| Popis: |
Studies of the effects of opioids on T lymphocytes have become increasingly important in light of statistical data which suggest that opioid users/abusers are at high risk for developing AIDS. Also, these studies are significant since T lymphocytes play a crucial role in both cellular and humoral immunity in patients with AIDS. The simian model of immunodeficiency virus infection, which has been followed thoroughly in our laboratory in a controlled fashion, has yielded important insights which may not be obtainable from a clinical setting involving human subjects. Using this system, we have studied the consequences of chronic morphine intake on the progression of AIDS in order to model a segment of the human population shown to be at risk. These studies are concerned with the possible modulation of the immuno-responses of primates toward lentiviral as well as opioid challenges. We have found that administration of morphine sulfate to rhesus monkeys may activate the quiescent lymphocyte for proliferation, induce a transient increase in the T cell proliferative response to mitogens, and cause an enhanced interleukin-2 (IL-2) release from the mitogen-stimulated lymphocytes (1). However, longitudinal studies of the animals dependent upon morphine have revealed an overall immunosuppression of both T helper cell functions (T cell proliferation and IL-2 release) and PMN (polymorphonuclear cells) chemotaxis and phagocytosis activities (1,2). In addition to cellular effects, opioid treatment also affects the humoral response of the treated subjects; relative to saline-treated animals, morphine-dependent animals had a lower titer of anti-SIV neutralizing antibody activity after SIV infection (3). |
