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The effects of delta 9-tetrahydrocannabinol (THC) on lymphocyte proliferation and interleukin (IL) 2 activity was investigated using adult murine spleen cells stimulated with either the mitogens concanavalin A, phytohemagglutinin, or anti-CD3 antibody. THC was found to suppress mitogen-induced proliferation, but to enhance anti-CD3-antibody-induced proliferation. These results reflected THC-induced suppression of Ly2 cells following concanavalin A or phytohemagglutinin stimulation and THC-induced enhancement of Ly2 cells following CD3 stimulation. The combination of THC and concanavalin A or phytohemagglutinin resulted in suppressed IL-2 activity, whereas the combination of THC and anti-CD3 antibody resulted in enhanced IL-2 activity. This drug-related modulation of IL-2 activity corresponded to the changes in blastogenic activity as well as to variations in numbers of Tac positive cells. These results suggest that the dysregulation in immune responses following THC treatment, either suppression or enhancement, may relate to the effects of THC on IL-2 production.

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Delta-9-tetrahydrocannabinol (THC), the major psychoactive component of marijuana, can suppress the immune response, both in vitro and in vivo. In the present study, THC was found to either up-regulate or down-regulate lymphocytes depending on the method of stimulation. When the mitogens concanavalin A (Con A) or phytohemagglutinin (PHA) were used to stimulate THC-treated splenocytes, a down-regulation of lymphocyte proliferation occurred, which reflected lower T-cell numbers in general and Ly2 positive cells specifically. When splenocytes were stimulated directly by using anti-CD3 antibody it was found that low concentrations of THC enhanced lymphocyte proliferation, T-cell numbers in general, and Ly2 cells specifically. These results emphasize that THC can either enhance or suppress aspects of the immune response, depending on the specific immune stimulants used and the specific parameter of immunity measured.

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Marijuana, and specifically its psychoactive component, THC, can up or down regulate lymphocyte proliferation in murine spleen cells depending in part on the method used to stimulate the cells. This study identifies a difference in THC induced disregulation using cells derived from two different secondary lymphoid organs, the spleen and the lymph node. It was found that THC treatment of mitogen (concanavalin A or phytohemagglutinin) stimulated cells derived from either organ resulted in suppression of the proliferative response. In contrast, spleen cells stimulated with anti-CD3 antibody and treated with low doses of THC displayed an enhanced proliferation whereas the response in lymph nodes did not change. The cell type involved with this THC immunoenhancement in spleen cells was found to be the Ly2 cell. Further differences in the THC modulation of Ly2 spleen cells as compared to lymph node cells were noted following stimulation with PHA. Proliferation of Ly2 cells of splenic origin was inhibited with low doses of THC whereas the Ly2 cells of lymph node origin were more resistant to this drug induced suppression. This study, therefore, demonstrates differences in the immunomodulatory capability of THC dependent upon the organ source of the lymphocytes.

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Marijuana components modulate a variety of immune response parameters. The cannabinoids delta 9-tetrahydrocannabinol (THC) and 11-hydroxy-tetrahydrocannabinol (11 OH-THC) are known to depress the in vitro proliferative response of murine lymphoid cells to the mitogens concanavalin A (Con A) and phytohemagglutinin (PHA). In the present report the effects of THC and 11 OH-THC on adult thymus and spleen cells were compared to effects on lymphoid cells of those organs from juvenile mice at various ages. The results demonstrate differences in susceptibility to cannabinoid-induced suppression by lymphoid cells from different organs and different age mice. In adults, thymus cells were suppressed more readily than spleen cells. Splenocytes from mice under 2 weeks old were suppressed much more readily than those from older mice. Cell populations from organs with higher proportions of L3T4+/Lyt2- cells were more difficult to suppress. The possible mechanisms involved and directions for future work are discussed.

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THC (delta-9-tetrahydrocannabinol), the major psychoactive component of marijuana, has been shown to suppress various immune functions in vivo and in vitro. THC suppresses murine T-lymphocyte proliferation; however, the effects on T-cell subsets remain unclear. We have stimulated cultured murine splenocytes with the mitogens concanavalin A (Con A) or phytohemagglutinin (PHA) while exposing them to varying concentrations of THC. After three days, the cells were analyzed by the fluorescent activated cell sorter for the following T-cell markers--Thy1, L3T4 and Ly2. The Ly2 cells represent the suppressor/effector T-cells while L3T4 cells represent the helper T-cell subpopulations. The results show that the dose response suppressive effect of THC on T-cell proliferation reflects a preferential inhibition of Ly2 vs L3T4 cells. The effects of THC on other functional parameters are in the process of investigation.

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Bordetella pertussis and Corynebacterium parvum are commonly used immunopotentiating agents. To explore the inflammatory environment induced by these agents, the peritoneal exudate response in mice following intraperitoneal injection of B. pertussis (PV) and C. parvum (CV) vaccines was investigated. The PV-induced exudate isolated by lavage was characterized by an early neutrophil influx followed by enhanced accumulation of mononuclear cells and fluid protein. The CV exudate was principally mononuclear in nature and displayed fewer numbers of cells and less fluid protein. Both vaccines also enhanced the leukocyte adherence inhibitory activity (LAIA) of peritoneal fluid as measured in vitro. The development of exudate LAIA was T lymphocyte independent. A similar LAIA was demonstrated in nonimmune mouse plasma and serum. Exudate fluid and serum LAIA were heat stable and trypsin sensitive. These studies suggest that significant differences exist in the composition of the local tissue environment following PV and CV injection and that exudate LAIA is serum derived. Further studies in this direction should result in a better understanding of the ways in which inflammatory cells and fluid substances affect lymphocyte-macrophage interaction subsequent to adjuvant administration.

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The percentage of neutrophils forming erythrocyte-antibody-complement complex (EAC) and with erythrocyte-antibody complex (EAG) was determined for 30 normal newborns and 10 normal adults. The cord values ranged from 84-100% EAC binding cells with a mean of 95%. The adult values ranged from 89-100% EAG binding cells with a mean of 96% rosetted neutrophils. The mean percentage of EAG binding cells in the cord samples was 81%, whereas in the seven adult samples the mean was 87%.

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Rana catesbiana adult frogs and tadpoles were immunized with the bacteriophage F2, 0X-174, and T4 and the haptens 2,4 dinitrophenyl (DNP) and fluorescein (FTC). The haptens were conjugated with bovine serum albumin (BSA), bovine gamma globulin (BGG), or horsehoe crab hemocyanin (Hycn). Sera were obtained from immunized animals at invervals up to six months after immunization. The antibody activities were measured by bacteriophage neutralization techniques. Sucrose density gradients were used to separate the antibody classes. Both adults and tadpoles responded to each of the antigens tested. High molecular weight antibodies were predominant in both groups of animals. Low molecular weight antibody activity was not found in adults until nine weeks post immunization but, thereafter, this fraction increased throughout the immune response. Low molecular weight antibodies could also be identified in serum of tadpoles, but only under certain conditions.

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