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PubMed1993

Contribution of serum inhibitory factors and immune cellular defects to the depressed cell-mediated immunity in patients with head and neck cancer.

The immune system of patients with head and neck cancer is frequently depressed. Serum inhibitory factors and immune cell dysfunction are known contributors to this depression, but their relative roles are unclear. We have examined these factors to determine whether a common pathway is involved. Is the defect an unresponding "switched-off cell" or is it a remedial defect responsive to the removal of serum inhibitory factors and/or to lymphokine restoration? Immune tests were performed in 66 patients with high-stage head and neck cancer. Serum inhibitory factors were measured by incubation of heat-inactivated serum (10%) with phytohemagglutinin (PHA)-stimulated lymphocytes or natural killer (NK) cells using the K562 assay. Lymphokine-activated killer (LAK) cell cytotoxicity was measured (in the presence/absence of serum) using chromium 51-labeled Raji tumor cells cultured 5 days with interleukin-2 (IL-2) (100 or 1,000 U/mL) and/or interferon-alpha (INF-alpha) (100 U/mL). IL-2 receptors, CD25 or p55 (low affinity) and p75 (high affinity), were measured by flow cytometry through fluorescence-activated cell sorter analysis. Serum inhibitory factors were detected in more than 50% of the patients. Head and neck cancer sera significantly inhibiting the normal lymphocyte response to PHA (11 of 22 patients), as well as significantly inhibiting the NK response of normal lymphocytes and the functional expression of the IL-2 receptor. LAK cell function at low-dose IL-2 was depressed in 45% of the patients (9 of 20) and was restored by increased IL-2 (1,000 U/mL) or a combination of IL-2 and INF-alpha. Twenty-five percent of the patients were unresponsive to maximum lymphokine stimulation. Half of the patients had depressed expression of the low-affinity IL-2 receptor (CD25). The cause of immune depression in patients with head and neck cancer is multifactorial and is related to serum inhibitory factors, as well as to inherent cellular defects. Based on these data, we would suggest a therapeutic approach in selected patients that includes the removal of serum inhibitory factors by plasmapheresis and restoration of cellular defects by combined IL-2 with or without INF-alpha.

Adult↗
PubMed2002

Corticosteroids, immune suppression, and psychosis.

The role of the immune system in psychiatric symptoms has been an area of much interest for many years. This review discusses medications and medical illnesses associated with immune system dysfunction, and their relationship to psychiatric symptoms, particularly psychosis. Medical illnesses including HIV infection, systemic lupus erythematosus (SLE), and Cushing's disease are all associated with psychiatric symptoms. In addition, high dosages of prescription corticosteroids (eg, prednisone and dexamethasone) are associated with mood changes, cognitive deficits, and even psychosis. However, the role of the immune system in mediating the psychiatric disturbances with each of these conditions is not clear. Directions for further research and treatment considerations are discussed.

Anti-Inflammatory Agents↗
PubMedDate not supplied

Autism: xenobiotic influences.

The advances in medical technology during the last four decades has provided evidence for an underlying neurological basis for autism. The etiology for the variations of neurofunctional anomalies found in the autistic spectrum behaviors appears inconclusive as of this date but growing evidence supports the proposal that chronic exposure to toxic agents, i.e., xenobiotic agents, to a developing central nervous system may be the best model for defining the physiological and behavioral data found in these populations. A total of 20 subjects (15 males and 5 females) who received a formal diagnosis of autism by a developmental pediatrician, pediatric neurologist, or licensed psychologist were included. The mean age for the sample was 6.35 yrs offnge = 3-12 years). This study employed several measures that collectively would provide evidence of burden levels of xenobiotic agents and abnormal liver detoxication processes. These included: (1) Glucaric Acid Analysis, (2) blood analyses for identification of specific xenobiotic agents, and (3) Comprehensive Liver Detoxification Evaluation. Kolmogorov-Smirnov testing for a chi-square and Normal distribution of the Glucaric Acid finding indicates that each of these distributions is significantly different from expected distributions (p < .01). It is most noteworthy that of the 20 cases examined for this study, 100% of the cases showed liver detoxication profiles outside of normal. An examination of 18 autistic children in blood analyses that were available showed that 16 of these children showed evidence of levels of toxic chemicals exceeding adult maximum tolerance. In the two cases where toxic chemical levels were not found, there was abnormal D-glucaric acid findings suggesting abnormal xenobiotic influences on liver detoxication processes. A proposed mechanism for the interaction of xenobiotic toxins with immune system dysfunction and continuous and/or progressive endogenous toxicity is presented as it relates to the development of behaviors found in the autistic spectrum.

Autistic Disorder↗
PubMed2004

Pineal attrition, loss of cognitive plasticity, and onset of puberty during the teen years: is it a modern maladaptation exposed by evolutionary displacement?

Cognitive plasticity, a developmental trait that promotes acquisition of complex skills such as language or playing musical instruments, diminishes substantially during puberty. The loss of plasticity has been attributed to surge of sex steroids during adolescence, but the phenomenon remains poorly understood. We hypothesize that pineal involution during puberty may contribute to plasticity decay. The pineal gland produces melatonin, the level of which declines dramatically during onset of puberty. Emerging evidence suggest that melatonin may modulate cognitive plasticity, independent of the effects of sex steroids, and low sex steroids and high melatonin may be simultaneously required to maintain cognitive plasticity. Potential mechanisms by which melatonin may modulate plasticity are examined within the sleep and hippocampal long-term potentiation frameworks. Implications for psychiatric conditions that involve sleep disorders and learning dysfunctions such as schizophrenia and autism are discussed, and the potential adaptive roles of postprandial and postcoital sleep are explored. From the Darwinian perspective, development and reproductive maturity may represent distinct phases that require tailored cognitive strategies to maximize fitness. While cognitive flexibility and susceptibility to new skills may be paramount during development, reduced cognitive flexibility and increased cognitive determinism may enable more efficient responses to stimuli during adulthood. Thus, cognitive plasticity and cognitive determinism may represent trade-off adaptations and different dimensions of intelligence. The decline of plasticity and emergence of puberty during the second decade may be relics of prehistoric times when the human lifespan was short and the environment was relatively simple and static. Today, when the environment is more complex and dynamic, and humans are living far longer, the early obsolescence of plasticity during puberty may represent a Darwinian inefficiency exposed by evolutionary displacement. Regulation of plasticity may be a systemic phenomenon, as exemplified by the association of learning disability with allergic conditions, a form of immune plasticity dysfunction. Ramifications for other plastic functions that decline during puberty such as wound healing and hyaline cartilage regeneration are explored. Like the plasticity of immunity and cognition, the plasticity of hyaline cartilage during youth may enable hosts to respond to ecologic opportunities and generate the optimally adapted adult phenotype. Pineal involution may represent a potential target for therapeutic extension or restoration of plasticity after puberty. Extending plasticity may have far-reaching consequences for human evolution.

Adolescent↗
PubMed2006

Chronic fatigue syndrome.

Chronic fatigue syndrome (CFS) is thought to have a worldwide prevalence of 0.4-1% with approximately 240,000 patients in the UK. Diagnosis is based on clinical criteria and critically depends on exclusion of other physical and psychiatric diseases. Studies of pathogenesis have revealed immune system abnormalities and chronic immune activation, dysfunction of the hypothalamic-pituitary-adrenal (HPA) axis, brain abnormalities, evidence of emotional stress (comprising host aspects) and evidence of exogenous insults, for example, various microbial infections (Epstein-Barr virus, enteroviruses, parvovirus B19, Coxiella burnetii and Chlamydia pneumoniae), vaccinations and exposure to organophosphate chemicals and other toxins (comprising environmental aspects). Emotional stress appears to be very important as it reduces the ability of the immune system to clear infections, it's presence has been shown to determine whether or not an individual develops symptoms upon virus infection, and it leads to activation of the HPA axis. But, emotional stress is distinct from depression, the presence of which precludes a diagnosis of CFS. There is no specific treatment for CFS other than the much underutilised approach of specific treatment of virus infections. Current priorities are to understand the molecular pathogenesis of disease in terms of human and virus gene expression, to develop a diagnostic test based on protein biomarkers, and to develop specific curative treatments.

Diagnosis, Differential↗
PubMed1986

Immune abnormalities in renal failure and hemodialysis.

Considerable work needs to be done in order to understand the immunosuppressive effect of 'uremia' and the lymphocyte changes induced by hemodialysis. For example, the lymphocyte population dynamics can be further defined using monoclonal antibodies specific for lymphocyte subgroups. In vitro assays are available for lymphokine detection (i.e. IL-1, IL-2 which are important for T cell function) and may be correlated with both the clinical state and overall immunobiological status of hemodialyzed patients. The possibility of specifically delineating the extent of the immune system dysfunction in renal failure patients (on or off dialysis) is at hand. With this knowledge it will be possible to manipulate their management so as to minimize function alterations.

Antibody Formation↗
PubMed2006

Identifying illness parameters in fatiguing syndromes using classical projection methods.

OBJECTIVES: To examine the potential of multivariate projection methods in identifying common patterns of change in clinical and gene expression data that capture the illness state of subjects with unexplained fatigue and nonfatigued control participants. METHODS: Data for 111 female subjects was examined. A total of 59 indicators, including multidimensional fatigue inventory (MFI), medical outcome Short Form 36 (SF-36), Centers for Disease Control and Prevention (CDC) symptom inventory and cognitive response described illness. Partial least squares (PLS) was used to construct two feature spaces: one describing the symptom space from gene expression in peripheral blood mononuclear cells (PBMC) and one based on 117 clinical variables. Multiplicative scatter correction followed by quantile normalization was applied for trend removal and range adjustment of microarray data. Microarray quality was assessed using mean Pearson correlation between samples. Benjamini-Hochberg multiple testing criteria served to identify significantly expressed probes. RESULTS: A single common trend in 59 symptom constructs isolates of nonfatigued subjects from the overall group. This segregation is supported by two co-regulation patterns representing 10% of the overall microarray variation. Of the 39 principal contributors, the 17 probes annotated related to basic cellular processes involved in cell signaling, ion transport and immune system function. The single most influential gene was sestrin 1 (SESN1), supporting recent evidence of oxidative stress involvement in chronic fatigue syndrome (CFS). Dominant variables in the clinical feature space described heart rate variability (HRV) during sleep. Potassium and free thyroxine (T4) also figure prominently. CONCLUSION: Combining multiple symptom, gene or clinical variables into composite features provides better discrimination of the illness state than even the most influential variable used alone. Although the exact mechanism is unclear, results suggest a common link between oxidative stress, immune system dysfunction and potassium imbalance in CFS patients leading to impaired sympatho-vagal balance strongly reflected in abnormal HRV.

Adult↗
PubMed2003

Effect of inhaled industrial chemicals on systemic and local immune response.

Using immunotoxic functional tests, namely IgM response to sheep red blood cells (SRBCs) and interferon-gamma (IFN-gamma) production, this study simultaneously evaluated the effects of inhaled chloroform (10, 20, and 50 ppm), carbon tetrachloride (100, 200, and 300 ppm), 1,1-dichloroethylene (5, 10, and 15 ppm), and styrene (100, 200, and 300 ppm) on the systemic (spleen) and local (lung-associated lymph nodes) immune response. At least one concentration of all the chemicals studied provoked a statistically significant increase in IgM response in the lymph nodes compared with the controls, as expressed by the number of plaque-forming cells (PFCs), whereas only the highest concentration of 1,1-dichloroethylene provoked an increase in the number of PFCs statistically different from the controls in the case of the spleens. The release of IFN-gamma in the lymph node cell cultures of the exposed mice exceeded that of the controls by more than 600%, whereas the release of IFN-gamma in the spleen cell cultures of the exposed mice was moderately different from the controls. It would appear from these results that the lung-associated lymph nodes are sensitive targets for chemical inhalation and that the results of systemic tests in the spleen may not mirror local immune response dysfunction. For risk assessment of inhaled chemicals, it is therefore important to take the local immunotoxic effects into consideration, in particular immunostimulation which may be involved in the rise in allergic diseases in industrialised countries.

Air Pollutants, Occupational↗
PubMed1997

Modification of cytokine patterns in subjects bearing the HLA-B8,DR3 phenotype: implications for autoimmunity.

The factors influencing the pathogenesis of autoimmune disease are not fully known, but the host genotype undoubtedly plays a role in determining the outcome of these diseases. The role of the host's major histocompatibility complex (MHC) genotype in the regulation of susceptibility to autoimmune diseases has been extensively studied in different populations, and certain HLA (the human MHC) alleles and haplotypes have been reported to be associated with several autoimmune diseases. In particular, the association with genes from the HLA-B8,DR3 haplotype has been reported by different research groups. This haplotype is associated in all Caucasian populations with a wide variety of diseases with autoimmune features, and in healthy subjects it is associated with a number of immune system dysfunctions. Mainly, peripheral blood mononuclear cells from HLA-B8,DR3-positive and -negative individuals differ in their ability to produce interleukin (IL)-2, IL-5, IL-12 and interferon-gamma upon stimulation with the mitogen phytohaemoagglutinin (PHA), while producing similar amounts of IL4, IL-6 and IL-10. Furthermore, in HLA-B8,DR3-positive subjects tumor necrosis factor alpha secretion is increased both with and without PHA stimulation. Accurate control of the functional repertoire of an immune response is a critical parameter in the response to infections as well as in immunopathology. MHC control of the class of the immune response at the level of cytokine production is a sophisticated way in which this occurs. This control might be involved in adaptive immune responses to infections as well as in immunopathology.

Animals↗
PubMed1980

Recurrent chronic pyoderma with cellular immunodeficiency. Successful therapy by levamisole.

In a 21-year-old male patient afflicted with widespread recurrent pyoderma resistent to antimicrobial therapy since 3 years, a deficient state of cellular immunity including dysfunctions of both microphages and T lymphocytes was disclosed. After 6 weeks of systemic treatment with levamisole all lesions cleared completely, whereas appropriate long-term antibiotic therapy previously administered had failed to succeed. The immunological parameters, as far as being reexamined, also returned to normal levels during levamisole therapy.

Adult↗
PubMed1995

Effects of aging on antibody avidity to Mycoplasma pulmonis.

Antibody avidity of serum and lung lavage responses was examined in rats to determine aging effects on functional differences in antibody to Mycoplasma pulmonis. Three age groups of animals (weanling, adult and senescent) were immunized with either of two doses of formalinized M. pulmonis as the antigen, or a placebo control. Total immunoglobulin levels and specific antibody responses were examined in serum and lung lavage fluids and subsequently avidity measurements of the same samples were made for the specific antibody to M. pulmonis. The concentration of NH4SCN that dissociated 50% of the antibody was used to determine the avidity index of the serum and lung lavage samples. Total serum IgG and IgA were decreased in the weanling animals when compared to the other two age groups of animals. In contrast, serum IgA levels were substantially increased in senescent animals. Significant increases in serum IgA levels were noted following immunization that was not observed for IgG levels. Substantial increases in both serum antibody and lung lavage antibody were observed in response to immunization with either dose of antigen, but only the lung lavage samples showed both IgG and IgA isotypes differences that were attributable to age. Serum IgG avidity indices gradually increased over time following immunization with higher indices being observed in the weanling animals immunized with the higher M. pulmonis dose. Serum IgA avidity indices also increased over time with no significant differences noted among the age groups. Lung lavage IgG avidity demonstrated slightly higher indices in the weanling animals, while lung lavage IgA avidity showed higher avidity indices in the senescent animals at the higher antigen dose. These data suggest that senescent animals are capable of producing an apparently functional antibody response and that differences noted in increased disease susceptibility in older animals may be attributed to mechanisms other than a dysfunctional humoral immune response at mucosal surfaces.

Age Factors↗
PubMed2002

Effects of nutritional rehabilitation on intestinal function and on CD4 cell number in children with HIV.

BACKGROUND: A complex interplay of malnutrition, intestinal dysfunction, and immune impairment increases the progression of human immunodeficiency virus (HIV) disease in children. The authors tested the hypothesis that nutritional support improves intestinal and immune functions in children infected with human immunodeficiency virus (HIV). METHODS: A questionnaire was circulated through reference centers for pediatric HIV infection to evaluate the effects of nutritional rehabilitation, total parenteral nutrition (TPN) and enteral nutrition (EN), in children. Information included changes in body weight, CD4 cell numbers, and intestinal absorption-as judged by the xylose load-before and after clinical nutritional support and the outcome of children. RESULTS: Sixty-two children underwent nutritional support: 46 received TPN and 16 received EN. All but three had full-blown acquired immunodeficiency syndrome, and all were severely malnourished. Baseline clinical conditions were worse in children receiving TPN than in those receiving EN. Intestinal dysfunction was detected in all children who received xylose oral load. A significant increase in CD4 cell count, xylose levels, and body weight followed EN. A similar pattern was observed after TPN, but none of the parameters significantly changed. Twenty-seven children who received TPN and three who received EN eventually died. Fourteen who received TPN and eight who received EN were shifted to oral feeding, and five who received TPN and five who received EN continued with clinical nutritional support at the end of the observation period. CONCLUSIONS: Nutritional intervention may restore intestinal absorption and increase CD4 cell numbers. The efficacy of nutritional intervention is enhanced if provided before a terminal stage of HIV infection. These data provide evidence of a close association among nutritional condition, intestinal absorption, and immune impairment.

Body Weight↗
PubMed2003

Defect in the lymphoid compartment might account for CD8+-mediated effects in the pathophysiology of pure red cell aplasia.

Pure red cell aplasia (PRCA) is a rare hematological syndrome characterized by the lack of red cell progenitors in an otherwise normocellular bone marrow. Many agents and mechanisms have been implicated in the pathophysiology of PRCA, including immune-mediated dysfunctions. This report describes three patients with PRCA with unknown underlying cause and showed that for each, increases in CD8+ cells blunted the maturation of early erythroid (BFU-E). Each patient subsequently responded to immunosuppressive therapy. Peripheral blood mononuclear cells from age- and sex-matched healthy controls showed comparable distribution of CD3, CD4 and CD16, but significant increase in CD8 and decreased CD19. The distribution of lymphocyte subsets correlated with mitogen responses, but showed no difference in allogeneic responses when compared to controls. The adherent population in PRCA is important for mediating the hyper-immune state of patients, when IL-2 levels were used as readout. There was a trend for decreased BFU-E in patients, but marked reduction for late erythroid progenitors (CFU-E). CD8+ cells from PRCA blunted the maturation of BFU-E, despite increasing erythropoietin concentrations. These results strongly suggest that there are defects in the lymphoid compartment that feedback on the erythroid lineage of PRCA.

Adult↗
PubMedDate not supplied

Possible role of bovine immunodeficiency virus in bovine paraplegic syndrome: evidence from immunochemical, virological and seroprevalence studies.

Bovine paraplegic syndrome (BPS) is a debilitating cattle disease of unknown origin that is characterized by leukocytosis, lymphocytopenia and monocytopenia. The major clinical signs are difficulties in locomotion affecting hind limbs, hypoalgesia in the hind quarters, posterior paralysis and death within 72 to 96 hours after recumbency. To investigate the aetiological basis of BPS, we examined a possible association of the syndrome with infection by bovine immunodeficiency virus (BIV), a lentivirus implicated in immune system dysfunction and central nervous system lesions in cattle. Serum samples (n = 1,278) were collected from both healthy and BPS-prevalent cattle herds in Venezuela, and organ extracts were prepared from euthanized animals (n = 11) suspected of having BPS. Sera were analysed for reactivity to recombinant BIV and bovine leukaemia virus gag precursor proteins by immunoblot procedures. Serum reactivity to BIV ranged from 12 to 66% between groups of BPS prevalent herds. The percentage of samples reactive to BLV antigen was much lower (2 to 17%). Rabbits inoculated with extracts from BPS-afflicted animals exhibited an anamnestic immune response to BIV antigens as well as the presence of BIV gag antigens in their tissues. We present evidence for a possible association between BPS disease and a viral agent related to BIV. The role of BIV, in combination with malnutrition, in BPS is discussed.

Animals↗
PubMed1996

Left ventricular dysfunction after heart transplantation: incidence and role of enhanced immunosuppression.

BACKGROUND: The purpose of this study was to examine the incidence, natural history, and outcome of left ventricular dysfunction in 102 consecutive heart transplant recipients. Left ventricular dysfunction (defined as a decline in the echocardiographic ejection fraction to < 0.45) occurred in 16 of 102 transplant recipients (16%) at a mean of 9.7 +/- 8.6 (standard deviation) months after transplantation. METHODS: Diagnostic evaluation included right heart catheterization and endomyocardial biopsy in all patients and coronary angiography in 13 patients. RESULTS: Four patients were found to have moderate cellular rejection (International Society for Heart and Lung Transplantation grade 2 or higher) and were treated with enhanced immunosuppression. Two patients had angiographically apparent coronary allograft vasculopathy; both died of electromechanical dissociation within 4 months. The remaining ten patients had no or mild cellular rejection (International Society for Heart and Lung Transplantation grade 0 or 1). Therapy in these ten patients included corticosteroids (n = 8). OKT3 (n = 5), and plasmapheresis (n = 2). Three patients died within 2 months of diagnosis, two from undetected severe coronary allograft vasculopathy and one from unrecognized constrictive pericarditis. The echocardiographic ejection fraction improved in the surviving patients after enhanced immunosuppressive therapy (0.33 to 0.53, p < 0.005). With the benefit of long-term clinical follow-up and autopsy data, the origins of left ventricular dysfunction in the 16 patients included moderate cellular rejection (n = 4), vascular rejection (n = 1), coronary allograft vasculopathy (n = 3), intercurrent cytomegalovirus infection (n = 1), constrictive pericarditis (n = 1), and either mild or no evident rejection (n = 6). Survival of the 16 patients with left ventricular dysfunction was similar to that of the 86 patients without left ventricular dysfunction. CONCLUSIONS: The cause of left ventricular dysfunction after heart transplantation includes cellular rejection, vascular rejection, coronary allograft vasculopathy, cytomegalovirus infection, constrictive pericarditis, and unexplained mechanisms. Given the improvement in left ventricular function observed after empiric therapy with enhanced immunosuppression in patients with left ventricular dysfunction, immune-mediated phenomena may play an important pathogenic role.

Biopsy↗
PubMed2004

Physiological levels of 5 alpha-dihydrotestosterone depress wound immune function and impair wound healing following trauma-hemorrhage.

HYPOTHESIS: Studies indicate that a depressed wound immune function contributes to an increased rate of wound complications and impaired wound healing following trauma-hemorrhage (T-H). Androgen, ie, 5 alpha-dihydrotestosterone, is responsible for producing the depressed systemic cell-mediated immune responses following T-H in males. The aim of the present study was to determine whether depletion of 5 alpha-dihydrotestosterone in males before T-H has any salutary effects on wound immune cell function and wound healing in male mice following T-H. DESIGN: Mice were castrated or sham castrated 14 days before midline laparotomy (ie, tissue trauma) and subcutaneous polyvinyl sponge implantation, followed by hemorrhage (mean +/- SEM blood pressure, 35 +/- 5 mm Hg for 90 minutes and resuscitation) or sham operation. At 24 hours thereafter, wound immune cells from the sponges were harvested and cultured with lipopolysaccharide A. Release of interleukin 1 beta (IL-1 beta) and IL-6 (in picograms per milliliter) was determined in the supernatants by enzyme-linked immunosorbent assay. In addition, IL-6 was assessed at the wound site by immunohistochemistry. Ten days after T-H, wound-breaking strength was measured. RESULTS: Precastration prevented the significantly suppressed capacity of wound immune cells to release IL-1 beta and IL-6. In addition, precastration normalized the elevated IL-6 expression at the wound site in the T-H mice. Moreover, wound-breaking strength was improved in castrated mice 10 days after T-H. CONCLUSIONS: Male sex steroids appear to be responsible for wound immune cell dysfunction following trauma and severe blood loss. Because decreasing androgen levels resulted in improved wound healing, our results suggest that the use of androgen receptor-blocking agents, eg, flutamide, following T-H might represent a novel adjunct for decreasing the rate of wound complications under those conditions.

Analysis of Variance↗
PubMed2006

Peripartum cardiomyopathy.

Peripartum cardiomyopathy (PPCM) is a disorder in which initial left ventricular systolic dysfunction and symptoms of heart failure occur between the late stages of pregnancy and the early postpartum period. It is common in some countries and rare in others. The causes and pathogenesis are poorly understood. Molecular markers of an inflammatory process are found in most patients. Clinical presentation includes usual signs and symptoms of heart failure, and unusual presentations relating to thromboembolism. Clinicians should consider PPCM in any peripartum patient with unexplained disease. Conventional heart failure treatment includes use of diuretics, beta blockers, and angiotensin-converting enzyme inhibitors. Effective treatment reduces mortality rates and increases the number of women who fully recover left ventricular systolic function. Outcomes for subsequent pregnancy after PPCM are better in women who have first fully recovered heart function. Areas for future research include immune system dysfunction, the role of viruses, non-conventional treatments such as immunosuppression, immunoadsorption, apheresis, antiviral treatment, suppression of proinflammatory cytokines, and strategies for control and prevention.

Adolescent↗
PubMed1993

[Immunology of multiple sclerosis. Recent data and therapeutic perspectives].

Numerous immune abnormalities have been described in multiple sclerosis, including dysfunction of humoral, cellular and non specific immunity. The main abnormality probably concerns suppressive T cell function. The decrease of this function could explain the breakdown of immunological tolerance towards myelin antigens. The primary responsibility of these abnormalities in the triggering of the disease has still to be demonstrated. Moreover, the antigenic target of immune dysfunction has not yet been determined. A better understanding of T cell traffic into the central nervous system and of the mechanisms of interactions between the T cells and the antigen on one hand, the T cells and the cells presenting antigen on the other hand, offer encouraging therapeutic possibilities.

Antibody Formation↗