Advances in neuroimmunology最新文献

{"title":"Stress and humoral immunity: A review of the human studies","authors":"Arthur A. Stone ,&nbsp;Dana H. Bovbjerg","doi":"10.1016/S0960-5428(06)80189-0","DOIUrl":"10.1016/S0960-5428(06)80189-0","url":null,"abstract":"<div><p>Many studies have examined the relationship between stress and immunity, however, only a few have explored associations between stress and Immoral immunity. In our review of this literature, three ways of characterizing the response of the humoral immunity system to stress were identified: total immunoglobulins, antibody to latent viruses and antibody to vaccines. These studies provide some support for the hypothesis that stress affects humoral immunity, particularly response to latent virus, but further research is required to confirm these observations. Several directions for future research are proposed.</p></div>","PeriodicalId":79314,"journal":{"name":"Advances in neuroimmunology","volume":"4 1","pages":"Pages 49-56"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0960-5428(06)80189-0","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19043526","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":"HIV infection of human brain capillary endothelial cell — Implications for AIDS dementia","authors":"Ashlee V. Moses,&nbsp;Jay A. Nelson","doi":"10.1016/S0960-5428(06)80262-7","DOIUrl":"10.1016/S0960-5428(06)80262-7","url":null,"abstract":"<div><p>We have demonstrated that human brain capillary endothelial (HBCE) cells, unlike umbilical or aortic endothelial cells are permissively infected by HIV. HIV infection of HBCE cells is noncytolytic and is mediated by a CD4- and GalCer-independent mechanism, implying that HBCE cell tropic strains utilize a unique receptor. The V3 loop of gp120 appears to be important in this reaction. T-cell tropic but not brain-derived macrophage tropic HIV strains selectively infect brain endothelium suggesting that T-cell tropism is important for HIV entry through the blood-brain barrier (BBB). The ability of HIV to infect cells that compose the BBB implies that the virus may be directly involved in the BBB dysfunction observed in</p><p>AIDS patients. HIV infection of HBCE cells may allow the flow of cytokines or toxic metabolites from the circulating blood into the brain parenchyma either by disrupting tight junctions or by altering the ability of the cells to regulate transport of substances across the BBB by transcytosis. HIV infection may also result in endothelial cell-induced astrocytosis by release of cytotoxic substances or modulation of abluminal surface antigens which contact astrocytic foot processes. Finally, HIV infection of the brain endothelium could facilitate virus entry to the CNS either by infection of HBCE cells or via entry of HIV-infected leucocytes. The establishment of our in vitro HIV-HBCE cell system will allow us to explore the potential mechanisms which mediate AIDS dementia.</p></div>","PeriodicalId":79314,"journal":{"name":"Advances in neuroimmunology","volume":"4 3","pages":"Pages 239-247"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0960-5428(06)80262-7","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18541902","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":"gp120-mediated alterations in astrocyte ion transport","authors":"D.J. Benos,&nbsp;B.H. Hahn,&nbsp;G.M. Shaw,&nbsp;J.K. Bubien,&nbsp;E.N. Benveniste","doi":"10.1016/S0960-5428(06)80254-8","DOIUrl":"10.1016/S0960-5428(06)80254-8","url":null,"abstract":"<div><p>The pathogenesis of the acquired immuno-deficiency syndrome (AIDS) dementia complex (ADC) is unknown. However, recent work indicates that neurons and astrocytes are functionally compromised by exposure to viral components or cellular factors released from HIV-1-infected macrophages/microglia. We show that exposure of primary cultured rat astrocytes to the major HIV envelope glycoprotein gp120 results in alterations of ion and solute transport that may contribute to neuronal cell injury.</p></div>","PeriodicalId":79314,"journal":{"name":"Advances in neuroimmunology","volume":"4 3","pages":"Pages 175-179"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0960-5428(06)80254-8","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18873486","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":"Update on current models of HIV-related neuronal injury: Platelet-activating factor, arachidonic acid and nitric oxide","authors":"Stuart A. Lipton ,&nbsp;Michael Yeh ,&nbsp;Evan B. Dreyer","doi":"10.1016/S0960-5428(06)80255-X","DOIUrl":"10.1016/S0960-5428(06)80255-X","url":null,"abstract":"<div><p>This review aims to summarize recent work related to the pathogenesis and possible treatment of neuronal injury in the acquired immunodeficiency syndrome (AIDS), especially with reference to potential neurotoxic substances released by HIV-infected or gp120-stimulated macrophages/microglia. Approximately a third of adults and half of children with AIDS eventually suffer from neurological manifestations, including dysfunction of cognition, movement, and sensation. Among the various pathologies reported in brains of patients with AIDS is neuronal injury and loss. A paradox arises, however, because neurons themselves are for all intents and purposes not infected by human immunodeficiency virus type 1 (HIV-1). This paper reviews recent evidence suggesting that at least part of the neuronal injury observed in the brains of AIDS patients is related to excessive influx of Ca²⁺ after the release of potentially noxious substances from HIV-infected or gp120-stimulated macrophages/microglia.</p><p>There is growing support for the existence of HIV- or immune-related toxins that lead indirectly to the injury or demise of neurons via a potentially complex web of interactions between macrophages (or microglia), astrocytes, and neurons. HIV-infected monocytoid cells (macrophages, microglia or monocytes), especially after interacting with astrocytes, secrete substances that potentially contribute to neurotoxicity. Not all of these substances are yet known, but they may include eicosanoids, i.e. arachidonic acid and its metabolites, as well as platelet-activating factor. Other candidate toxins include nitric oxide (NO·), superoxide anion (02·⁻), and the <em>N</em>-methyl-scd-aspartate (NMDA) agonist, cysteine. Similarly, macrophages activated by HIV-1 envelope protein gp120 also appear to release arachidonic acid and its metabolites, and cysteine. These factors can lead to increased glutamate release or decreased glutamate re-uptake. In addition, interferon-γ (IFN-γ) stimulation of macrophages induces release of the NMDA-like agonist, quinolinate. HIV-infected or gp120-stimulated macrophages also produce cytokines, including TNF-α and ILI-β, which contribute to astrocytosis. A final common pathway for neuronal susceptibility appears to be operative, similar to that observed in stroke, trauma, epilepsy, neuropathic pain and several neurodegenerative diseases, possibly including Huntington's disease, Parkinson's disease, and amyotrophic lateral sclerosis. This mechanism involves the activation of voltage-dependent Ca²⁺ channels and NMDA receptor-operated channels with resultant generation of free radicals, and therefore offers hope for future pharmacological intervention.</p></div>","PeriodicalId":79314,"journal":{"name":"Advances in neuroimmunology","volume":"4 3","pages":"Pages 181-188"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0960-5428(06)80255-X","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18873487","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":"Effects of chronic zidovudine administration on CNS function and virus burden after perinatal SIV infection in rhesus monkeys","authors":"Dianne M. Rausch ,&nbsp;Melvyn Heyes ,&nbsp;Lee E. Eiden","doi":"10.1016/S0960-5428(06)80261-5","DOIUrl":"10.1016/S0960-5428(06)80261-5","url":null,"abstract":"<div><p>Continuous intravenous administration of zidovudine (AZT) has been reported to improve cognitive function in HIV-infected pediatric patients (Pizzo <em>et al.</em>, 1988). The effects of long-term zidovudine treatment in the perinatally infected pediatric population, including antiviral efficacy and effects on cognitive and motor function has not been systematically examined. These questions were addressed in rhesus macaque infants infected at birth with SIV_SMM/B670, a primate model for infantile HIV infection and disease (Eiden <em>et al.</em>, 1993a). Continuous or intermittent administration of AZT during the first 6 months following infection resulted in about a doubling of lifespan, a delay in the occurrence of motor impairment, and lower virus burden and quinolinic acid levels in cerebrospinal fluid (CSF) following administration of the antiviral drug.</p></div>","PeriodicalId":79314,"journal":{"name":"Advances in neuroimmunology","volume":"4 3","pages":"Pages 233-237"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0960-5428(06)80261-5","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18874051","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":"Activation of HIV-1 transcription by Tat in cells derived from the CNS: Evidence for the participation of NF-κB — A review","authors":"J. Paul Taylor,&nbsp;Kamel Khalili","doi":"10.1016/S0960-5428(06)80270-6","DOIUrl":"https://doi.org/10.1016/S0960-5428(06)80270-6","url":null,"abstract":"","PeriodicalId":79314,"journal":{"name":"Advances in neuroimmunology","volume":"4 3","pages":"Pages 291-303"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0960-5428(06)80270-6","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"92115691","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 recognition of acetylcholine receptor. Recognition by α-neurotoxins and by immune and autoimmune responses and manipulation of the responses","authors":"M.Zouhair Atassi","doi":"10.1016/0960-5428(94)00037-O","DOIUrl":"10.1016/0960-5428(94)00037-O","url":null,"abstract":"","PeriodicalId":79314,"journal":{"name":"Advances in neuroimmunology","volume":"4 4","pages":"Pages 403-432"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0960-5428(94)00037-O","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18543744","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":"Detection of HIV-1 DNA in pediatric AIDS brain tissue by two-step ISPCR","authors":"Leroy R. Sharer ,&nbsp;Yoshihiro Saito ,&nbsp;Leon G. Epstein ,&nbsp;Benjamin M. Blumberg","doi":"10.1016/S0960-5428(06)80268-8","DOIUrl":"10.1016/S0960-5428(06)80268-8","url":null,"abstract":"<div><p>In order to detect latent infection in neurons or other cell types in formalin-fixed brain tissue, we performed polymerase chain reaction amplification with incorporation of digoxigenin-conjugated deoxynucleotides, followed by <em>in situ</em> hybridization with biotinylated probes. The use of this two-step technique in brain tissue from a child with severe HIV-1 encephalitis revealed signal in both nuclear and perinuclear regions of cells identified as monocytes and astrocytes, and also in perineuronal satellite cells of glial morphology, but HIV-1 infection of neurons was not detected.</p></div>","PeriodicalId":79314,"journal":{"name":"Advances in neuroimmunology","volume":"4 3","pages":"Pages 283-285"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0960-5428(06)80268-8","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18872181","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 experimental model system for HIV-1-induced brain injury","authors":"Howard E. Gendelman ,&nbsp;Peter Genis ,&nbsp;Marti Jett ,&nbsp;Qi-hui Zhai ,&nbsp;Hans S.L.M. Nottet","doi":"10.1016/S0960-5428(06)80256-1","DOIUrl":"10.1016/S0960-5428(06)80256-1","url":null,"abstract":"<div><p>The pathological hallmark of HIV infection in brain is productive viral replication in cells of mononuclear phagocyte lineage including brain macrophages, microglia and multinucleated giant cells (Koenig <em>et al.</em>, 1986; Wiley <em>et al.</em>, 1986; Gabuzda <em>et al.</em>, 1986; Stoler <em>et al.</em>, 1986). These cells secrete viral and cell encoded neurotoxins that lead to neuronal injury, glial proliferation and myelin pallor during advancing disease (Genis <em>et al.</em>, 1992; Giulian <em>et al.</em>, 1990, 1993; Pulliam <em>et al.</em>, 1991). The apparent paradox between the distribution and numbers of virus infected cells and brain tissue pathology support indirect mechanisms for CNS damage (Epstein, 1993; Geleziunas <em>et al.</em>, 1992; Merrill and Chen, 1992; Michaels <em>et al.</em>, 1988; Price <em>et al.</em>, 1988). First, brain macrophages and microglia can produce neurotoxins by secretion of viral proteins (for example, gp120) (Dawson <em>et al.</em>, 1991; Merrill <em>et al.</em>, 1989; Lipton <em>et al.</em>, 1990; Lipton, 1993). Second, HIV primes macrophages for immune activation to produce neurotoxins including: cytokines (TNF(α and IL-1β), eicosanoids, quinolinate and nitric oxide (NO). Chronic immune stimulation mediated by opportunistic infections and chronic interferon gamma (IFNγ) production (in and outside the CNS) continues the process of macrophage activation leading to progressive neural injury. The hyperresponsiveness of HIV-infected macrophages to activation results in production of cellular factors that activate uninfected macrophages. This suggests that HIV-infected macrophages are both perpetrators and amplifiers for neurotoxic activities.</p></div>","PeriodicalId":79314,"journal":{"name":"Advances in neuroimmunology","volume":"4 3","pages":"Pages 189-193"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0960-5428(06)80256-1","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18873488","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":"Interrelations among patterns of change in neurocognitive, CT brain imaging and CD4 measures associated with anti-retroviral therapy in children with symptomatic HIV infection","authors":"Pim Brouwers,&nbsp;Charles DeCarli ,&nbsp;Gareth Tudor-Williams ,&nbsp;Lucy Civitello ,&nbsp;Howard Moss ,&nbsp;Philip Pizzo","doi":"10.1016/S0960-5428(06)80260-3","DOIUrl":"10.1016/S0960-5428(06)80260-3","url":null,"abstract":"<div><p>The interrelationships of patterns of change and variability between baseline and after 6 months of anti-retroviral therapy in neurocognitive, brain imaging, and immune measures were studied in 77 children with symptomatic HIV disease.</p><p>Overall improvement in CNS structure/function after 6 months of anti-retroviral therapy was limited; new intracerebral calcifications tended to occur and old ones tended to progress in young children with vertically acquired HIV infection, despite treatment. Substantial inter-individual differences in change were however observed. Factors which explained part of the variance in the magnitude and direction of change were baseline structural and functional abnormalities, rating of degree of CNS penetration of the drug protocol, and concurrent changes on other variables. These preliminary data suggest that CNS specific effects of therapies as well as pretreatment status of CNS function/structure need to be taken into consideration when evaluating future trials of anti-retroviral therapy for children with symptomatic HIV infection.</p></div>","PeriodicalId":79314,"journal":{"name":"Advances in neuroimmunology","volume":"4 3","pages":"Pages 223-231"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0960-5428(06)80260-3","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18874050","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}