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At least 1,369 records · Page 76Linked to original sources
PubMed1986

Depletion of suppressor T cells by 2'-deoxyguanosine abrogates tolerance in mice fed ovalbumin and permits the induction of intestinal delayed-type hypersensitivity.

We have re-examined the role of suppressor T cells (Ts) in regulating immune responses to fed proteins by investigating the effect of 2'-deoxyguanosine (dGuo) on systemic and intestinal immunity in mice fed ovalbumin (OVA). Administration of dGuo for 10 days abrogated the suppression of systemic delayed-type hypersensitivity (DTH) and antibody responses normally found after feeding OVA, and also prevented the generation of OVA-specific Ts. In parallel, mice given dGuo and fed OVA developed sensitization to OVA in the gut-associated lymphoid tissues (GALT) after oral challenge with OVA and had increased intraepithelial lymphocyte (IEL) counts and crypt cell production rates (CCPR) in the jejunal mucosa, indicating the presence of a local DTH response. These findings confirm the importance of Ts in preventing hypersensitivity to dietary protein antigens and suggest that enteropathies associated with food hypersensitivity are due to a defect in Ts activity.

Animals↗
PubMed1988

Cyclophosphamide (Cy)-facilitated adoptive immunotherapy of a Cy-resistant tumour. Evidence that Cy permits the expression of adoptive T-cell mediated immunity by removing suppressor T cells rather than by reducing tumour burden.

A cyclophosphamide (Cy)-resistant immunogenic tumour, the L5178Y lymphoma, was used to demonstrate that Cy-treatment of a host bearing this tumour enables passively transferred tumour-sensitized T cells to cause complete tumour regression without any need for Cy to cause a reduction in tumour burden. It was shown that whereas infusion of tumour-sensitized T cells from immune donors had very little effect on growth of the tumour, and whereas treatment with 150 mg/kg of Cy caused appreciable enhancement of tumour growth, combination therapy with Cy plus immune T cells caused complete tumour regression and resulted in long-term survival. Evidence that Cy treatment facilitated the expression of adoptive immunity against the L5178Y lymphoma by eliminating tumour-induced suppressor T cells consisted of the demonstration that tumour regression caused by combination treatment with Cy and immune T cells could be inhibited by infusing the recipient with Cy-sensitive, L3T4+ T cells from tumour-bearing but not from normal donors.

Animals↗
PubMed1985

[Microautoradiographic method permitting the study of migration of 99m-technetium labelled leukocytes].

Cell migration studies are very important in inflammatory phenomena. Methods currently used are not quantitative and have been subject to much controversy. Homogeneity of 99mTc leukocyte labelling was verified by a microautoradiographic method (MAR), which was performed in our laboratory. This method was used in cell migration studies to verify if the migrating cells were indeed the labelled cells.

Autoradiography↗
PubMed1987

Treatment with dilute alkali-nuclease S1 permits the analysis of DNA damage: cells treated with platinum analogues.

We describe here an approach to characterize various lesions induced in DNA by drug treatments, using three parameters: (a) release of single-stranded DNA fragments by cell lysis in dilute alkali, which result from enzymatic strand scission during DNA repair or chemical alterations of DNA; (b) the presence of high molecular weight DNA in cells after lysis in dilute alkali followed by nuclease S1 treatment which, due to drug-induced DNA cross-links and its level is a measure of the amount of DNA-containing cross-links; and (c) the appearance of small double-stranded DNA fragments, when the cell lysis is followed by digestion with nuclease S1 to remove single-stranded DNA. This DNA shows the same characteristics as DNA of untreated cells, but it may contain monoadducts. By following the flow of label through the three parameters, one can characterize both the lesions induced in DNA and how the lesions are repaired. We report here results of three platinum analogues: cis-Pt(II), trans-Pt(II), and cis-FLAP(II). A large proportion of DNA in treated cells appears as fragments (parameter c). The cis- compounds and trans- compounds differ with regard to appearance of high molecular weight DNA (parameter b) and the initial release of fragments (parameter a).

Cell Line↗
PubMed1986

[The ultrasensitive determination of TSH permits the prediction of the response to TSH in the TRH test].

A new ultrasensitive TSH immunoradiometric assay (IRMA) using two monoclonal antibodies is now able to distinguish between euthyroid and hyperthyroid patients. The aim of this study was to compare data given by ultrasensitive basal TSH (IRMA) and by the response of TSH to TRH test considered until now as the more reliable test in case of mild or atypical hyperthyroidism. Basal plasma TSH levels were determined in euthyroid (n = 80), hyperthyroid (n = 30), hypothyroid (n = 14) and pituitary deficient patients (n = 8) before and 30 minutes after a TRH test (250 micrograms i.v.). A close linear correlation was found between basal and post-stimulative TSH levels. Normal TSH response ranged from 2 to 22 uU/ml. The sensibility and the specificity of these two parameters appeared comparable in the case of primary dysthyroidism; on the contrary basal TSH levels were not sufficient for the diagnosis of central hypothyroidism. In conclusion, excepted for pituitary deficiency, basal plasma TSH (IRMA) levels are accurate and sufficient in the evaluation of the thyroid function and make the TRH-test useless.

Humans↗
PubMed1988

Restoration of adenylate cyclase responsiveness in murine myeloid leukemia permits inhibition of proliferation by hormone. Butyrate augments catalytic activity of adenylate cyclase.

Mechanisms of leukemic cell clonal dominance may include aberrations of transmembrane signaling. In particular, neoplastic transformation has been associated with reduced capacity for hormone-stimulated adenylate cyclase activity. In the present study, prostaglandin E, a hormonal activator of adenylate cyclase that has antiproliferative activity in myeloid cells, and cholera toxin, an adenylate cyclase agonist that functions at a postreceptor site by activating the adenylate cyclase stimulatory GTP-binding protein (Gs), were studied for antiproliferative activity in two murine myeloid cell lines. FDC-P1, an interleukin 3 (IL 3)-dependent myeloid cell line and a tumorigenic IL 3-independent subline, FI, were resistant to these antiproliferative agents. The in vitro ability of the "differentiation" agent, sodium butyrate, to reverse their resistance to adenylate cyclase agonists was studied. The antiproliferative action of butyrate involved augmentation of transmembrane adenylate cyclase activity. Increased adenylate cyclase catalyst activity was the primary alteration of this transmembrane signaling group leading to the functional inhibitory effects on leukemia cells, although alterations in regulatory G-proteins appear to play a secondary role.

Adenylyl Cyclases↗
PubMed1987

The role of sulfhydryl groups in permitting transformation and DNA binding of the glucocorticoid receptor.

Treatment of rat liver cytosol containing temperature-transformed, [3H]dexamethasone-bound receptors at 0 degree C with the sulfhydryl-modifying reagent methyl methanethiosulfonate (MMTS) inhibits the DNA-binding activity of the receptor, and DNA-binding activity is restored after addition of dithiothreitol (DTT). When cytosol containing untransformed receptors is heated at 25 degrees C in the presence of MMTS, the 90-kDa heat shock protein dissociates from the receptor in the same manner as in the absence of MMTS, and the receptor will bind to DNA-cellulose if DTT is added subsequently at 0 degree C. These observations are consistent with the conclusion of Bodwell et al. (Bodwell, J. E., Holbrook. N. J. and Munck, A. (1984) Biochemistry 23, 1392-1398) that sulfhydryl moieties on the receptor are absolutely required for the receptor to bind to DNA, and they show that the sulfhydryl-modifying reagent does not inhibit the temperature-mediated dissociation of the heteromeric receptor complex that accompanies transformation to the DNA-binding state. When steroid-receptor complexes that are prebound to DNA-cellulose are exposed to MMTS, the steroid rapidly dissociates, but the receptor remains bound to DNA. Thus, the presence of steroid is not required for the receptor to remain bound to DNA in a high affinity manner. Treatment of cytosol containing transformed glucocorticoid-receptor complexes at 0 degrees C with 20 mM hydrogen peroxide also inactivates the DNA-binding activity of the receptor. The peroxide-induced inactivation is reversed by DTT. Incubation of rat liver cytosol containing untransformed glucocorticoid-receptor complexes at 25 degrees C with hydrogen peroxide prevents their transformation to the DNA-binding form as shown by their inability to bind to DNA-cellulose after addition of DTT. The presence of peroxide during heating of the cytosol also prevents dissociation of the receptor complex as assayed both by reduction in sedimentation value of the receptor and by dissociation of the 90-kDa heat shock protein from the steroid-binding protein. These results strongly suggest that critical sulfur moieties in the receptor complex must be in a reduced form for the temperature-mediated dissociation of the receptor to occur.

Animals↗