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Biomedical subjects

M Malkovsky

Publications and source records attributed to M Malkovsky.

At least 37 records · Page 2Linked to original sources
PubMed1988

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↗
PubMed1988

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↗
PubMed1987

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↗
PubMed1987

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↗
PubMed1987

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↗
PubMed1987

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↗
PubMed1986

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↗
PubMed1986

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↗
PubMed1985

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↗
PubMed1985

In vivo activity of interleukin-2: conversion of a stimulus causing unresponsiveness to a stimulus causing contact hypersensitivity by the injection of interleukin-2.

The intravenous injection of hapten-modified (picrylated) cells causes unresponsiveness. When conventional or recombinant interleukin-2 (IL-2) is also injected, strong contact sensitivity occurs. This IL-2 is effective when given 7 hr after the injection of the picrylated cells or 2 days later, but has no effect when given beforehand. It is suggested that picrylated cells given intravenously fail to induce contact sensitivity secondary to a failure of IL-2 production, and that IL-2 may be one of the second signals which converts a 'tolerogenic' stimulus into an immunogenic stimulus.

Animals↗
PubMed1984

The role of B cell differentiation factors and specific T cell help in the pathogenesis of primary hypogammaglobulinemia.

We have examined the function of T and B cells from patients with late onset primary acquired hypogammaglobulinemia (PHG). T cells from these patients give effective help to normal B cells for antigen-dependent antibody synthesis. PHG mononuclear cells also synthesize normal quantities of B cell differentiation factors, which enhance IgG, IgM and antigen-dependent antibody synthesis by normal lymphocytes. While patient T cells appear to behave appropriately, the responsiveness of patient B cells is abnormal. Although they respond to differentiation factors with increased synthesis of IgM, overall levels are 10-50-fold lower than normal B cells, and they produce little or no IgG. This pattern of response is not altered if normal T cells are the source of help. The poor response of the B cell appears to represent immaturity rather than an inherent defect, as IgG-secreting clones can be obtained after Epstein-Barr virus transformation of lymphocytes from certain patients, and some of these clones respond to differentiation factors with increased IgG production. The lack of any functional defect in the T population, and the apparent immaturity rather than abnormality of the B cells, may implicate accessory cells in the pathogenesis of the disease.

Agammaglobulinemia↗
PubMed1984

T helper factor in contact sensitivity: antigen-specific I-A+ helper factor is made by an Lyt-1+2-, I-A+, I-J- T cell.

Antigen-specific T helper factor appears in the 24 hr supernatant of lymph node cells taken 4 days after immunization with contact sensitizer. The factor is assayed by its ability to augment the contact sensitivity response induced by haptenized spleen cells. In practice, picrylated or oxazolonated spleen cells are treated with the factor for 1 hr at 4 degrees and 4 x 10(6) cells are injected into the footpads of recipient mice. Contact sensitivity is assessed 5 days later. The factor first appears 3 days after immunization and its production depends on an Lyt-1+2-, I-A+, I-J- T cell. It is antigen-specific in its action in a criss-cross experiment, and can be absorbed with and eluted from haptenized beads. It bears I-A determinant(s) and the I-A determinant and the antigen binding site(s) occur on the same molecule. The molecular weight is around 60,000. The possible role of T helper factors in the activation of the antigen-presenting cell in the induction stage of the immune response is discussed.

Animals↗
PubMed1984

Suppressor cells induced by BCG release non-specific factors in vitro which inhibit DNA synthesis and interleukin-2 production.

Mice injected intravenously with a high dose (5 X 10(7) ) of BCG fail to develop delayed hypersensitivity to BCG and are described as anergic or unresponsive. Spleen cells from these mice release factors on culture which suppress DNA synthesis induced by concanavalin A in vitro. Cell separation experiments showed that both macrophages and T cells produce inhibitory factors. However, the macrophage factor has a molecular weight 10,000-30,000, while the T cell factor has a molecular weight of 50,000-70,000. Further evidence that these two factors are different is provided by the kinetics of their action. The T cell factor only acts when given within 12 hr of stimulation with concanavalin A, while the macrophage factor acts even when given at 48 hr. In the case of the T cell factor, the inhibition of DNA synthesis may be attributed to its ability to block the interleukin-2 production induced by Con A. As similar T cell and macrophage factors are produced in mice responding to simple chemically reactive haptenes (contact sensitizers), it is possible that a similar suppressor circuit is involved in the control of the response to contact sensitizers and in the production of unresponsiveness (anergy) in mice given large doses of BCG.

Animals↗