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Biomedical subjects

J R Huddlestone

Publications and source records attributed to J R Huddlestone.

12 recordsLinked to original sources
PubMed1984

Systemic alpha-interferon therapy of multiple sclerosis.

A randomized, double-blind, placebo-controlled crossover study tested the efficacy of natural alpha interferon in altering exacerbating-remitting MS. Twenty-four patients with frequent exacerbations were treated for 6-month periods, beginning with either 5 X 10(6) IU of interferon daily or placebo. A 6-month washout period followed each treatment. Exacerbation rates were reduced during interferon and placebo phases compared with pre-study rates; a greater reduction occurred on interferon, particularly following placebo, possibly reflecting a learning phenomenon. Fifteen patients with a strictly exacerbating-remitting course had fewer and milder exacerbations on interferon compared with those on placebo, whereas 9 patients with a progressive component continued to have active disease. These results suggest that interferon might reduce exacerbations in certain patients and indicate guidelines for future trials of interferon in MS.

Adult↗
PubMed1982

Suppressor T cells are activated in vivo in patients with multiple sclerosis coinciding with remission from acute attack.

By a variety of assays, investigators (1-4) from several laboratories previously observed changes in numbers of thymus-derived suppressor lymphocytes (Ts) in patients with acute active multiple sclerosis (MS). Changes in numbers of Ts in the peripheral blood compartment of such patients closely follow disease activity. Extending these observations we now report Ts are activated in the peripheral blood of certain patients with MS. This activation occurred in vivo in the majority of patients with active disease, but only during remission after an acute episode of MS. In contrast, activated Ts were found infrequently in patients with chronic progressive or stable MS, with neurologic diseases other than MS, or healthy individuals. The suppressor activity found in peripheral blood T cells during the acute remitting stage of disease was associated with elevated numbers of lymphocytes bearing Fc receptors for IgG and/or OKT8 markers.

Humans↗
PubMed1981

Interferon acts directly on human B lymphocytes to modulate immunoglobulin synthesis.

At different times of exposure, interferon (IFN) enhanced and suppressed pokeweed mitogen- (PWM) induced IgG synthesis by human peripheral blood lymphocytes (PBL). Pretreatment of PBL and IFN frequently increased antibody production by more than 100% when compared with that by untreated PBL. Results of experiments in which PBL were separated into T and B subpopulations indicated that IFN preparations acted directly on B cells. Thus, mixtures of IFN-treated B cells and untreated T cells from 5 of 7 persons tested produced 81% to 500% more IgG than untreated, matched control cells. However, IFN-treated monocytes mixed with untreated B and T cells or IFN-treated T cells mixed with untreated B cells failed to enhance IgG production significantly in similar assays. In contrast to the pretreatment protocol, when IFN was present in the incubation mixture throughout the PWM assay, IgG production decreased. Sephadex chromatography of the IFN and tests of the resulting fractions indicated that the IgG production-enhancing activity was located in the fraction carrying the antiviral activity.

Adolescent↗
PubMed1979

Induction and kinetics of natural killer cells in humans following interferon therapy.

Natural killer (NK) cells are non-B, non-T lymphocytes that effect spontaneous cytolysis of both virus-infected and neoplastically transformed target cells. These NK lymphocytes have been detected in several species including man. Interferon is a primary regulator of natural killer activity. Because NK cells have been implicated in the regulation of tumour cell expression and can be induced by interferon in murine models, we have studied patients receiving large doses of interferon to determine (1) whether interferon could induce NK lymphocytes in the peripheral blood of man, and (2) whether there are characteristic kinetics for the appearance, disappearance and reactivation of NK lymphocytes following interferon therapy. We report here the activation of human NK cells by the systemic inoculation of human subjects with interferon. Five patients received interferon as therapy for non-Hodgkin's lymphoma. All showed a marked increase in NK cell activity 12--24 h after inoculation. Peak NK activity occurred 18 h after introducing interferon, and thereafter declined rapidly but remained above pre-interferon levels. Induced NK activity occurred with reintroduction of interferon but at lower levels of activity and with different kinetics.

Humans↗
PubMed1979

T suppressor (TG) lymphocytes fluctuate in parallel with changes in the clinical course of patients with multiple sclerosis.

Aberrant immune responses to several unrelated antigens observed in patients with multiple sclerosis have suggested faulty regulation of immunocompetent cells. Recently human T lymphocytes have been segregated into subpopulations. T lymphocytes that bear Fc receptors for IgG suppress B lymphocyte proliferation and the production of IgG. Here we report studies on the percentage of TG cells in the peripheral blood of 25 patients all of whom met stringent clinical criteria for the diagnosis of multiple sclerosis (MS). Many of these patients were followed for more than 14 months. In the total group, nine patients experienced definite acute exacerbations of disease followed by periods of remission. The mean percentages +/- 1 standard deviation of TG cells found in all MS patients during remission, 16 +/- 6 was significantly higher than the mean found in normal subjects, 12 +/- 2. In contrast, the mean found in patients experiencing an acute attack, 6 +/- 2 was significantly lower than the mean TG level of normal subjects. Moreover, when individual patients were followed through their clinical illness, levels of TG lymphocytes that were low during acute exacerbations invariably increased to relatively high levels with the onset of clinical remission.

Blood Cell Count↗