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Mast cells are a heterogeneous population of granulocytic cells in the immune system. Mast cell granules contain numerous mediators, including neurotransmitters, cytokines, chemokines and lipid-derived factors. In addition to their well-known role in immune inflammation, the presence of mast cells in the meninges and perivascular space in the central nervous system points to their role in brain physiology and their potential involvement in the development of neurological disorders. Of interest, activation of mast cells and their interaction with glial cells have been shown to be involved in altering the permeability of blood brain barrier, a phenomenon which is a key part of neuroinflammatory/degenerative processes. Mast cells have also been reported to exert protective effects against neuroinflammation likely through releasing anti-inflammatory compounds or degrading inflammatory mediators. While diseases like multiple sclerosis, Alzheimer’s disease and stroke are considered as classical examples of neuroinflammation, the role of low-grade inflammation in the pathogenesis of psychiatric disorders has recently attracted the attention of investigators. Herein, we summarize some of the findings about the role of mast cells in the pathogenesis of psychiatric disorders including anxiety disorders.

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Mesenchymal stem cells can be obtained from deferent tissues like adipose tissue, umbilical cord, placenta, skin, bone marrow, etc. These cells have regulatory effects on all types of immune cells such as dendritic cell, natural killers and lymphocytes. Mesenchymal stem cells induce inhibitory phenotypes of Antigen Presenting Cells (APCs) following their activity. They also change T cells phenotype from pre-inflammatory form to anti-inflammatory form by decreasing interferon gamma (INFY) production and increasing IL4 production. They increase T reg cells proliferation and decrease Natural Killer Cells proliferation and differentiation of alloantigen Induced Lymphocytes. MSC decrease destruction of axon and myelin and also improve regeneration of them. The role of mesenchymal stem cell in suppression of neuroinflammation is obvious. They have great immunomodulatory impact. Mesenchymal stem cells increase neurons survival by secreting neuroprotective factors and significantly decrease their apoptosis. These type of stem cell can play an important role in treatment of neuroinflamatory disease. Studies have shown that the use of mesenchymal cells are safe but more studies are needed to show they long term influences.

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1. Intravenous Immunoglobulin (IVIG): Using IVIG neutralizes Pro-inflammatory antibodies, thus regulating the inflammation. It is widely used in treating Guillain-Barre syndrome.
2. Plasma Exchange: In this method antibodies are removed; Therefore significantly reducing the inflammation. This method is mainly used in treating central and peripheral nervous system inflammations such as Guillain-Barre syndrome and Neuromyelitis optica.
3. < > The main effect of interferons is the regulation of cell-mediated immunity as in treating Multiple Sclerosis.Monoclonal antibodies: Introduction of new monoclonal antibodies has made treatments far more specific, helping us to target immune cells that have key roles in immunosuppressive disorders such as CD19 and CD20. These drugs act either by preventing sensitized cells from entering CNS like Natalizumab or directly inactivating these cells. In conclusion, these novel methods may pave the way for better and more effective treatments in the future.

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Multiple Sclerosis (MS) is a complex neurological disease in which neuro inflammation that leads to neurodegeneration _ plays a key role and its prevalence is 2 million in the world. Vitamin A is a fat-soluble vitamin that is multifunctional. One of the important functions is in immune system, both in immunological tolerance and in adaptive immune responses. 264 patients will be enrolled that suffer from MS and divided them into two groups. Group (A) will take interferon beta and Vitamin A and group (B) will take interferon beta and placebo. we will follow them for one year and every six months we will check the inflammatory factors in the serum. In this project, we expect that vitamin A regulate CCL2 (as a chemokine) which means vitamin A will increases amount of CCL2 in serum and then CCL2 will effect on TH cells (stimulate TH2 and TReg) and then IL-10 that is anti-inflammatory cytokine will increase and IL-2 that is pro-inflammatory cytokine will be inhibited by IL-10. We guess if vitamin A increases the amount of CCL2 about 50 pg/ml we can see the expected changes. Based on other researches, we expect that vitamin A regulate the inflammatory factors and then reduce the rate and intensity of relapsing in patients.