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Biomedical subjects

G H Heppner

Publications and source records attributed to G H Heppner.

107 records · Page 6Linked to original sources
PubMed1969

Serum-mediated protection of neoplastic cells from inhibition by lymphocytes immune to their tumor-specific antigens.

The combined effect of immune lymphocytes (lymphnode cells or blood lymphocytes) and serum from tumor-bearing donors was assessed in four tumor systems with the use of the colony inhibition assay: (a) Moloney virus-induced sarcomas in mice, (b) Shope papillomas in rabbits, (c) spontaneous mammary carcinomas in mice, and (d) two adenocarcinomas of the colon and two adenocarcinomas of the lung in humans. The neoplasms studied had previously been shown to possess tumor-specific antigens, against which cellular immunity could be detected in vitro. In all four systems, it was found that sera from hosts with progressively growing neoplasms could abrogate the inhibitory effect of lymphocytes which were immune to the specific antigens of the corresponding tumor type. Studies with Moloney sarcomas, in particular, showed that the serum effect had at least some degree of specificity.

Adenocarcinoma↗
PubMedDate not supplied

Alterations in murine delayed type hypersensitivity responses by delta-8-THC and cannabinol.

The ability of cannabinol and delta-8-tetrahydrocannabinol (delta-8-THC), two cannabinoid marihuana components, to modify delayed-type hypersensitivity (DTH) to sheep red blood cells (SRBC) was investigated in mice. Reduction of DTH reactivity by cannabinol required multiple, daily, postimmunization drug administration. Neither multiple preimmunization dosings nor a single postimmunization dosing was effective. Delta-8-THC produced moderate (13-33%) suppression of DTH reactivity only upon multiple, preimmunization treatments, whereas postimmunization administration only delayed peak DTH reactivity 24 hours without altering the absolute response level. These results indicate that delta-8-THC and cannabinol possess slight to moderate activity in the suppression of DTH.

Animals↗
PubMedDate not supplied

Mechanisms of lymphocyte traffic in neoplasia.

The composition of tumor infiltrating lymphocyte populations is often reported to be different from that of the lymphocyte pool of peripheral blood. This suggests that infiltration-regulating mechanisms reside in or near the tumor microenvironment. Available evidence indicates that these mechanisms exert their effects on lymphocyte traffic. Two models of regulation are proposed. In the selective immigration model, different lymphocyte types display different tendencies to extravasate into the tumor. Selective immigration could reflect heterogeneity of such lymphocyte properties as binding to vascular endothelium, response to chemotactic factors, or spontaneous locomotion. In the other model, selective entrapment, different types of lymphocytes exit from the tumor microenvironment at different rates. Entrapment could be regulated by selectively acting adhesive, locomotion-inhibiting, or negatively chemotactic factors. Available information supporting each model is presented. The composition of infiltrate may also be influenced by the composition of the circulating lymphocyte pool. Evidence is presented that this pool in turn may be influenced by tumor-induced systemic changes in lymphocyte traffic. Deliberate manipulation of lymphocyte traffic should improve the effectiveness of immunotherapeutic regimes. One promising method of traffic manipulation is the modulation of spontaneous motility. A collagen gel assay for spontaneous lymphocyte motility is described.

Animals↗