of mice show increased IL-2 activated killer (LAK) activity following immunization with the contact sensitizing agents, 'oxazolone' and picryl chloride. This is best elicited with 500 mu/ml human recombinant IL-2 and can be demonstrated with both YAC-1 and K562 targets. There is also a lesser increase in NK activity.
Animals↗
AIDS, Portugal, and Africa.
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Acquired Immunodeficiency Syndrome↗
Isolation of retroviruses from two patients with "common variable" hypogammaglobulinaemia.
Retroviruses related to human T-lymphotropic virus III/lymphadenopathy-associated virus (HTLV-III/LAV) have been isolated from peripheral-blood mononuclear cells of two patients with "common variable" hypogammaglobulinaemia who were being treated with intravenous gammaglobulin. One has had three different opportunistic infections. In both patients hypogammaglobulinaemia developed within 6 years of a longlasting undiagnosed viral-like illness in adolescence, and it is suggested that the virus causing that illness also gave rise to the hypogammaglobulinaemia. However, iatrogenic infection from intravenous gammaglobulin cannot be ruled out.
Adolescent↗
Acquired immunodeficiency with disseminated cryptococcosis.
A 9 year old Portuguese boy presented with severe wasting and a disseminated cryptococcal infection that resolved after massive doses of intrathecal and parenteral antifungal agents. Clinical and laboratory findings were consistent with AIDS. Apart from neonatal blood transfusions, there were no identified risk factors for HTLV III infection.
Acquired Immunodeficiency Syndrome↗
The role of dendritic cells in the initiation of immune responses to contact sensitizers. I. In vivo exposure to antigen.
Twenty-four hours after skin painting mice with picryl chloride (PIC) there was a four- to fivefold increase in the numbers of dendritic cells (DC) isolated from the lymph nodes. These DC initiated primary proliferative and cytotoxic responses when added to cultures of normal syngeneic lymph node cells. The proliferative response was enhanced when the donors of the responding lymph node cells were sensitized with the same antigen. Contact sensitivity developed in syngeneic mice injected into the footpads with 30,000-50,000 DC from lymph nodes of mice painted with picryl chloride 1 day previously. Thus, 1 day after skin painting mice, there were dendritic cells in the draining lymph nodes which were able both to initiate primary stimulation of lymphocytes in vitro and to sensitize recipient mice to give specific delayed hypersensitivity reactions.
Animals↗
Augmentation of interleukin-2 production and delayed hypersensitivity in mice infected with Mycobacterium bovis and fed a diet supplemented with vitamin A acetate.
High-dose Mycobacterium bovis-infected mice fed a vitamin A acetate-supplemented diet developed a positive skin reaction to purified protein derivative of mycobacteria, and their spleen cells showed an increased IL-2 production in vitro.
Animals↗