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PubMed1983

Isolation and assay of a human plasma factor affecting human thymus-derived lymphocytes.

An amino acid-containing factor has been isolated from a dialysate of defibrinated human plasma using Sephadex G-25 and Sephadex CM-25 column chromatography. This factor is capable of enhancing "avid" E-rosette formation by normal human lymphocytes, where avid E-rosettes are defined as lymphocytes binding 10 or more sheep red cells. This factor is effective at concentrations as low as 10(-12) g/ml. It resembles the porcine and murine "facteur thymique sérique" (e.g. J.-F. Bach, M. Dardenne, J.-M. Pleau, and J. Rosa, Nature (London) 266, 55, 1977) in its elution characteristics, its capacity to enhance avid E-rosette formation and, tentatively, its amino acid composition.

Animals↗
PubMed1983

The effect of a human plasma thymic factor on human peripheral blood mononuclear cell subpopulations.

Human plasma thymic factor in vitro (human "facteur thymique sérique," or FTS) (at concentrations between 0.25 and 0.25 X 10(5) pg/ml) significantly increased "avid" E-rosette formation by human peripheral blood mononuclear cells (PBMC). It also increased the percentage of OKT8+ cells but did not affect the percentages of OKT3+, OKT4+, OKT11+, OKIa1+, or OKM+ cells. In the low-density immature PBMC, FTS increased both total and avid E-rosette formation, while increasing the percentages of OKT3+ and OKT8+ cells and decreasing the percentage of OKT4+ cells. Theophylline decreased E-rosette formation and the percentages of OKT3+ and OKT4+ among PBMC, and increased the percentages of OKT3+ and OKT4+ among the low-density cells. Human FTS may be capable of inducing maturation of immature PBMC into E-rosette-forming OKT3+8+ cells, while increasing the percentage of mature cells which may be doubly labeled OKT4+8+. The function of such doubly labeled cells remains to be determined. Human FTS may act by increasing intracellular cAMP in immature cells, but probably has a different mode of action in mature cells.

Adult↗
PubMed1983

Studies of the thymus in mice bearing the Lewis lung carcinoma. II. Modulation of thymic natural killer activity by thymulin (FTS-Zn) and the antimetastatic effect of zinc.

Modulation of thymic natural killer (NK) cell activity by the serum thymic factor (thymulin or FTS-Zn) was demonstrated in mice carrying the Lewis lung carcinoma (3LL). Thymulin decreased the increased NK activity found in amputated (tumor) tumor-bearing mice and induced a significant NK activity in nonamputated mice, normally devoid of such activity. Zinc had no effect in either case. Histological studies revealed that zinc prevented the tumor-induced thymic atrophy. A clear-cut decrease in the number of lung metastases was observed in zinc-treated mice. This effect was suppressed by concomitant administration of thymulin to amputated mice. The thymic dependency of the anti-metastatic action of zinc as well as the mode of action of thymulin on NK cell activity in tumor-bearing animals is discussed.

Animals↗
PubMed1984

Studies of the thymus in mice bearing the Lewis lung carcinoma. III. Possible mechanisms of tumor-induced thymic atrophy.

Adrenalectomy prevents thymic atrophy but not splenomegaly in mice implanted with Lewis Lung carcinoma cells. Surprisingly, the presence of the tumor does not lead to increased levels of corticosterone, which argues against an exclusive role of stress in the tumor-induced involution of the thymus. Interestingly, serum from tumor-bearing hosts in vitro displays strong cytolytic activity against normal syngeneic thymocytes. This thymocytotoxicity depends upon the stage of tumor development, i.e., the size of the local tumor, and is concomitant with the severe thymic atrophy. Treatment of donor mice with zinc chloride or excision of the local tumor, both of which have been shown to prevent this involution of the thymus, also abolishes the cytotoxic effect of the serum. The active component of the serum is a nonimmunoglobulin fraction of molecular weight greater than 25,000 Da. The possible mechanisms of tumor-dependent thymic atrophy as well as the in vivo relevance of this serum-mediated thymocytotoxicity are discussed.

Adrenalectomy↗
PubMed1989

Male BXSB mice develop a thymic hormonal dysfunction with presence of intraepithelial crystalline inclusions.

The thymus is morphologically abnormal in male BXSB mice with cortical involution densification of the epithelium and the presence of intraepithelial crystals. The thymic endocrine function in BXSB mice was appraised using a biological assay to measure the level of the zinc-dependent thymic hormone, thymulin, and an indirect immunofluorescence technique to evaluate the number of cells synthesizing the hormone within the thymus. Unlike the dramatically accelerated age-linked decline of thymulin production reported in females of other autoimmune strains (measured as early as 6 weeks of age), only male BXSB were affected, as compared to normal strains. The number of hormone-producing cells was significantly reduced in male BXSB thymuses, in parallel with this hormonal decrease. Thymulin inhibitory molecules were detected in male BXSB sera, as early as 8 weeks of age, as evaluated by their capacity to absorb in vitro and in vivo the biological activity of the hormone. These inhibitors are thymus dependent since they disappear after adult thymectomy. They are low MW molecules (less than 10 kDa), as previously found in normal aging mice, rather than autoantibodies, as evidenced in two autoimmune strains (B/W and db/db mice). These findings demonstrate that male BXSB mice develop thymic abnormalities very similar to those observed in other autoimmune strains. The presence of intrathymic crystals and of low MW inhibitors suggests the role of abnormal storage and the excretion of thymulin. This thymic dysfunction may play a role in the maintenance of B cell hyperactivity previously shown in BXSB males.

Aging↗
PubMed1989

Thymic hormones and prostaglandins. I. Lack of stimulation of prostaglandin production by thymic hormones.

Prostaglandins (PGs) have been implicated as possible mediators of the biological activity of thymic hormones. It has been shown that type E-PGs are able to mimic the action of several thymic hormones and that indomethacin prevents in vivo or in vitro the appearance of Thy-1+ antigen induced by some of these factors. We thus investigated a possible role for PGs in the mechanism of action of different thymic extracts and peptides. Attempts to modulate prostaglandin production showed that neither thymosin fraction 5 (0.01-100 micrograms/ml), nor thymosin alpha 1 (1-10 micrograms/ml), thymulin (0.001-100 ng/ml), thymopoietin II (10-1000 ng/ml) or TP5 (10-1000 ng/ml) affect PGE2, 6-keto-PGF1 alpha, PGF2 alpha and TXB2 production by spleen cells from control and thymectomized mice. These results do not support the hypothesis that prostaglandins could act as mediators of thymic hormones.

Animals↗
PubMed1990

Thymic hormones and prostaglandins. II. Synergistic effect on mouse spontaneous rosette forming cells.

Prostaglandins (PGs) have been assumed to play a role in the biological activity of thymic hormones (TH). Indeed, it has been shown that type E-PGs are able to mimic the action of several TH. Moreover, indomethacin interferes in the rosette assay, which still represents the most commonly used bioassay for the evaluation of TH and, in particular thymulin levels, in biological fluids. Previously, our attempt to modulate PG production by different TH showed that none of the TH tested affect PGE2, 6-keto-PGF1 alpha, PGF2 alpha and TXB2 production by spleen cells from control and thymectomized (Tx) mice, while indomethacin was able to inhibit the spontaneous PG production. Here, we investigated a possible role for each endogenously produced PG in the experimental conditions of the rosette assay, in order to define: 1) whether or not there was a specificity of action of a given PG; and 2) to analyze the pattern of action between thymulin and the endogenously produced PGs. We demonstrated that PGE2 and 6-keto-PGF1 alpha are the PGs which are physiologically involved in the rosette assay, according to their levels of endogenous production, and that they are able to synergize with thymulin. This synergy was demonstrated in two ways: 1) by adding anti-PGE2 and anti-6-keto PGF1 alpha-antibodies, which prevent part of the thymulin effect, or 2) by simultaneous addition of PG and thymulin, at concentrations far lower than those which correspond to their thymulin-like effect. Moreover, PGE2 addition, at concentration close to that found to be endogenously produced, partially reversed the indomethacin-induced effect in the rosette assay. In conclusion, if PGs do not act as mediators of thymulin, they are able to synergize in one of its biological action.

Animals↗
PubMed1989

Serum thymic hormone thymulin activity is normal in children with asthma.

In asthma, it has been hypothesized that suppressor T-lymphocytes play a protective role and have been reported to be functionally abnormal. Thymic hormone thymulin plays a role in the differentiation of T-lymphocytes and plasmatic thymulin concentration and is related to the functional state of the thymus. To assess the participation of the thymus in the impairment of T-lymphocyte function, we measured plasma thymulin activity in children with allergic asthma (N = 40). The plasma thymulin activity was compared with plasma thymulin activity of children with nonallergic asthma (N = 6), children with atopic dermatitis (N = 9) or allergic rhinitis (N = 7), and in age-matched healthy control children (N = 18) (age range of children studied, 2 to 19 years). Thymulin activity was found within the normal range (1/16 to 1/64) in all control children and in all children with allergic asthma and allergic rhinitis, as well as in all children with intrinsic asthma and atopic dermatitis. Our findings are at variance with the low thymulin activity previously reported in allergic asthma, and we could not explain these discrepancies. (Both studies used the same bioassay, and the population studied did not appear to be different.) T-lymphocyte abnormalities in subjects with asthma must be assessed by other means than measurement of thymic function.

Adolescent↗
PubMedDate not supplied

The effect of synthetic thymulin on cell surface marker expression by avian T-cell precursors.

The effects of the in vitro exposure of avian bone marrow (BM) cells and thymocytes to synthetic thymulin were studied. Two T-cell differentiation markers, PNA binding site and CT-1a expression, were used to examine cell maturation. Enhanced PNA binding to both BM cells and thymocytes resulted following an in vitro thymulin exposure but cell proliferation was not affected. Scatchard analysis supported the conclusion that PNA binding affinity was significantly increased and thus responsible for the observed increase in PNA binding. Flow cytometric analysis suggested that the induced PNA+ thymocyte population may be a different population from the one exhibiting enhanced CT-1a expression following thymulin exposure. Taken together, the observations suggest that cells can express their further differentiation states without undergoing proliferation following in vitro thymulin stimulation.

Animals↗