Cannabinoid дали имаш некакви податоци
како влијае марихуаната на имунитетот?
Позитивно влијае.
1. Human leukocytes express cannabinoid (CB) receptors, suggesting a role for both endogenous ligands and Delta 9-tetrahydrocannabinol (THC) as immune modulators. To evaluate this, human T cells were stimulated with allogeneic dendritic cells (DC) in the presence or absence of THC (0.625-5 microg/ml). THC suppressed T cell proliferation, inhibited the production of interferon-gamma and shifted the balance of T helper 1 (Th1)/T helper 2 (Th2) cytokines. Intracellular cytokine staining demonstrated that THC reduced both the percentage and mean fluorescence intensity of activated T cells capable of producing interferon-gamma, with variable effects on the number of T cells capable of producing interleukin-4. Exposure to THC also decreased steady-state levels of mRNA encoding for Th1 cytokines, while increasing mRNA levels for Th2 cytokines. The CB2 receptor antagonist, SR144528, abrogated the majority of these effects. We conclude that cannabinoids have the potential to regulate the activation and balance of human Th1/Th2 cells by a CB2 receptor-dependent pathway.
2. Delta 9-Tetrahydrocannabinol (THC), an active component of marijuana, has been shown to be immunosuppressive. To test THC's ability to suppress an immune-mediated disease, experimental autoimmune encephalomyelitis (EAE), the laboratory model of MS, was used. Lewis rats and strain 13 guinea pigs were administered THC either before inoculation for EAE or treated with THC after injection. Control animals received placebo. The effect of dose, in addition to the timing of treatment, was also investigated. All animals treated with placebo developed severe clinical EAE 10-12 days post-injection (d.p.i.) and more than 98% died by 15 d.p.i. THC-treated animals had either no clinical signs or mild signs with delayed onset (13-15 d.p.i.) with survival greater than 95%. Examination of central nervous system tissue revealed a marked reduction of inflammation in the THC-treated animals. Therefore, as THC has been shown to inhibit both clinical and histologic EAE, it may prove to be a new and relatively innocuous agent for the treatment of immune-mediated diseases.
Пошто знаеш англиски, бујрум + линкчиња:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2219542/?tool=pmcentrez
http://www.ncbi.nlm.nih.gov/sites/entrez/12446015?dopt=Abstract&holding=f1000,f1000m,isrctn
http://brain.oxfordjournals.org/content/130/10/2543.abstract
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2219542/?tool=pmcentrez
3. Resident immune and CNS cells express functional CB2 receptors. The activation of CB2 receptors results in the modulation of the inflammatory response, restraining one of the agents responsible for the progress of demyelination and neuronal death, the ultimate causes of the symptoms in pathologies such as MS and EAE. The modulation of inflammatory molecules through CB2 receptors could also enhance remyelination, stimulating the survival of oligodendrocyte precursors and neural stem/precursor cells, and their development into mature oligodendrocytes.
However, the role of CB2 in controlling demyelination and enhancing remyelination is not limited to autoimmune diseases and it is not restricted to the control of the immune system (
Figure 2). Both in MS, EAE and other non-immune-mediated demyelinating diseases, the protective effect of CB2 agonists on neural cells is a remarkable advantage. Moreover, CB2 receptor activation may be a relevant strategy in cellular replacement. However, before proposing the usefulness of CB2 agonists for myelin disorders, it is necessary to obtain a deeper understanding of what effects may be attributable to the activation of CB2 receptors alone, and which are also due to the participation of the CB1 receptor. Furthermore, we must be aware of what effects may be mediated by other receptors, since there is increasing evidence that cannabinoids can induce certain effects independently of CB1 or CB2. Nevertheless, given our current understanding of CB2 receptors and the pathogenesis of immune-mediated or other demyelinating disorders, these receptors seem to be of potential therapeutic interest.
Се надевам бев од некаква помош.
