Activation of immune competence by thymus factors.
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Aging↗
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Results for “Thymus Extracts”
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Influence of the thymus-corticothropin-growth hormone interaction on the rejection of skin allografts in the rat.
Skin allograft rejection was noticeably delayed in rats following hypophysectomy. Daily injections of hypophyseal growth hormone restored the normal reaction. Additional thymectomy had no influence on the rejection of hypophysectomized rats. In these animals growth hormone by itself had no significant influence on the graft rejection. It only restored a normal reaction when given together with thymic hormone. Corticotropin injections accelerated the allograft rejection. On this action of corticotropin thymic hormone has shown a significant inhibitory influence. The thymus was thus proved to be a synergist to growth hormone and an antagonist to corticotropin. Previous observations made with usual endocrinological test- are thus confirmed with an immunological test.
Adrenocorticotropic Hormone↗
The effect of antithymosin globulin on the recovery of T-cells in ATS-treated mice.
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Animals↗
The endocrine thymus: potential role for thymosin in the treatment of autoimmune disease.
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Amyloidosis↗
New perspectives on use of thymic factors in immune deficiency.
Current knowledge on the role of thymic factors in the immune response is inadequate and remains relatively primitive when compared with present technical possibilities for assessing lymphocyte subsets or cytokine interaction. New studies support the potential importance of thymic factors as regulators of immune interactions. Indirect evidence supports the concept that thymic factors may work at the level of IL-2. The functional identity of cells responsive to thymic factors and the relation of observed effects to cytokine network interactions need to be established. The use of thymic factors in the future will depend on the development of criteria to identify appropriate settings in which to use such factors and the implementation of appropriate measures of immune functional response.
CD4-CD8 Ratio↗
Lymphocyte-differentiating hormone of bursa of fabricius.
Induction of early lymphocyte differentiation was studied in vitro in fractionated bone marrow cells of newly hatched chickens, with alloantiserums to identify newly differentiated B cells (Bu-1+) and T cells (Th-1+). Thymus extract induced selective T cell differentiation; the activity of the extract corresponds to that of thymopoietin. Bursal extract induced both B cell and T cell differentiation, but at lower concentrations B cell differentiation was always greater. This activity is ascribed to a lymphocyte-differentiating hormone of the bursa of Fabricius, for which the name bursopoietin is suggested.
Animals↗
Antiviral guanosine analogs as substrates for deoxyguanosine kinase: implications for chemotherapy.
A highly active form of human recombinant deoxyguanosine kinase (dGK) phosphorylated purine nucleoside analogs active against cytomegalovirus, hepatitis B virus, and human immunodeficiency virus, such as penciclovir, 2',3'-dideoxyguanosine and 3'-fluoro-2',3'-dideoxyguanosine. The antiherpesvirus drug ganciclovir, which is also used in gene therapy, was a substrate for dGK, but with low efficiency. ATP and UTP were both good phosphate donors, with apparent K(m) values of 6 and 4 microM and V(max) values of 34 and 90 nmol of dGMP/mg of dGK/min, respectively. With a mixture of 5 mM ATP and 0.05 mM UTP, which represent physiologically relevant concentrations, the activities of dGK with ganciclovir and penciclovir was 1% and approximately 10%, respectively, of that with dGuo. The levels of dGK in different tissues were determined with a selective enzyme assay and the total activities per gram of tissues were similar in liver, brain, heart, and thymus extracts. The fact that the cellular dGK enzyme can phosphorylate antiviral guanosine analogs may help to explain the efficacies and side effects of several forms of chemotherapy.
Adenosine Triphosphate↗
Cellular immunity in systemic lupus erythematosus as evidenced in vitro by leucocyte migration inhibition tests.
A leucocyte migration inhibition test was performed on 26 patients with systemic lupus erythematosus (SLE) and on 35 control subjects using three different antigens, fetal calf thymus DNA, baker's yeast RNA, and calf thymus extractable nuclear antigen (ENA). Leucocyte migration was inhibited by DNA in 17 out of 26 SLE patients (65-3%), and in only 2 of the 35 controls (5-7%). When RNA or ENA was added none of the patients or controls showed inhibition. In SLE patients migration inhibition by DNA was significantly correlated with the presence of proteinuria and/or granular casts in urinary sediment. When the migration inhibition test was positive, immunofluorescence verified active histology of the glomeruli obtained by a percutaneous renal biopsy.
Adult↗
Autoantibodies in patients with juvenile chronic arthritis and their immediate family relatives.
Antibodies to nuclear antigens were assessed in 23 children with juvenile chronic arthritis (JCA) and 66 of their first degree relatives. Serum samples from 16 patients with JCA (70%) and nine relatives (14%) had antinuclear antibodies by indirect immunofluorescence. Antibodies against nuclear antigens in rabbit thymus extract or an erythroblastoid cell line (K562) were detected by countercurrent immunoelectrophoresis and immunoblotting in 16 patients (70%) and 39 family relatives (59%). Immunoblotting did not show any banding patterns common to all patients with JCA, though bands in the 43-45 kD range were detected in 5/23 patients. Anticardiolipin antibodies were found in 7/23 patients. In total, 18/20 families (90%) had members other than the probands with detectable autoantibodies. In five families immunoblotting showed common banding patterns between the probands and other members. This suggests that there might be an inherited trend towards autoimmune responses in some families of patients with JCA.
Antibodies, Antinuclear↗
Thymostimulin effects on the pituitary-ovarian axis in hyperprolactinemic young female rats.
This work was undertaken to study the effects of thymostimulin on the pituitary-ovarian axis of young female rats, and to elucidate possible prolactin-mediated effects. 30-day-old rats implanted with an ectopic pituitary from a littermate male donor under the kidney capsule or sham-operated animals were injected with thymostimulin or vehicle for 2 and 8 days. Chronic thymostimulin treatment to sham-operated rats increased plasma prolactin and estradiol levels, and decreased gonadotropin levels. Thymostimulin administration to pituitary-grafted rats did not further modify the increase in plasma prolactin and the decrease in plasma luteinizing hormone levels induced by the presence of an ectopic pituitary, suggesting a hypothalamic and/or hypophysial site of action of the thymic fraction. An increase in plasma estradiol and progesterone levels was observed with the in vivo thymostimulin treatment, although differential in vitro effects on estradiol responses to human chorionic gonadotropin in the various groups studied were observed. These effects seem to be mediated through the changes in plasma prolactin and gonadotropin concentrations observed. The above-mentioned changes induced by the thymic fraction on plasma estradiol and progesterone levels might counteract prolactin effects on the thymus. These data suggest that thymostimulin treatment of young female rats changes hypophysial and sex hormone secretion, as well as the response of the ovaries to human chorionic gonadotropin, probably modifying the normal process of sexual maturation.
Animals↗
Antimyenteric neuronal antibodies in scleroderma.
The pathogenesis of gastrointestinal (GI) dysmotility in scleroderma is incompletely understood, although previous studies have proposed a neuropathic mechanism. We studied patients with scleroderma as compared with other connective tissue disease patients and normal controls for the presence of circulating antibodies to myenteric neurons. Serial dilutions of sera were overlaid on rat intestine, double-labeled with antineurofilament antibody as a myenteric plexus marker, and imaged using indirect immunofluorescence techniques. High titer sera (> or = 1:50) from 19 out of 41 scleroderma patients stained myenteric neurons, whereas none of 22 normals or 5 patients with idiopathic GI dysmotility were positive. Although 6 out of 20 SLE and 6 out of 10 mixed connective tissue disease patients' sera stained myenteric plexus neurons, when positive sera were absorbed with calf thymus extract to remove antinuclear antibody, 15 scleroderma sera, 0 SLE, and 2 mixed connective tissue disease patients retained positive staining of myenteric neurons. Western blotting using actin and neuronal intermediate filament preparations failed to show immunoreactivity with scleroderma sera containing antimyenteric neuronal antibodies. Paraneoplastic sera associated with GI dysmotility stained myenteric neurons in a different pattern than seen with scleroderma sera. A positive correlation between the presence of Raynaud's phenomenon and antimyenteric neuronal antibodies was observed in scleroderma patients. Our results indicate that IgG antibodies reacting with myenteric neurons are present in many patients with scleroderma. Although the neuronal antigen has not yet been identified, the presence of myenteric neuronal antibodies in patients with GI dysmotility and scleroderma suggests a neuropathic process.
Adolescent↗
Effect of thymic humoral factor on cellular immune factors of normal children and of pediatric patients with ataxia telangiectasia and Down's syndrome.
Cellular immune functions of nine Down's syndrome patients and of nine was Ataxia telangiectasia vs. nine normal children and nine cord bloods, were evaluated using in vitro assays of peripheral blood lymphocytes. The in vitro assays included E rosette formation, antilymphocytic cytotoxicity by an antithymic antiserum and leukocyte migration inhibition factor (LIF) production. The mitogens and antigens used were phytohemagglutinin, purified protein derivative, and monilia antigen. The effect of a thymic hormone (THF) on these parameters was evaluated and it was administered therapeutically to three Down's syndrome patients and to two patients with Ataxia telangiectasia. Most deficient T-cell functions were reversed to normal after incubation of the lymphocytes with THF, or after THF therapeutic administration. In two Down's syndrome cases, the clinical course was not altered by THF administration, while one seemed to benefit from it markedly. One of the Atactic patients recovered from a severe viral infection, while the other died from intractable bronchopneumonia.
Ataxia Telangiectasia↗
Thymostimulin effects on lymphoid organs in Ames dwarf mice.
This work was undertaken to study the effects of thymostimulin (TP-1) on the immune function in Ames dwarf mice, and to relate these effects to PRL and/or GH deficiency in these animals. Male Ames dwarf mice implanted with pituitaries from normal mice under the kidney capsule, sham-operated dwarf mice and normal immature or adult mice were injected daily for five days with TP-1. In comparison to normal animals, sham-operated dwarf mice had markedly lower body, thymus and spleen weights, as well as a lower number of lymphocytes in the spleen and in the thymus and the natural killer (NK) activity of spleen lymphocytes. Ectopic pituitary transplants produced the expected enhancement of body weight gain and increased spleen and thymus weights, which reached the values found in normal (non-dwarf) animals. The numbers of lymphocytes in the spleen and thymus were significantly increased in pituitary-grafted dwarf mice, but the grafts did not modify the cytotoxic activity of NK spleen cells, or the number of peripheral white blood cells (PWBC). In sham-operated dwarf mice, TP-1 treatment did not modify the number of cells in the spleen and thymus, or the NK activity. In pituitary-grafted dwarf mice, treatment with TP-1 induced an increase in the number of spleen lymphocytes and in the NK activity of spleen cells without affecting the weight of lymphoid organs or the number of thymic cells. Plasma prolactin (PRL) and growth hormone (GH) levels of pituitary-grafted dwarf mice were not changed after TP-1 administration.(ABSTRACT TRUNCATED AT 250 WORDS)
Analysis of Variance↗
Thymalfasin for the treatment of chronic hepatitis B.
Chronic hepatitis B virus infection is a serious problem because of its worldwide distribution and possible adverse chronic sequelae, such as cirrhosis and hepatocellular carcinoma. Chronic hepatitis B infection is a dynamic state of interactions between the virus, hepatocyte and host immune response. Interferon-alpha and direct antiviral agents, such as lamivudine (Epivir, GlaxoSmithKline), are effective in the therapy of chronic HBV infection but the efficacy is far from satisfactory. Thymalfasin (thymosin alpha1; Talpha1, Zadaxintrade mark, SciClone Pharmaceuticals, Inc.) is a 28-amino acid polypeptide produced synthetically but originally isolated from thymosin fraction 5, a bovine thymus extract containing a number of immunologically active peptides. In vitro studies have shown that Talpha1 can influence T-cell production and maturation, stimulate production of Th1 cytokines such as interferon-gamma and interleukin-2, and activate natural killer cell-mediated cytotoxicity. Seven randomized controlled studies on Talpha1 monotherapy in patients with chronic hepatitis B showed that 6 months treatment with Talpha1 (1.6 mg twice-weekly) resulted in a significantly higher sustained response rate than untreated controls. The benefits of Talpha1 therapy is usually not immediately apparent during therapy. There is a trend for complete virological response to increase or accumulate gradually after the end of thymosin therapy. The results of Talpha1 and interferon combination therapy in two open-label trials were also promising. In terms of the mechanisms of action, a combination of Talpha1 and nucleoside or nucleotide analogs is a logical approach in the control of chronic HBV infection and a randomized control study is ongoing.
Animals↗
Thymic peptides as anti-aging drugs: effect of thymic hormones on immunity and life span.
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Aging↗
Update and future perspectives of a thymic biological response modifier (Thymomodulin).
Thymomodulin (Ellem Industria Farmaceutica spa, Milan, Italy) is a calf thymus acid lysate with immunomodulating activities. It is composed of several peptides with a molecular weight range of 1-10kD. Extensive studies in animal systems showed that Thymomodulin exhibited no, or very little toxicity even when used at high doses. Studies done in vitro and in vivo demonstrated that Thymomodulin is a biologically active compound which regulates the maturation of human and murine pre T lymphocytes, as well as modulate the functions of apparently mature human and animal B and T lymphocytes. It was observed that Thymomodulin can promote myelopoiesis as demonstrated by an increase of granulocyte-macrophage colonies in agar. Although additional studies to examine its target cell lineage are required, it appears that Thymomodulin exhibits specificity toward T cells. Therefore, enhancement of other cell lineage functions by Thymomodulin may be indirect, and mainly due to its effect on T cells. Of major importance is to note that Thymomodulin is prepared in a manner which allows it to maintain its biological activity when administered orally.
Acquired Immunodeficiency Syndrome↗