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PubMed2005

Immune cell activation and subsequent epithelial dysfunction by Staphylococcus enterotoxin B is attenuated by the green tea polyphenol (-)-epigallocatechin gallate.

Bacterial superantigens (SAg) are potent T cell activators and when delivered systemically elicit a self-limiting enteropathy in mice. Also, SAg-stimulated human peripheral blood mononuclear cells (PBMC) increase enteric epithelial cell monolayer permeability in vitro. Epigallocatechin gallate (EGCG), the major polyphenol component of green tea (Camilla sinesis) leaf, has been presented as an anti-inflammatory agent. We tested the hypothesis that EGCG (10-100 microM) would block PBMC activation by the SAg, Staphylococcus aureus enterotoxin B (SEB, 1 microg/ml), thus preventing disruption of the epithelial barrier. Pretreatment or co-treatment of human PBMC or murine lymphnode cells with EGCG significantly reduced SEB-induced proliferation and IL-2, IFNgamma, and TNFalpha production. ConA-induced proliferation was also inhibited by EGCG (50 microM) co-treatment. These effects of EGCG were not due to induction of immune cell apoptosis, and were independent of EGCGs anti-oxidant activity, and inhibition of NF-kappaB or AP-1 activation. Moreover, addition of exogenous IL-2 (20 ng/ml) to the cultures could not overcome the immunosuppressive effect of EGCG. Culture supernatant from PBMC stimulated in the presence of EGCG failed to increase the permeability of T84 epithelial cell monolayers: a finding consistent with the reduced IFNgamma and TNFalpha production by SAg+EGCG treated PBMC. These data promote EGCG as a suppressor of T cell activation, and given the prominent role that bacteria and T cells play in inflammatory disease we suggest that EGCG could be a useful addition to current treatments for enteric immune disorders and T cell driven immunopathologies.

Animals↗

PubMed1980

Interaction of circulating immune complexes with granulocyte function in patients with rheumatoid arthritis.

The sera and peripheral blood granulocytes of 10 patients with rheumatoid arthritis and of 10 healthy controls were investigated for the presence of soluble immune complexes and for cellular dysfunction. Using the Rajicell-radioimmunoassay, immune complexes were detected in 7 out of 10 rheumatoid sera. In one patient the presence of immune complexes was demonstrated by immunofluorescence. In all rheumatoid patients with circulating immune complexes decreased chemotactic reactivity and diminished bactericidal capacity of the neutrophils were observed. Incubation of rheumatoid granulocytes with pooled AB-serum or pretreatment of neutrophils of healthy controls with immune complexes containing rheumatoid sera resulted in a reduced number of comparable cellular dysfunctions including increased release of lysosomal enzymes, strongly correlated with the presence of intracellular phagocytosed immune complexes. Phagocytosis and increase of oxidative cell metabolism during phagocytosis were not influenced by circulating immune complexes. Based on our in vitro findings we suggest that the described immune complex-dependent granulocyte dysfunctions are possible responsible for the high risk of local or systemic bacterial diseases in patients with rheumatoid arthritis.

Adult↗

PubMed1994

The role of brain-immune interactions in immunotoxicology.

Certain xenobiotics (or the metabolites) can damage immunocompetence by directly interacting with one or more of the cells of the immune system and adversely affecting its function. It has also been proposed that xenobiotics may indirectly affect immune function by affecting other organ systems that will in turn affect immunocompetence. This review surveys evidence that supports the existence of a functional link between the brain and the immune system. In addition, we review data that support the concept that a xenobiotic-induced dysfunction in the neuroendocrine system may be associated with an immune dysfunction as well. Such chemicals do not necessarily interact directly with immunocompetent cells but would instead act to disrupt regulatory brain-immune interactions. This class of indirectly acting immunotoxic xenobiotics would not be detected in the typical in vitro screening assays.

Animals↗

PubMed1991

Expression of TGF-beta 2 in human glioblastoma: a role in resistance to immune rejection?

Glioblastomas are among the most malignant tumours for which no curative treatment exists. A dysfunction of cellular immunity with decreased skin reactivity and lymphocyte blastogenesis has been described in patients with glioblastomas. In culture human glioblastoma cells release a factor termed glioblastoma-derived T cell suppressor factor (G-TsF) which inhibits the antigen-dependent growth of both helper and cytotoxic T cells. Purification and cloning indicated that G-TsF is a novel member of the TGF-beta family with a well-conserved mature sequence but less homology in the precursor segments. The factor was renamed TGF-beta 2. The two glioblastoma cell lines investigated expressed mRNAs for both G-TsF/TGF-beta 2 and TGF-beta 1 but only G-TsF/TGF-beta 2 protein was secreted. Neuroblastoma cells express only the mRNA for TGF-beta 1 but not the protein, nor the mRNA for G-TsF/TGF-beta 2. Recombinant G-TsF/TGF-beta 2 inhibits the generation of virus-specific cytotoxic T cells when injected into mice infected with lymphocytic choriomeningitis virus. Thus G-TsF/TGF-beta 2 might contribute to the impairment of tumour immune surveillance. Some T cell clones may escape the immunosuppressive effects of TGF-beta: ovalbumin-specific T helper cell lines that showed different degrees of susceptibility to TGF-beta contained clones which had lost receptor(s) for TGF-beta.

Animals↗

PubMed1999

Peter Paul Rickham Prize--1998. Neutrophil dysfunction the cellular mechanism of impaired immunity during total parenteral nutrition in infancy.

BACKGROUND: Studies have shown that total parenteral nutrition (TPN) in infancy is associated with impaired immunity. The causes of this acquired immunodeficiency are poorly understood. Bacterial infection is a major complication of TPN suggesting neutrophils may be affected by this feeding modality. PURPOSE: The aim of this study was to test the hypothesis that TPN-related impaired bactericidal activity is related to impairment of neutrophil function, particularly intracellular killing. METHODS: Studies were performed in five infants (age <2 months) who received long-term TPN (>10 days), five control infants who received a normal enteral diet, and five healthy adults. Patients on long-term TPN were clinically stable with no evidence of sepsis. The experimental study used an in vitro whole-blood model of septicaemia. Coagulase-negative staphylococci were the bacterial challenge. Whole-blood killing of coagulase-negative staphylococci was measured after 45 minutes using the Miles-Misra technique. Neutrophils were separated from whole blood after 15, 30, 45, and 60 minutes of bacterial challenge. The survival rate of the bacteria within the neutrophils was analysed by flow cytometry and the percentage of the bacteria killed by neutrophil intracellular killing assessed at each time-point. RESULTS: Whole-blood killing was significantly lower (P = .05) in infants who received long-term TPN (33.3%) compared with control infants (69.7%) and adults (67.7%). In all subjects studied, neutrophil intracellular killing increased with incubation time. At each time point the intracellular killing in infants on long-term TPN was significantly lower (P < .05) than in normal control infants and adults. CONCLUSION: Future strategies to prevent TPN-related infection should aim to minimise this acquired neutrophil dysfunction.

Adult↗

PubMed2001

Immunotherapy for prostate cancer.

The components of an effective immune response have been elucidated in recent years. An understanding of the dysfunction of the immune response in cancer in one or more of these components has led to a variety of immunotherapeutic approaches. These therapeutic strategies are designed to stimulate dendritic cell proliferation, promote antigen uptake and processing, stimulate an effector cell response via direct antigen presentation, or target tumor cells via antibody therapy. Many approaches in prostate cancer have demonstrated successful induction of the desired immune response. Limited clinical success has also been seen.

Antigen Presentation↗

PubMed2001

Infections in diabetes.

Diabetics are predisposed to infections because of various immune deficiencies, including neutrophil and monocyte dysfunction. Some of these immune deficiencies are improved by tight glucose control. This article is a review of the immune deficiencies seen in diabetes and an overview of selected infections that are commonly or predominantly seen in diabetics.

Bacterial Infections↗

PubMed1986

Pharmacological treatment of immune-mediated inner ear disorders. A clinical immunology and audiology survey.

Cellular and humoral immune reactions may play an etiologic role in an audio-vestibular dysfunction. That immune-mediated inner ear disorders can both be of cochlear and retro-cochlear origin is illustrated on the basis of immunological, immunopathological and audiological data of three case reports, completely differing in their pathogenesis. Autoimmunity may play a certain role, but not in all cases. Anti-inflammatory treatment (corticosteroids) remains the mainstay in therapy.

Adolescent↗

PubMed1995

Neuroendocrine-immune system interactions and autoimmunity.

The concept of an integrated bidirectionally regulated neuroendocrine-immune adaptive response to stress has strong experimental support. The quality and intensity of this coordinated response to stress varies depending upon age, gender, reproductive status, and other genetically determined factors as well as the types and magnitudes of environmental challenges. These factors and dysfunctional communication between the nervous, endocrine, and immune systems appear to contribute to the development of autoimmune diseases in the Lewis and BB rats, the OS chicken, and the NOD, MRL, NZB, NZW, and NZB/NZW F1 mice. Neuroendocrine-immune dysfunction also contributes to the pathogenesis of human autoimmune diseases such as rheumatoid arthritis, systemic lupus erythematosus, thyroid diseases, and others. This review highlights these concepts. It includes discussions on various aspects of the stress response, the hypothalamic-pituitary-adrenal and -gonadal axes, corticotropin releasing hormone, luteinizing hormone releasing hormone, interleukin-1 and -6, corticosteroids, estrogens, testosterone, dehydroepiandrosterone, growth hormone, prolactin, and thyroid hormone. The role of the nervous and endocrine systems in regulating thymopoiesis and T cell development is also emphasized.

Animals↗

PubMed2003

Tolerogenic immunosuppression for organ transplantation.

BACKGROUND: Insight into the mechanisms of organ engraftment and acquired tolerance has made it possible to facilitate these mechanisms, by tailoring the timing and dosage of immunosuppression in accordance with two therapeutic principles: recipient pretreatment, and minimum use of post-transplant immunosuppression. We aimed to apply these principles in recipients of renal and extrarenal organ transplants. METHODS: 82 patients awaiting kidney, liver, pancreas, or intestinal transplantation were pretreated with about 5 mg/kg of a broadly reacting rabbit antithymocyte globulin during several hours. Post-transplant immunosuppression was restricted to tacrolimus unless additional drugs were needed to treat breakthrough rejection. After 4 months, patients on tacrolimus monotherapy were considered for dose-spacing to every other day or longer intervals. FINDINGS: We frequently saw evidence of immune activation in graft biopsy samples, but unless this was associated with graft dysfunction or serious immune destruction, treatment usually was not intensified. Immunosuppression-related morbidity was virtually eliminated. 78 (95%) of 82 patients survived at 1 year and at 13-18 months. Graft survival was 73 (89%) of 82 at 1 year and 72 (88%) of 82 at 13-18 months. Of the 72 recipients with surviving grafts, 43 are on spaced doses of tacrolimus monotherapy: every other day (n=6), three times per week (11), twice per week (15), or once per week (11). INTERPRETATION: The striking ability to wean immunosuppression in these recipients indicates variable induction of tolerance. The simple therapeutic principles are neither drug-specific nor organ-specific. Systematic application of these principles should allow improvements in quality of life and long-term survival after organ transplantation.

Antilymphocyte Serum↗

PubMedDate not supplied

Prolactin secretion and the immune system.

Prolactin receptors were identified on the membranes of lymphocytes have been demonstrated to secrete prolactin. The decrease, as well as the increase of the prolactin level in the plasma are responsible for immune disorders. Prolactin dysfunction has been described in some autoimmune diseases, such as systemic lupus erythematosus, immune arthritis, uveitis, experimental allergic encephalomyelitis and thyroid disease. The normal prolactin secretion is trophic for the lymphocytes, while the high and also the low levels of prolactin may play an immunosuppressive role.

Animals↗

PubMed1988

[Immunoreactive systems in the healing of aseptic and infected wounds in an experiment].

Main parameters of systemic immune reactivity were studied in 240 mature Wistar male rats with simulated aseptic and infected surface wounds before surgical intervention, and 1-10, 12 and 15 days after it. It was stated that aseptic wounds were responsible for nonspecific systemic response to the stress, whereas the presence of bacterial flora in the wound inhibited the development of humoral immune response in the presence of T-cell activation thus causing the dysfunction of the immune system and therefore affecting the course of wound progress. The consideration of all factors mentioned permits averting wound purulent complications in postsurgical period.

Animals↗

PubMed2000

Failure of female baboons (Papio anubis) to conceive following immunization with recombinant non-human primate zona pellucida glycoprotein-B expressed in Escherichia coli.

Progress in the development of an immunocontraceptive vaccine based on zona pellucida glycoproteins has been hampered due to observed ovarian dysfunction associated with immunization using these as immunogens. In this study four female baboons (Papio anubis) were immunized with recombinant bonnet monkey (Macaca radiata) zona pellucida glycoprotein-B (r-bmZPB) expressed in Escherichia coli and conjugated to diphtheria toxoid (DT) using Arlacel-A and Squalene as adjuvants. All the immunized animals elicited a good antibody response against r-bmZPB, continued to have ovulatory cycles and showed no disturbance in the cyclicity. In presence of high titres of circulating anti-bmZPB antibodies (>2x10(3) antibody units), the immunized animals failed to conceive following mating with males of proven fertility. Pregnancy was observed in the immunized animals subsequent to the decline in anti-r-bmZPB antibody titres. These results, though preliminary, suggest that immunization with ZPB may be used for immunocontraception without obvious ovarian dysfunction.

Animals↗

PubMed2026

Convergent evolution of immune evasion in ESKAPE pathogens: A cross-pathogen architecture of conserved host-defense checkpoints.

Antimicrobial resistance in ESKAPE pathogens is primarily attributed to resistance genes, yet persistent infections despite appropriate therapy implicate immune evasion as an independent driver of treatment failure. Although immune-evasion mechanisms have been extensively characterized in individual pathogens, their shared architecture across the ESKAPE group remains insufficiently integrated. This review synthesizes current evidence to show that phylogenetically diverse ESKAPE pathogens have convergently evolved conserved strategies to evade host immunity under comparable selective pressures. A cross-pathogen immune-evasion framework emerges, encompassing impaired pathogen recognition, complement inhibition, phagocyte dysfunction, immunometabolic reprogramming, biofilm-mediated protection, and persistence-promoting inflammation, together with pathogen-specific virulence mechanisms. These processes intersect with adaptive immune dysfunction and emerging concepts, including quorum-sensing-mediated immunomodulation, trained immunity, and the itaconate-succinate immunometabolic axis, forming an interconnected persistence network rather than isolated virulence traits. This systems-level perspective identifies conserved host-directed therapeutic targets that may complement conventional antimicrobial therapy across species. However, host-directed therapies, immunotherapeutics, and vaccines remain largely preclinical or have shown inconsistent clinical efficacy. Mechanistic evidence is strongest for Staphylococcus aureus, Pseudomonas aeruginosa, and Klebsiella pneumoniae, whereas substantial knowledge gaps persist for Enterococcus faecium, Acinetobacter baumannii, and Enterobacter spp. Overcoming persistent ESKAPE infections will require targeting conserved host-pathogen interactions alongside pathogen-specific antimicrobial resistance mechanisms.

Convergent immune evasion↗

PubMed1982

T-cell dysfunction and hyperimmunoglobulinemia E in paracoccidioidomycosis.

Various aspects of T and B cell mediated immunity were investigated in 20 well documented cases of active (10) or inactive (10) paracoccidioidomycosis (Pcm), as well as in 8 healthy individuals living in the endemic area of the disease. The results confirm previous reports that active Pcm produces diverse grades of depression of T cell mediated immunity. Such T cell dysfunction is not associated with a reduction in the number of peripheral E rosette-forming cells, and the immunodepression is reversed by chemotherapy. Sera from Pcm (active or inactive) patients have significantly increased levels of total IgE, but the actual proportion of IgE antibodies against P. brasiliensis was very low (0.4-0.6%). The highest levels of total IgE were found in active patients with disease-related immune depression, suggesting that T cell dysfunction might contribute to the excessive IgE production.

Adolescent↗

PubMed1985

Immunological abnormalities in massive cutaneous hyalinosis.

Immunological studies in a patient with massive cutaneous hyalinosis, a disease characterized by principally dermal and subcutaneous accumulations of monoclonal kappa light chains and a gliadin-binding mannose-rich 90 kD glycoprotein, show that the ratio of helper to suppressor T cells is decreased and the proliferative responses of the peripheral mononuclear cells to T cell and T cell-dependent B cell mitogens are depressed. High levels of circulating immune complexes were demonstrated by C1q-binding and rheumatoid factor enzyme linked immunoassays. IgM and IgA class antibodies against the hyalin components, the mannosyl-90 kD glycoprotein and type I collagen, and against keratin and gluten were present in high titres. The reactivity of mononuclear cells to phytohemagglutinin normalized and the antibody levels to hyalin proteins, keratin and gluten fell during low-dose steroid therapy. However, the concanavalin A response was not reversed, neither did the levels of circulating immune complexes and anti-intercellular substance antibodies decrease. The results demonstrate a very complex dysfunction of the immune system in massive cutaneous hyalinosis.

Aged↗

PubMed1994

Induction of feline acquired immune deficiency syndrome by feline leukemia virus: immuno- and neuroendocrine dysfunctions.

Young cats, when chronically infected with feline leukemia virus (FeLV), developed feline acquired immune deficiency syndrome (FAIDS). The syndrome was associated with a sequence of dysfunctions in the hypothalamic-pituitary-gonadal (HPG) and the immune system, manifested in the reduction of luteinizing hormone-releasing hormone (LHRH), follicle stimulating hormone (FSH), luteinizing hormone (LH), and testosterone in blood plasma. The average FSH and LH (in plasma or lymphocyte), testosterone, and LHRH concentrations in the 20 FeLV-infected cats were measured by radioimmunoassay. The results were compared with those of the 12 control cats that were not FeLV-infected. Four weeks after infection, the plasma LHRH concentration in the infected cats showed a 43% reduction. Five to six weeks after infection, the content of FSH and LH in lymphocyte was reduced by 50% and 28%, respectively, whereas, the plasma FSH and LH was reduced by 52% and 42%, respectively. A significant reduction in testosterone content was detected at Week 11 of infection. The onset of the immuno- and neuroendocrine dysfunctions in FAIDs cats followed this sequence: hypothalamus, lymphocyte, pituitary, adrenal gland, and gonads. Indirect immunofluorescence assay showed the presence of FeLV cytoplasmic antigens in the fibers of the hypothalamic preoptic region and the Leydig cells. The possible causal relationship between the dysfunction of the lymphocyte and HPG systems and the presence of FeLV was discussed.

Animals↗

PubMed2000

Insights into the role of gammadelta T lymphocytes in the immunopathogenic response to thermal injury.

Studies have shown that cell-mediated immunity is markedly suppressed after thermal injury. T lymphocyte dysfunction and macrophage hyperactivity have been implicated as causative factors. Previous studies have primarily examined the effects of thermal injury on alphabeta T lymphocytes; however, the role of gammadelta T lymphocytes in the immune response after thermal injury is unclear. Therefore, wild-type mice and mice lacking the TCR delta gene (TCR delta-/-) were subjected to a third-degree scald burn and cell-mediated immune responses assessed at 7 days post-injury. TCR delta-/- mice had 75% mortality after burn injury compared with 25% mortality in the wild-type group. Plasma interleukin-6 (IL-6) levels were significantly elevated at 2, 4, and 18 h post-injury, whereas no difference was observed in tumor necrosis factor alpha (TNF-alpha) and prostaglandin E2 (PGE2) plasma levels. Plasma levels of these inflammatory mediators were similar in wild-type and TCR delta-/- mice post-injury. Splenic macrophage PGE2, IL-6, TNF-alpha, and IL-10 production was significantly increased in wild-type mice at 7 days post-injury, whereas macrophages from injured TCR delta-/- mice had a significantly attenuated capacity to produce IL-6 and TNF-alpha. In contrast, the increased release of PGE2 and IL-10 by macrophages post-injury was not reduced in TCR delta-/- mice. These results implicate a dual role for gammadelta T lymphocytes in the immunopathogenic response to burn injury: (1) they contribute to survival from the insult; and (2) they mediate the induction of a pro-inflammatory macrophage phenotype at 7 days post-injury. Thus, gammadelta T lymphocytes, in part through the modulation of macrophage activity, appear to contribute to the immune dysfunction after thermal injury.

Animals↗