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Chronic fatigue immune dysfunction syndrome (CFIDS) is a recently recognized illness characterized by debilitating fatigue as well as immunological and neurological abnormalities [Straus, S.E. (1988) J. Inf. Dis. 157, 405-412]. Once thought to be caused by Epstein-Barr virus, it is now thought to have a different but unknown etiology. We evaluated 30 adult and pediatric CFIDS patients from six eastern states for the presence of human T-lymphotropic virus (HTLV) types I and II by Western immunoblotting, polymearse chain reaction, and in situ hybridization of blood samples. The majority of patients were positive for HTLV antibodies by Western blotting and for HTLV-II gag sequences by polymerase chain reaction and in situ hybridization. Twenty nonexposure healthy controls were negative in all assays. These data support an association between an HTLV-II-like virus and CFIDS.
Chronic fatigue and immune dysfunction syndrome (CFIDS) is a disease presenting with systemic, sensory, cognitive, and psychological manifestations. Ocular symptomatology is reported in the visual, functional, perceptual, and pathological aspects of the visual system. The purpose of the research was to evaluate ocular symptoms in patients with CFIDS. One hundred and ninety CFIDS patients [155 females, 35 males; mean age of 41 years (range 15 to 72)] and 198 healthy controls [133 females, 65 males; mean age of 42 years (range 8 to 89)] were surveyed via written questionnaire. Evaluation of data showed statistical significance at levels ranging from 0.0001 to 0.007 for all but one symptom surveyed. It appears that the ocular symptoms of CFIDS are genuine. Further research is needed to determine the etiology and appropriate treatment of this disease.
Advances in the understanding of the interrelationship between immunology and nutrition indicate that immune dysfunction in critically ill patients is linked with nutrient deficiency and abnormal acute-phase response to illness. Immune dysfunction requires special nutrition therapy and metabolic support; immunoregulation by nutrition manipulation may lead to specific immunotherapies for defined groups of patients. The success of dietary strategies must be measured not only by metabolic indexes but also by effects on immune function. The health profession must combat immune dysfunction and inflammation for the sick and frail patients under its care.
Immune system function is thought to be depressed after hemorrhagic shock. We evaluated the delayed effect of hemorrhagic shock on the immune system in rats with and without spleens and investigated the effect of the colloid hetastarch on reticuloendothelial system (RES) function. There were six groups: controls (N = 30, no shock), two groups of shocked animals resuscitated with either hetastarch (HES, N = 13) or lactated Ringer's (LR, N = 13); the remaining three groups were identical except that splenectomy had been performed (N = 16, N = 14, and N = 16, respectively). One week after shock and resuscitation, all groups were challenged with intravenous Streptococcus pneumoniae; quantitative blood and tissue (liver, lung, and spleen) cultures were then obtained. There were no differences between the HES and LR groups. In nonsplenectomized animals, colony counts in the blood, liver, lung, and spleen were significantly higher in shocked animals when compared with controls. Splenectomized rats had no significant differences between shocked groups and controls. These data demonstrate that delayed immune function is depressed in nonsplenectomized rats. Splenectomy causes more severe immune dysfunction than does shock. Also, in similar animals without splenectomy, hetastarch does not appear to alter delayed RES function.
The effects of age and dietary restriction on immune response were investigated using an animal model of accelerated senescence (senescence accelerated mouse, SAM). The experimental groups consisted of control (ad libitum fed) and restricted groups (fed 60% of energy intake of the controls). Spleen weight and total number of splenic cells were significantly lower in the food-restricted group at 8 mo of age. Percentages of T (Thy-1.1+) and B (surface Ig+) cells in the splenic cells were not significantly different between the two groups. The number of direct hemolytic plaque-forming cells per 10(6) spleen cells 4 d following immunization with sheep red blood cells and dinitrophenyl-Ficoll was significantly greater in the 8-mo-old mice in the food-restricted group than in the control group. In the latter group, antibody responses Progressively decreased with age. Mitogen responses to concanavalin A and lipopolysaccharide were maintained in the food-restricted group but were depressed in the control group at 8 mo. In addition, though autoantibody to single-stranded DNA increased in the control group with advancing age, there was a steady decrease in the food-restricted group until 8 mo. Serum immunoglobulin (IgA and IgM) concentrations were significantly lower in the food-restricted group than in controls at 8 mo of age. Therefore, our results suggest that when senescence accelerated mice are subjected to food restriction, there may be a modulatory effect on the immune dysfunction associated with advancing age.
This study was undertaken in order to correlate the immune status of persons with various types of immune dysfunctions with the incidence of dental caries. Preliminary data on caries experience and the microbial composition of plaque in these individuals are presented. The findings suggest that persons with immunoglobulin dysfunctions have a greater susceptibility to dental caries and have a greater frequency of harboring S mutans than do normal persons.
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Using the murine LP-BM5 retrovirus-induced immunodeficiency model, the therapeutic value of zidovudine (AZT) was analyzed. Continuous low dose (60 mg/kg per day) oral AZT administration for 6 weeks increased survival time by 5-6 weeks. Decreasing the duration of therapy to 3 weeks decreased the mean survival time. Extending the therapy from 6 to 14 weeks increased the median survival time (8 weeks). This dose was nontoxic and reduced virus titers, splenomegaly, and lymphadenopathy. AZT also retarded the immune dysfunction syndrome characteristic of this model. Hypergammaglobulinemia was reduced by AZT and was also a marker for disease progression. AZT reduced hyperproliferation of large blast cells and delayed the loss of splenic B cells.
A well-characterized murine model of graft-vs-host disease (GVHD) that develops in response to minor histocompatibility antigens was used to study the mechanism of an immunodeficiency syndrome that is associated with GVHD. Lethally irradiated mice were transplanted with a combination of bone marrow and spleen cells from H-2 compatible donors that differed at multiple minor histocompatibility antigens, or from syngeneic donors. Four to 12 weeks later, the humoral responses of transplanted and control mice to the T dependent antigens bacteriophage phiX174 and TNP-sheep red blood cells (TNP-SRBC), and to the T independent antigen TNP-Brucella abortus (TNP-BA) were determined. The results demonstrate that mice with GVHD have relatively intact B Cell function and a profound defect in T helper cell function. The immune response to T dependent antigens normalized with repeated immunization. We conclude that immune dysfunction in mice with GVHD is due to a reversible defect in T helper cell function.
The effect of the graft-versus-host reaction in response to minor histocompatibility antigens on the antibody response to a T-dependent antigen was studied in four strains of mice. Lethally irradiated mice were transplanted with bone marrow plus graded numbers of spleen cells from H-2-compatible donors. Recipients of syngeneic bone marrow transplants and recipients of allogeneic bone marrow depleted of T cells made normal antibody responses to bacteriophage phi chi 174 when immunized on day 28 (primary) and day 56 (secondary) after marrow transplantation. Recipients of allogeneic bone marrow plus spleen cells made only small amounts of specific antibody and failed to make IgG antibody after secondary immunization. The pattern of the depressed antibody response suggests that the primary mechanism of immune dysfunction in mice with the minor antigen GVHR is a lack of T helper cell function.
Specific pathogen-free domestic cats with experimentally induced feline immunodeficiency virus (FIV) infections of short duration (less than or equal to 10 months) exhibited depressed total leukocyte and neutrophil numbers and a marginally decreased lymphocyte proliferative response to pokeweed mitogen (PWM), while cats with infections of more lengthy duration (greater than or equal to 25 months) exhibited normal leukocyte and neutrophil numbers but a dramatic loss of responsiveness to both PWM and concanavalin A (Con A). Cats with short-term infections exhibited a decrease in the percentage of CD4+ lymphocytes in peripheral blood and a corresponding depression of the CD4+:CD8+ ratio. Cats with long-term infections exhibited a similar but more profound perturbation of the CD4+ lymphocyte subset that also included a decrease in the absolute number of CD4+ cells. The decreased responsiveness to Con A and PWM in cats infected long term paralleled the decline in CD4+ cell counts, and the duration of infection was directly correlated with the decrease in the percentage of CD4+ cells. These data provide evidence supporting the hypothesis that FIV is the cause of an immune dysfunction in cats, with distinct similarities to that produced by human immunodeficiency virus (HIV) in people.
Emerging evidence highlights the crucial role of peripheral immune cells in maintaining brain homeostasis and their influence on the pathology of Alzheimer disease (AD). Genome-wide association studies have identified numerous AD risk variants in genes expressed by immune cells, implicating innate and adaptive immune pathways in disease progression. Advances in neuroimmunology have revealed that immune cell crosstalk involving T cells, B cells, monocytes and/or macrophages and neutrophils can modulate the hallmark features of AD, including amyloid plaque accumulation, tau pathology and chronic neuroinflammation. Mechanistic insights suggest that chronic peripheral inflammation, immune exhaustion, metabolic dysfunction and epigenetic reprogramming exacerbate neurodegeneration in AD by promoting toxic inflammation and impairing protein clearance in the brain. These findings may catalyse the development of novel immunomodulatory strategies, such as immune checkpoint inhibition and cytokine targeting, among others, for AD. This Review examines peripheral immune alterations in AD, evaluates related therapeutic opportunities and highlights key knowledge gaps, particularly the need for human-derived data to advance translational progress. Future research should prioritize personalized approaches that integrate genetic risk, immune profiling and ageing to inform next-generation therapies for AD.
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The effects of short-term thymic hormone administration on age-associated immune function were evaluated. Two groups of individuals greater than 65 years of age were treated for 30 days with thymic extracts (TP1) or placebo; before and after this treatment a panel of in vitro and in vivo parameters was determined according to a very rigorous experimental protocol. In most individuals, TP1 treatment was associated with an improvement in cutaneous delayed-type response to PPD. Moreover, an increase in a circulating T cell subpopulation bearing the CD45R surface antigen ("virgin" T cells), and in NK cell cytotoxic activity was also observed in some subjects. Finally, lymphocyte responsiveness to PHA tended to increase, while no effect on lymphocyte ability to produce IL-2 following mitogen stimulation was observed. These findings suggest that TP1 treatment may influence age-related alterations in immune function parameters in some subjects.
We investigated the hypothesis that alcohol-induced changes of the immune system result in IgA nephropathy (IAN). Wistar rats were infused with liquid diet containing alcohol: "alcoholics." Control rats received an isocaloric diet with glucose instead of alcohol. IAN was diagnosed by mesangial IgA deposition. When compared to controls, serum IgA in alcoholic rats with IAN had a fourfold increase and a twofold increase in alcoholics without IAN. The intestinal lamina propria showed overall lymphocyte depletion in alcoholic rats. The decrease was not uniform for all the lymphocyte subgroups: it resulted in a relative increase in IgA-B cells in alcoholic rats with IAN but not in alcoholic rats without IAN. No significant differences were observed between alcoholic and control rats in the percentages of spleen lymphocyte subtypes. We suggest that dysfunction of the mucosal immune system may be related to the induction of IAN in chronic alcohol consumption.
Viruses can persist for years without provoking an effective host immune response or otherwise causing the cell destruction characteristic of an acute viral infection. Clinically relevant principles, generalizable to many persistent viruses, are exemplified by measles and lymphocyte choriomeningitis viruses. The LCMV model indicates that viral persistence and the anergic state are reversible.