Microglia, the resident immune effective cells of the central nervous system, play crucial roles in mediating immune-related process. It becomes activated quickly in response to even minor pathological insults and participates in series of immune responses. Under physiological conditions, most microglia stay in a typical resting state, with ramified processes continuously extending and retracting from surrounding neural tissues, suggesting an important function of resting microglia. Recent studies indicate that resting microglia can regulate many physiological processes, including neural development, neural circuit formation, neuronal activity and plasticity, and animal grooming behavior. Here, we review the properties of resting microglia and further discuss how microglia participate in the above-mentioned functional regulation under physiological conditions.
Animals ; Central Nervous System ; cytology ; Humans ; Microglia ; immunology ; physiology

Objective: Due to the special anatomical structure and pathophysiological mechanism of the central nervous system (CNS), there is a big difference between the repair of brain injury and other systems of the body. More and more evidence shows that targetedly reducing the autoimmune response of brain tissue without affecting the immune function in other parts of the body will be the best optimized treatment for brain injury. Data Sources: This review was based on data in articles published in PubMed up to June 5, 2017, with the following keywords: "immune tolerance", "traumatic brain injury", and "central nervous system". Study Selection: Original articles and critical reviews on immune tolerance and brain damage were selected for this review. References of the retrieved articles were also screened to search for potentially relevant papers. Results: The CNS is isolated from the immune system through the blood-brain barrier. After brain injury, brain antigens are released into the systemic circulation to induce damaging immune responses. Immune tolerance can effectively reduce the brain edema and neurological inflammatory response after brain injury, which is beneficial to the recovery of neurological function. The clinical application prospect and theoretical research value of the treatment of immune tolerance on traumatic brain injury (TBI) is worth attention. Conclusions The establishment of immune tolerance mechanism has a high clinical value in the treatment of TBI. It opens up new opportunities for the treatment of brain damage.
Brain ; immunology ; Brain Injuries, Traumatic ; immunology ; therapy ; Central Nervous System ; Humans ; Immune Tolerance ; Immunotherapy

Neuroimmunology is a rapidly expanding field in the medicine and there has been great advancement in the understanding of the pathogenesis of autoimmune diseases during the past decade. In neurology, immune mechanism has been implicated in the pathogenesis of more than twenty neurological diseases. The understanding of the immunological mechanism of these diseases has helped clinicians in management of these diseases. In many neurological diseases with immunological deterioration, multiple sclerosis and Guillain-Barre syndrome are relatively common diseases that share common features like demyelination. But multiple sclerosis is a disease of central nervous system and Guillain-Barre syndrome is a syndrome developed in peripheral nervous system. This review will describe the recent advances in clinical immunology with regard to general aspects of autoimmune diseases of neurological system, pathogenesis of two common autoimmune diseases, multiple sclerosis and Guillain-Barre syndrome.
Allergy and Immunology ; Autoimmune Diseases ; Central Nervous System ; Demyelinating Diseases ; Guillain-Barre Syndrome* ; Multiple Sclerosis* ; Neurology ; Peripheral Nervous System

Malignant gliomas are the most common type of primary brain tumor and are in great need of novel therapeutic approaches. Advances in treatment have been very modest, significant improvement in survival has been lacking for many decades, and prognosis remains dismal. Despite "gross total" surgical resections and currently available radio-chemotherapy, malignant gliomas inevitably recur due to reservoirs of notoriously invasive tumor cells that infiltrate adjacent and non-adjacent areas of normal brain parenchyma. In principle, the immune system is uniquely qualified to recognize and target these infiltrative pockets of tumors cells, which have generally eluded conventional treatment approaches. In the span of the last 10 years, our understanding of the cancer-immune system relationship has increased exponentially; and yet we are only beginning to tease apart the intricacies of the central nervous system and immune cell interactions. This article reviews the complex associations of the immune system with brain tumors. We provide an overview of currently available treatment options for malignant gliomas, existing gaps in our knowledge of brain tumor immunology, and strategies that might be exploited for improved design of "custom immunotherapeutics." We will also examine major new immunotherapy approaches that are being actively investigated to treat patients with malignant glioma, and identify some current and future research priorities in this area.
Allergy and Immunology ; Biomarkers ; Brain ; Brain Neoplasms ; Cell Communication ; Central Nervous System Neoplasms* ; Central Nervous System* ; Glioma ; Humans ; Immune System ; Immunotherapy ; Prognosis ; Vaccines

An experimental allergic encephalomyelitis was induced by bovine myelin basic protein (MBP) and bovine galactocerebroside (GC) on male guinea pigs. Animals were divided into five experimental and one control groups. Among the five experimental groups, three were inoculated with 75 micrograms, 150 micrograms and 300 micrograms of MBP, respectively, to see the dose dependency of demyelination. The fourth group was inoculated with mixture of 75 micrograms of MBP and 180 micrograms of GC and the fifth group with 180 micrograms GC. All inocula was injected intradermally in emulsion state mixed with equal amount of complete Freund adjuvant. Control group was injected with adjuvant only. Clinical symptoms began to appear from 15th day after inoculation and animals were sacrificed on maximum neurologic deficit or 4 to 5 days after the onset of symptoms. Demyelination was observed in 6 out of 8 animals inoculated with MBP/GC mixture, while only 3 out of 24 animals inoculated with various dosage of MBP showed demyelination. The difference was statistically significant. Serum antibodies to MBP and GC were measured by ELISA method. All of the eight animals inoculated with MBP/GC mixture and two animals inoculated with GC had low titer of anti-GC antibodies, while all animals inoculated with MBP, MBP alone or MBP/GC mixture, had high titer of anti-MBP antibodies. Therefor it is concluded that the demyelination is augmented by GC and is not significantly dose-dependent on MBP.
Animals ; Autoantibodies/*immunology ; Central Nervous System/*immunology/pathology ; Cerebrosides/*immunology ; Dose-Response Relationship, Drug ; Encephalomyelitis, Autoimmune, Experimental/*metabolism/pathology ; Galactosylceramides/*immunology ; Guinea Pigs ; Male ; Myelin Basic Protein/*immunology

An experimental allergic encephalomyelitis was induced by bovine myelin basic protein (MBP) and bovine galactocerebroside (GC) on male guinea pigs. Animals were divided into five experimental and one control groups. Among the five experimental groups, three were inoculated with 75 micrograms, 150 micrograms and 300 micrograms of MBP, respectively, to see the dose dependency of demyelination. The fourth group was inoculated with mixture of 75 micrograms of MBP and 180 micrograms of GC and the fifth group with 180 micrograms GC. All inocula was injected intradermally in emulsion state mixed with equal amount of complete Freund adjuvant. Control group was injected with adjuvant only. Clinical symptoms began to appear from 15th day after inoculation and animals were sacrificed on maximum neurologic deficit or 4 to 5 days after the onset of symptoms. Demyelination was observed in 6 out of 8 animals inoculated with MBP/GC mixture, while only 3 out of 24 animals inoculated with various dosage of MBP showed demyelination. The difference was statistically significant. Serum antibodies to MBP and GC were measured by ELISA method. All of the eight animals inoculated with MBP/GC mixture and two animals inoculated with GC had low titer of anti-GC antibodies, while all animals inoculated with MBP, MBP alone or MBP/GC mixture, had high titer of anti-MBP antibodies. Therefor it is concluded that the demyelination is augmented by GC and is not significantly dose-dependent on MBP.
Animals ; Autoantibodies/*immunology ; Central Nervous System/*immunology/pathology ; Cerebrosides/*immunology ; Dose-Response Relationship, Drug ; Encephalomyelitis, Autoimmune, Experimental/*metabolism/pathology ; Galactosylceramides/*immunology ; Guinea Pigs ; Male ; Myelin Basic Protein/*immunology

No abstract available.
Animal ; Central Nervous System/virology ; Central Nervous System/pathology ; Central Nervous System/immunology ; Cytokines/metabolism ; Cytokines/immunology ; Demyelinating Diseases/virology* ; Demyelinating Diseases/immunology ; Disease Models, Animal ; Human ; Inflammation/virology ; Multiple Sclerosis/virology ; Multiple Sclerosis/immunology ; T-Lymphocytes/immunology ; Theiler Murine Encephalomyelitis Virus/pathogenicity ; Theiler Murine Encephalomyelitis Virus/immunology*

BACKGROUNDTo investigate the relationship between immune status and rubella virus (RV) infection of central nervous system (CNS).

METHODSBALB/c mice were given dexamethaxone and cytoxan before RV JR23 strain infection. Immune functions and RV invasion to CNS were assayed at 21 days postinfection via abdominal cavity and their relationship was analyzed.

RESULTST cell functions of cytoxan group were obviously worse than those of other groups (P <0.05) by MTT method. Infection rates of dexamethaxone and cytoxan and the group without any intervention were 60%, 90% and 50% (P >0.05), respectively. Cellular immune functions of the mice with CNS infection were obviously worse than those of the mice without CNS infection (P <0.001). Specific antibodies (Ab) were assayed in all groups with ELISA and the results showed that there were no significant differences among groups (P >0.05), neither between the groups with and without CNS infections.

CONCLUSIONSRV infection of CNS may relate to cellular immune status before specific antibody was produced in the body.

Animals ; Antibody Specificity ; Central Nervous System Infections ; immunology ; virology ; Female ; Immunity, Cellular ; Male ; Mice ; Mice, Inbred BALB C ; Rubella ; immunology ; Rubella virus ; immunology ; T-Lymphocytes ; immunology

BACKGROUNDConventional magnetic resonance imaging (MRI) is the preferred neuroimaging method in the evaluation of neuropsychiatric systemic lupus erythematosus (NPSLE). The purpose of this study was to investigate the association between clinical and immunological features with MRI abnormalities in female patients with NPSLE, to screen for the value of conventional MRI in NPSLE.

METHODSA total of 59 female NPSLE patients with conventional MRI examinations were enrolled in this retrospective study. All patients were classified into different groups according to MRI abnormalities. Both clinical and immunological features were compared between MRI abnormal and normal groups. One-way analysis of variance was used to compare the systemic lupus erythematosus disease activity index (SLEDAI) score for MRI abnormalities. Multivariate logistic regression analysis investigated the correlation between immunological features, neuropsychiatric manifestations, and MRI abnormalities.

RESULTSThirty-six NPSLE patients (61%) showed a variety of MRI abnormalities. There were statistically significant differences in SLEDAI scores (P < 0.001), incidence of neurologic disorders (P = 0.001), levels of 24-h proteinuria (P = 0.001) and immunoglobulin M (P = 0.004), and incidence of acute confusional state (P = 0.002), cerebrovascular disease (P = 0.004), and seizure disorder (P = 0.028) between MRI abnormal and normal groups. In the MRI abnormal group, SLEDAI scores for cerebral atrophy (CA), cortex involvement, and restricted diffusion (RD) were much higher than in the MRI normal group (P < 0.001, P = 0.002, P = 0.038, respectively). Statistically significant positive correlations between seizure disorder and cortex involvement (odds ratio [OR] = 14.90; 95% confidence interval [CI], 1.50-151.70; P = 0.023) and cerebrovascular disease and infratentorial involvement (OR = 10.00; 95% CI, 1.70-60.00; P = 0.012) were found.

CONCLUSIONSMRI abnormalities in NPSLE, especially CA, cortex involvement, and RD might be markers of high systemic lupus erythematosus activity. Some MRI abnormalities might correspond to neuropsychiatric manifestations and might be helpful in understanding the pathophysiology of NPSLE.

Adolescent ; Adult ; Child ; Child, Preschool ; Female ; Humans ; Lupus Erythematosus, Systemic ; immunology ; pathology ; Lupus Vasculitis, Central Nervous System ; immunology ; pathology ; Magnetic Resonance Imaging ; Middle Aged ; Retrospective Studies

With extended life of HIV-infected patients due to highly active anti-retroviral therapy (HAART), the rate of HIV associated neurocognitive disorder (HAND) remains high and attracts much attention. The evidence is clear that cytokines are elevated in the blood of patients with HIV infection, which contribute to elevating the permeability of blood-brain barrier. Benefiting from that, cells in the brain are infected with HIV that has accelerated through the blood-brain barrier both as cell-free virus and infected immune cells including monocytes and T cells. Upon migration into the central nervous system, HIV-infected monocytes and T cells not only infect brain resident cells but also produce proinflammatory cytokines such as TNF and IL-1ß, which further activate microglia and astrocytes. These activated brain glial cells and perivascular macrophages, which release inflammatory mediators, are the main contributors to neuroinflammation resulting in neuronal dysfunction. The pathogenesis of HAND is multifaceted, however, mounting evidence indicates that HIV related neuroinflammation plays a major role, which should be the focus of therapeutic research for HAND in future.
Astrocytes ; Blood-Brain Barrier ; Brain ; Cell Movement ; Central Nervous System ; Cytokines ; HIV Infections ; immunology ; HIV-1 ; Humans ; Macrophages ; Microglia ; Monocytes ; Neurocognitive Disorders ; immunology ; Neurons ; T-Lymphocytes