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Biomedical subjects

A Newell

Publications and source records attributed to A Newell.

11 recordsLinked to original sources
PubMed1992

Inhibitory activity of HIV envelope gp120 dominates over its antigenicity for human T cells.

HIV-1 envelope glycoprotein (gp120), as a CD4-binding reactant, has been shown to inhibit in its native form human T cell responses to several antigens. Here we show that gp120 in soluble form also inhibits activation of a specific human T cell line that responds to gp120-pulsed autologous antigen-presenting cells. In addition the inhibitory property of gp120 for antigen-driven T cell proliferation depends upon its ability to bind CD4 and is lost when CD4-binding capacity is abolished by denaturation, or blocked by complexing with soluble CD4 or with polyclonal antibodies. In contrast, antigenicity of denatured or complexed gp120 for specific human T cells is preserved. Similar effects are also observed with another CD4-binding reactant (i.e. anti-Leu 3a MoAb), which stimulates and/or inhibits human T cells specific for mouse immunoglobulins depending on native or denatured conformation.

Antibodies, Monoclonal↗
PubMed1992

HIV-induced deletion of antigen-specific T cell function is MHC restricted.

When antigen-specific T cells are pulsed by antigen-presenting cells (APC) in the presence of HIV they are functionally deleted following subsequent exposure to syngeneic APC in the absence of HIV. Recombinant soluble HIV envelope (gp120) is able to induce a similar effect which, unlike that induced by HIV, is reversible. Neither HIV nor gp120 affect the ability to respond to IL-2. Thus it is only antigen-specific responses involving the T cell receptor pathways and CD4/MHC class II interaction that appear to be inhibited by HIV-1 and gp120. Furthermore, the functional impairment caused by HIV-1 is specific to the T cells that respond to the antigen in co-culture with HIV, as there is no apparent effect on 'bystander'-activated T cells specific for another antigen. Antigen-specific T cell lines may be deleted by a signalling mechanism which involves molecules other than gp120/CD4 but still requires MHC class II restriction.

Animals↗
PubMed1992

HTLV-I infection and neurological disease in Rio de Janeiro.

Fifty patients with chronic neurological diseases attending a clinic in Rio de Janeiro, Brazil, were examined for evidence of HTLV-I infection. Fifteen of 27 with progressive paraparesis of obscure origin had antibodies to HTLV-I in high titre in their serum samples, and 10 of 13 studied had antibodies in their cerebrospinal fluid. The clinical features of the antibody positive patients were similar to those of patients with HTLV-I associated myelopathy from other countries except that half of the Brazilian patients were white. Seven patients had multiple sclerosis and one of these had antibodies to HTLV-I in the serum. None of the eight patients with motor neuron disease and four with polymyositis had HTLV-I antibodies in their serum samples.

Africa↗
PubMed1988

HTLV-1 infection in tropical spastic paraparesis: lymphocyte culture and serologic response.

All 17 patients with tropical spastic paraparesis (TSP) in a series seen in the United Kingdom have antibodies to the human T cell leukemia virus type 1 (HTLV-1). Cultured peripheral blood lymphocytes from these patients formed multinucleated giant cells and reacted with sera and monoclonal antibodies to HTLV-1 in a manner identical to adult T cell leukemia-lymphoma (ATLL) patient lymphocytes. Western blot analysis failed to reveal any marked difference in the antigens recognized by sera from TSP and ATLL patients. The sera from TSP patients, their asymptomatic relatives and ATLL patients were titrated using the following assays: enzyme-linked immunosorbent assays (ELISA), particle agglutination, antibody-dependent cell-mediated cytotoxicity, and pseudotype neutralization. There were significantly stronger serologic responses in the TSP patients than in their relatives or ATLL patients. High antibody titers in the presence of replicating virus often reflect the antigen load; however, these data are also consistent with the suggestion that neurologic damage in TSP may be immunologically mediated.

Adult↗
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↗
PubMed1967

Computer science.

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Computers↗