PubMed Health⌕ Search

PubMed · 7492898

Melatonin: implications at the oral level.

Abstract

The strong relationship between the pineal gland and the immune system continues to establish itself more and more. In situations of a pinealectomy or in those of inhibition of the production of melatonin, a state of immunosuppression is produced which disappears when the patient receives this hormone. Likewise, melatonin counteracts the negative effects that immunosuppressive drug treatment produce over the immunity. It is due to these facts that one postulates the possibility of utilizing melatonin in primary and secondary immunodeficiency states as well as in cancerous immunotherapy. The action of this hormone over the immune system is carried out through the T-helper lymphocytes, lymphokines and also it seems through certain pituitary hormones. On the other hand, lymphokines such as gamma-interferon and interleukin-2, as well as the thymus, can modulate the synthesis of melatonin at the level of the pineal gland. Without doubt, all these actions have important consequences at the time of treatment of our high-risk dental patients who have, in one way or another, an altered immunologic system. The altered immune system has direct implications in primary oral pathologies, or in others derived directly from our dental treatment.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

A Cutando, F J Silvestre. Melatonin: implications at the oral level.. https://pubmed.ncbi.nlm.nih.gov/7492898/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Immunostimulatory RNA oligonucleotides trigger an antigen-specific cytotoxic T-cell and IgG2a response.

Single-stranded RNA oligonucleotides containing an immunostimulatory motif (immunostimulatory RNA [isRNA]) are potent inducers of interferon-alpha via the Toll-like receptor 7. We investigated the effect of isRNA on the development of an immune response. We show that isRNA activates dendritic cells and induces production of Th1-type cytokines both in vitro and in vivo. Cytokine production led to bystander activation of T and B cells. We further demonstrate that isRNA triggers the generation of antigen-specific cytotoxic T cells and of an IgG2a-biased antibody response to antigen in a sequence-dependent manner. In summary, we provide evidence for the first time that isRNA oligonucleotides can simultaneously activate the innate and adaptive arms of the immune system.

Adjuvants, Immunologic↗

Mechanism of third signals provided by IL-12 and OX-40R ligation in eliciting therapeutic immunity following dendritic-tumor fusion vaccination.

Dendritic-tumor heterokaryons generated by electrofusion are highly immunogenic. In animal studies, a single vaccination was therapeutic for tumors established in the lung, skin, and brain. However, effective therapy required a third signal which could be provided by exogenous IL-12 or the agonistic anti-OX-40R monoclonal antibody (mAb). In this study, we investigated the mechanism and mode of actions of these two seemingly distinct adjuvants. In immunotherapy of the MCA205 sarcoma, administration of the neutralizing anti-IL-12 mAb nearly completely blocked the adjuvant effect of IL-12, but had minimal inhibitory effects on anti-OX-40R mAb. By contrast, in vivo administration of the antagonistic anti-OX-40L mAb inhibited the adjuvant effects of both IL-12 and anti-OX-40R mAb. Thus, a common pathway of endogenous OX-40 interaction is critical for the development of a therapeutic immune response. Analysis of the third signal mechanism revealed that in the absence of an adjuvant, vaccination with fusion hybrids led to IL-10 production without eliciting IFN-gamma secreting cells. The addition of IL-12 to vaccination suppressed IL-10 production and initiated sensitization of specific IFN-gamma secreting cells, resulting in a type 1-like antitumor immunity. These findings underscore the significance of the third signal in the design of dendritic cell-based cancer vaccines.

Adjuvants, Immunologic↗