Advances in Neuroimmune Biology最新文献

{"title":"New Aspects of Immunoregulation by Growth and Lactogenic Hormones","authors":"I. Bérczi, A. Stephano, R. Campos, K. Kovacs","doi":"10.3233/NIB-140086","DOIUrl":"https://doi.org/10.3233/NIB-140086","url":null,"abstract":"Growth hormone and prolactin maintain adaptive immunity, which incudes cell mediated immunity, antibody- and autoimmune reactions, maintain thymus and bone marrow function. Insulin like growth factor-1 participate in the regulatory action of growth hormone and prolactin. The hypothalamus-pituitary-adrenal axis stimulates innate immunity and suppresses adaptive immunity. Dopamine also inhibits adaptive immunity and regulates innate immunity. Catecholamine's and corticosteroids support innate immunity and stimulate suppressor-regulatory T cells, which inhibit adaptive immunity. Adrenalectomy sensitized mice to Lipid A, which was mediated by exaggerated production of tumor necrosis factor-alpha, due to the lack of functional hypothalamic pituitary adrenal axis. Growth and lactogenic hormones share signal transduction pathways with type I (gamma-c) cytokines. This indicates functional overlap. The hypothalamic pituitary adrenal axis produces glucocorticoids, which stimulate innate immunity, and play a primary role during the acute phase response. Vasopressin supports the acute phase response, maintains chronic inflammatory reactions and coordinates heeling. Vasopressin maintains immunocompetence during homeostasis as it stimulates the hypothalamus-pituitary- adrenal axis and also prolactin. Vasopressin stimulates innate immune cytokine production. Oxytocin is immunoregulatory. Thyroidectomy in rats suppresses immune function and thyroxin releases growth hormone and prolactin from transplanted pituitary grafts in rats and also restores immunocompetence. This indicates that thyroxin is an indirect immunoregulator. The growth hormone secretagouge, ghrelin, is immunoregulatory. Dopamine is a neurotransmitter and immunoregulator. Dopamine has a role in normal immune function and in stress, inflammatory diseases, schizophrenia, Parkinson disease, Tourette syndrome, Lupus, Multiple Sclerosis, AIDS, and generalized anxiety syndrome.","PeriodicalId":38645,"journal":{"name":"Advances in Neuroimmune Biology","volume":"29 1 1","pages":"43-60"},"PeriodicalIF":0.0,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3233/NIB-140086","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70145339","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"An Update of Neural Regulators of the Hypothalamic-Pituitary-Adrenal Axis","authors":"I. Bérczi","doi":"10.1016/B978-0-12-801770-8.00004-5","DOIUrl":"https://doi.org/10.1016/B978-0-12-801770-8.00004-5","url":null,"abstract":"","PeriodicalId":38645,"journal":{"name":"Advances in Neuroimmune Biology","volume":"5 1","pages":"217-228"},"PeriodicalIF":0.0,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/B978-0-12-801770-8.00004-5","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"54162293","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Myelin Mutant Rat Taiep as a Model of Neuroimmunological Disease","authors":"Eguibar R. Jose, C. Carmen, Ugarte Araceli, León-Chávez Alicia","doi":"10.3233/NIB-140081","DOIUrl":"https://doi.org/10.3233/NIB-140081","url":null,"abstract":"Taiep rat is a myelin mutant with a progressive motor syndrome characterized by tremor, ataxia, immobility episodes, epilepsy and paralysis of the hind limbs. The rats show an initial hypomyelination, followed by a progressive demyelination of the central nervous system, but not peripheral nerves. All myelin alterations are due to an accumulation of microtubules in the cytoplasm and their process in oligodendrocytes, which disrupt the transporting mechanism from endoplasmic reticulum to Cis portion of the Golgi apparatus. Because of these microtubule alterations, all major myelin proteins decreased progressively. In fact, several brain regions of taiep rats showed an increment in the expression of glial fibrillary acidic protein (GFAP) suggesting glia activation. Additionally, when glial cells from taiep rats were cultured and exposed to lipopolysaccharide (LPS) or interferon gamma (IFN)-gamma, they produced higher amounts of nitrites and nitrates than control glial cells, suggesting an activation of glia cells in taiep rats. There are also an activation of interleukins and changes in their receptors that correlated with the progressive demyelination in this myelin mutant. The activation of immune responses in older rats correlated with the electrophysiological alterations such as changes in the sleep-wake pattern and absence seizures, or locomotion pattern and ataxia. Additionally, the frequency and mean duration of immobility episodes (IE's) increased after 6 month of age, which is an expression of rapid eye movement (REM) sleep alteration, suggesting that taiep rats suffer of narcolepsy-cataplexy. These results clearly showed that taiep rats are suitable model of neuro-immune alterations associated to chronic demyelination, and it is alternative model to experimental allergic encephalomyelitis to study glia-neuron interaction. In conclusion, taiep rat showed progressive immunological, electrophysiological and behavioral alterations due to demyeli- nation associated with normal lifespan that allow us to do diverse studies from different approaches.","PeriodicalId":38645,"journal":{"name":"Advances in Neuroimmune Biology","volume":"5 1","pages":"9-17"},"PeriodicalIF":0.0,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3233/NIB-140081","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70144970","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Epigenetic Regulation of the Th2 Locus in Fetal and Neonatal T Cells","authors":"B. Adkins, M. Yoshimoto","doi":"10.3233/NIB-140078","DOIUrl":"https://doi.org/10.3233/NIB-140078","url":null,"abstract":"I n na¨ ove adult CD4 + T cells, the Th2 locus, containing the Il5, Il13, and Il4 genes, is in a transcriptionally quiescent state. When naT cells differentiate into Th2 cells, the Th2 locus undergoes extensive epigenetic modifications which are permissive for gene expression. These modifications, which include the induction of DNase I hypersensitivity, permissive histone modifications, and DNA demethylation at CpG residues, are associated with Th2 differentiation and secretion of Th2 cytokines. Regulatory regions, such as the Il4 and Il13 promoters, the locus control region (LCR), and intra- and intergenic enhancers are the primary targets of these modifications. Unlike adult animals, neonates are considered to be Th2 biased due to the robust development of Th2 lineage cells coupled with a deficiency in Th1 differentiation. This Th2 bias is reflected in the epigenetic status of the Th2 locus. In naneonatal CD4 + T cells in thymus and lymph nodes, key regulatory regions in the Th2 locus pre- exist in a hypomethylated state and these cells are already primed for Th2 status. Here, we focus on the epigenetic modifications in fetal and neonatal T cells and the association of the Th2 locus hypomethylated status with the characteristics of neonatal Th2 biased immunity.","PeriodicalId":38645,"journal":{"name":"Advances in Neuroimmune Biology","volume":"5 1","pages":"69-73"},"PeriodicalIF":0.0,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3233/NIB-140078","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70145101","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Links between Obesity, Inflammation and Breast Cancer","authors":"Julie Romero, Karen Elizabeth Nava Castro, J. M. Montor, E. McCarron","doi":"10.3233/NIB-140080","DOIUrl":"https://doi.org/10.3233/NIB-140080","url":null,"abstract":"","PeriodicalId":38645,"journal":{"name":"Advances in Neuroimmune Biology","volume":"5 1","pages":"1-7"},"PeriodicalIF":0.0,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3233/NIB-140080","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70145254","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neurosteroids and Host Immune Resistance","authors":"R. Loria","doi":"10.3233/NIB-140084","DOIUrl":"https://doi.org/10.3233/NIB-140084","url":null,"abstract":"Androstene steroids up-regulate immunity to increase host resistance against lethal infection by viruses, bacteria, and parasites. They also repair injury after lethal radiation exposure by mediating a rapid recovery of hematopoietic precursor cells. Androstenes increase the levels of the TH1 cytokines, IL-2, IL-3, IFN and counteract hydrocortisone mediated immune suppression. Increased host resistance results in protection from lethal infection by DNA or RNA viruses such as herpes virus, coxsackievirus B4, influenza, and arthropod borne viruses. They provide similar protection against lethal Gram positive and negative bacteria as well as parasitic infections. During shock response, the hypothalamic-pituitary-adrenal axis (HPA) causes unchecked inflammation and sepsis. Androstenetriol treatment reduces Th2 and increases in Th1 cytokines, and significantly increases survival after severe trauma hemorrhage and shock by modulating the HPA response. In contrast to its epimer, 17 androstenediol inhibits proliferation and mediates apoptosis in tumor cells of murine and human origin and autophagy in human glioblastoma. The anti-proliferative functions or the immune up regulation by these neurosteroids are independent of either the estrogen or androgen receptors for activity. Results demonstrate that endoplasmic reticulum (ER) stress is linked to 17 androstenediol induced autophagy by PERK/eIF2 signaling in human malignant glioma cells and transformed fibroblast. The androstene hormones increase host resistance to infections by enhancing cell mediated immunity while androstene exerts an anti- tumor effect by apoptosis, autophagy and increase ER stress.","PeriodicalId":38645,"journal":{"name":"Advances in Neuroimmune Biology","volume":"5 1","pages":"33-42"},"PeriodicalIF":0.0,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3233/NIB-140084","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70145275","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Immunoendocrine Network in Breast Cancer","authors":"K. Nava-Castro, M. I. Palacios-Arreola, P. Ostoa-Saloma, S. Muñiz-Hernández, M. Cerbón, G. Gómez-Icazbalceta, S. Muñoz-Cruz, H. Aguilar-Díaz, L. Pavón, Julieta Ivone Castro-Romero, J. Morales-Montor","doi":"10.3233/NIB-140097","DOIUrl":"https://doi.org/10.3233/NIB-140097","url":null,"abstract":"Breast cancer is a disease in which abnormal cell proliferation leads to uncontrolled growth of breast tissue. Breast cancer can start in various areas of the breast, such as the ducts, lobes, and, in some cases, the intervening tissue. For many years, inflammatory infiltrates in tumors have been suggested to reflect the origin of cancer; however, little is known about the function of chronic inflammation in malignant transformation. Sex hormones are associated with many types of cancer, such as colon, cervical, and especially breast. Estrogen-dependent breast cancer (EDBC) constitutes approximately 50% to 80% of all cases of breast cancer. Furthermore, estrogen-dependency is linked to the initiation of malignancy by promoting the growth and proliferation of mammary cells and it is related to prognosis and treatment. The correlation between sex hormones and breast cancer has been recognized for decades, but the mechanisms of this association remain unknown. In recent years, a more enriched landscape of this relationship has emerged. Intervention by the immune system in cancer begins with the detection of transformed cells and their proliferation-—not with the defense and effort to restrain an established tumoral mass. In the late 1950s, Burnet introduced the immunosurveillance theory, which proposes that immune system cells detect and attack transformed cells, eliciting an adaptive response that succeeds and eliminates them or fails, leading to the formation of a tumoral mass and cancer onset. Conversely, sex hormones are important modulators of the immune system. Growing evidence demonstrates a reciprocal relationship between sex steroids and the immune system. Because the innate immune response determines the type of adaptive immunity that develops, hormonal effects on the former can affect adaptive responses. The sex steroids estrogens, progesterone, and testosterone regulate the growth, differentiation, survival, and function of many cell types that mediate homeostasis, immunity, and breast cancer. The presence of sex steroid receptors on immune cells indicates that sex steroids exert their effects by binding to them. Sex steroids and immunity are inextricably linked, and their mutual regulation influences the maintenance of the immune balance. Understanding the mechanisms of action of sex steroids on immune cells is paramount to developing novel therapies for chronic diseases that are associated to immune dysregulation, such as breast cancer. This chapter describes the risk factors in breast cancer, the hormonal factors that are involved, the immunological response toward cancer, and the effects of sex steroids on immune system cells and their implications for the incidence of breast cancer.","PeriodicalId":38645,"journal":{"name":"Advances in Neuroimmune Biology","volume":"5 1","pages":"109-131"},"PeriodicalIF":0.0,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3233/NIB-140097","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70145486","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Molecular and Neuronal Mechanisms of Chronic Fatigue Syndrome: From Bench to Bedside","authors":"T. Katafuchi, Y. Kataoka","doi":"10.3233/NIB-139001","DOIUrl":"https://doi.org/10.3233/NIB-139001","url":null,"abstract":"Fatigue is one of the symptoms produced by our bioalarm system. However, we may not have paid enough attention to the importance of fatigue, since fatigue normally disappears after rest or sleeping overnight. It has been recognized that patients with chronic fatigue syndrome (CFS), showing debilitating and long-lasting fatigue which is not relieved by rest, has been producing a huge amount of economic loss in our modern society. The CFS is characterized by not only severe fatigue, but also the impairment of neuroendocrine, autonomic, cognitive and immune functions, suggesting a diturbance in the neuronal-endocrine-immune interactions. One of the reasons for not having a specific medicine may be because of the unknown etiology of this syndrome. Clinical symptoms have suggested an association of viral infection with the cause of CFS. Although researchers have not identified the specific pathogen yet, many possible viruses have been reported to induce CFS. In this special issue co-organized by Dr. Yosky Kataoka (RIKEN, Kobe, Japan) and me, we present recent findings on molecular and neuronal mechanisms of CFS using animal models and human patients. It is well known that chronic stress is deeply associated with the onset or exacerbation of CFS. Ogawa et al. demonstrated that rats given a sleep-depriving continuous stress showed morphologically atrophic and functionally suppressed somatotrophs as well as hyperactive melanotrophs including secretion of -MSH (see the chapter by Ogawa et al.). They also suggested that the serum level of -MSH can be a bio-marker for CFS at the early stage. Transforming growth factor(TGF) was also suggested as a possible bio-marker for CFS. TGFwas identified from cerebrospinal fluid in physically exhausted rats, which was found to induce fatigue when administered to normal rats. Those findings in the animal models have been supported by the clinical study showing an elevation of active TGFin the serum of CFS patients (see the chapter by Inoue). Neuroinflammation is characterized by activation of glial cells secreting cytokines, chemokines, radicals, growth factors and proteases in the central nervous system (CNS). It has been indicated that neuroinflammation plays an important role in various neurodegenerative diseases such as Parkinson’s and Alzheimer’s diseases and it is likely that CFS also involves neuroinflammation. Kataoka et al. showed presence of neuroinflammation using positron emission tomography (PET) during central fatigue, which was induced by excessive stimulation with cortical spreading depression of the brain. They also demonstrated that central fatigue induced by systemic injection of synthetic double-stranded RNA, polyriboinosinic:polyribocytidylic acid (poly I:C), was suppressed by minocycline (an inhibitor of microglial activation). In this immunologically induced fatigue model, it is suggested that the balance of interleuikin1 (IL-1 ) and its intrinsic antagonist, IL-1 receptor antagonist, is important","PeriodicalId":38645,"journal":{"name":"Advances in Neuroimmune Biology","volume":"4 1","pages":"217-218"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70144545","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Immune System in Patients with Chronic Fatigue Syndrome","authors":"A. Bradley, B. Ford, A. Bansal","doi":"10.3233/NIB-130068","DOIUrl":"https://doi.org/10.3233/NIB-130068","url":null,"abstract":"","PeriodicalId":38645,"journal":{"name":"Advances in Neuroimmune Biology","volume":"4 1","pages":"255-263"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3233/NIB-130068","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70144659","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Central Fatigue and TGF-β","authors":"Kazuo Inoue","doi":"10.3233/NIB-130069","DOIUrl":"https://doi.org/10.3233/NIB-130069","url":null,"abstract":"","PeriodicalId":38645,"journal":{"name":"Advances in Neuroimmune Biology","volume":"40 1","pages":"229-236"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3233/NIB-130069","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70144702","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}