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At least 91 records · Page 5Linked to original sources
PubMed1990

Intra-articular immunization induces strong systemic immune response in humans.

There is no information available about immunological interactions between the synovial tissue compartment and systemic immunity in health and in disease. The aim of the present study was to evaluate effects of intra-articular immunization on the systemic immune responses in humans. Control subjects were immunized with the same dose of immunogen subcutaneously. Peripheral blood lymphocytes were analysed by spot-ELISA with respect to numbers of immunoglobulin-producing cells and antigen-specific antibody-secreting cells before and 1 week after immunization. Serum and salivary antibody levels were measured by an ELISA before and 14 days after the antigenic exposure. In addition, serum levels of interleukin-6 (IL-6) were analysed before and after immunization. The results indicate that the influenza virus antigen deposited in the joint space induces strong systemic antibody response of IgG, IgA and IgM classes. This response is significantly higher (P less than 0.05) than that of control subjects immunized subcutaneously. In contrast, no significant differences were detected between intra-articularly and subcutaneously immunized subjects with respect to mucosal immune responses. Increased serum levels of IL-6 were observed 1-2 weeks after the vaccination in both experimental groups. We conclude that human joints possess very efficient antigen-presenting properties enhancing systemic B cell reactivity.

Adult↗
PubMed2004

Effect of laparoscopy on the immune system.

Surgery induces alterations in local and systemic immune responses. These changes appear to be associated with an increase in postoperative morbidity. Minimally invasive techniques are considered to improve the preservation of immune function compared with open surgery and may therefore be beneficial for patient recovery. As laparoscopic techniques are increasingly used in abdominal surgery, more research has focussed on the immunologic consequences of these techniques. Nevertheless, the changes that occur in response to trauma are still not completely understood. The immunologic benefits of laparoscopic surgery are the most obvious for minor surgical procedures such as cholecystectomy and antireflux surgery. For more complex procedures such as colorectal surgery for cancer, the benefits are not immediately obvious. Although laparoscopic surgery for colorectal malignancies may be associated with higher survival rates and lower recurrence rates because of improved immune function, it has also been related to high incidences of port-site metastases. Reviews in the literature have now shown that incidences of port-site metastases are comparable to incidences of wound metastases after open surgery. However, it will be necessary to wait for the long-term results of randomized, clinical trials to provide further clarification of how immune function is altered after laparoscopic and open surgery for colorectal cancer.

Acute-Phase Reaction↗
PubMed1987

An in vivo and in vitro analysis of systemic immune function in mice with histologic evidence of neural transplant rejection.

Histologic and immunocytochemical analyses of fetal neocortical tissue transplanted to the lateral ventricle of inbred adult mice indicate that this tissue survives transplantation well if the donor and host are isogeneic. The major histocompatibility complex (MHC) of the mouse is known as the H-2 locus. H-2-incompatible neural transplants (allografts), unlike their H-2-identical counterpart (isografts), are characterized by the presence of T cells comprising both major T-cell subsets and macrophages, and by a marked increase in the expression of both class I and class II (Ia) MHC antigens. These findings suggest a recognition of H-2 alloantigens by the host's immune system followed by an appropriate effector response. We report here our attempts to demonstrate systemic host sensitization to alloantigens in mice bearing H-2-incompatible intraventricular neural transplants. We measured the time to rejection of orthotopic skin grafts subsequent to neural transplantation, splenocyte proliferative responses to alloantigens in mixed lymphocyte cultures (MLC), and class I-restricted antigen-specific cytolytic T lymphocyte (CTL) activity. No significant differences were found in any of these tests of host systemic sensitization between mice with allogeneic neural transplants and those with isogeneic transplants or control animals. We conclude that intraventricular neural transplants, while recognized and affected by cells of the host's immune system, do not elicit a detectable systemic sensitization to class I H-2 alloantigens. Rejection of neural transplants may depend on sensitization to class II H-2 alloantigens, to so-called minor histocompatibility antigens, or some combination thereof.

Animals↗
PubMed2001

Infliximab induces potent anti-inflammatory and local immunomodulatory activity but no systemic immune suppression in patients with Crohn's disease.

BACKGROUND: Anti-TNFalpha therapy with infliximab is effective for Crohn's disease. Infliximab neutralizes the biological activities of TNFalpha, a cytokine involved in host-defence against certain infections. AIM: To evaluate the effects of infliximab on the gut and peripheral immune system functions. METHODS: Biopsies and blood samples from three clinical trials of infliximab in Crohn's disease were analysed. Pharmacokinetics, changes in leucocyte counts and T cell subsets, T cell function, and cytokine profiles of lamina propria mononuclear cells (LPMC) and peripheral blood mononuclear cells (PBMC) were analysed. RESULTS: Infliximab has a serum half-life of 9.5 days and is still detectable in serum 8 weeks after infusion. Leucocyte counts showed consistent changes from baseline toward normal values after therapy. Monocytes and lymphocytes were modestly increased, while neutrophils were decreased 4 weeks after treatment. Lymphocyte subsets and T cell proliferative responses were not altered after therapy. The proportion of PBMCs capable of producing IFNgamma and TNFalpha did not change, while Th1 cytokine production by stimulated LPMC was decreased after infliximab therapy. CONCLUSION: The clinical efficacy of infliximab is based on local anti-inflammatory and immunomodulatory effects in the bowel mucosa, without generalized suppression of systemic immune functions in Crohn's disease patients.

Antibodies, Monoclonal↗
PubMed2003

Protective efficacy of anti-Helicobacter pylori immunity following systemic immunization of neonatal mice.

Helicobacter pylori infection of the gastric mucosa is a significant cause of morbidity and mortality because of its etiologic role in symptomatic gastritis, peptic ulcer disease, and gastric adenocarcinoma. Infection occurs in young children; therefore, a prophylactic vaccine would have to be administered within the first year of life, a period thought to be immunologically privileged. We investigated vaccine formulations administered by different routes to confer protective anti-H. pylori immunity in neonatal mice. Neonatal mice immunized with a single dose of vaccine in complete Freund's adjuvant (CFA) generated antigen-specific gamma interferon-, interleukin-2 (IL-2)-, IL-4-, and IL-5-secreting T cells in numbers similar to those in immunized adult mice, while vaccine administered to neonates in incomplete Freund's adjuvant (IFA) induced such cells in reduced numbers compared to those in adult mice. Both IFA and CFA, however, provided partial protection from a challenge with infectious H. pylori when the vaccine was administered subcutaneously. Neonatal immunized mice also had reduced bacterial loads when immunized intraperitoneally with CFA. In all cases, protection was equivalent to that achieved when adult counterparts were immunized. These studies suggest that an efficacious vaccine might be successfully administered to very young children to prevent perinatal infection of H. pylori.

Aluminum Hydroxide↗
PubMed1989

The secretory immune system.

Several features distinguish mucosal from systemic immunity, depending on the anatomical and functional characteristics of the organs involved. Secretory IgA immunoglobulins are the main effectors of the mucosal immune system and their protective aspects are well documented. Serum IgA have received less attention but are equally important, since they control and remove in a non-phlogistic way antigens crossing the mucosal barriers.

Humans↗
PubMed2006

Robustness trade-offs and host-microbial symbiosis in the immune system.

The immune system provides organisms with robustness against pathogen threats, yet it also often adversely affects the organism as in autoimmune diseases. Recently, the molecular interactions involved in the immune system have been uncovered. At the same time, the role of the bacterial flora and its interactions with the host immune system have been identified. In this article, we try to reconcile these findings to draw a consistent picture of the host defense system. Specifically, we first argue that the network of molecular interactions involved in immune functions has a bow-tie architecture that entails inherent trade-offs among robustness, fragility, resource limitation, and performance. Second, we discuss the possibility that commensal bacteria and the host immune system constitute an integrated defense system. This symbiotic association has evolved to optimize its robustness against pathogen attacks and nutrient perturbations by harboring a broad range of microorganisms. Owing to the inherent propensity of a host immune system toward hyperactivity, maintenance of bacterial flora homeostasis might be particularly important in the development of preventive strategies against immune disorders such as autoimmune diseases.

Bacteria↗
PubMed1997

The biology of the immune system.

Intact immunity is fundamental for survival. The human immune system has evolved with the sophisticated biologic capacity to distinguish self from nonself and for memory through the process of clonal expansion. The ability to distinguish even subtle differences from self, and among myriad antigens, is possible by the rearrangement of genes that encode immunoglobulins and T-cell receptors, as well as by the requirement for T cells to recognize antigens in the context of presentation by HLA molecules encoded within the major histocompatibility complex. Modulation of immune function initiated by antigenic stimulation and cell-cell interactions is facilitated by a plethora of soluble mediators such as cytokines. This overview of the biology of the immune system provides a framework for understanding physiologic immune responses and how lacunar defects within the immune system explain the pathogenesis of immunologic disorders. Through such understanding, potential targets can be identified for therapeutic modulation of the immune system.

Apoptosis↗
PubMed1983

The immune system and the nervous system.

The immune system may interfere with brain function. The central nervous system may also influence the activity of the immune system. The central nervous system is functionally protected by the blood-brain barrier. The central nervous system is functionally protected by the blood-brain barrier. The endothelial cells of the brain capillaries are linked by tight junctions, resulting in an almost continuous interior wall which restricts the transfer of plasma proteins. The barrier function is modified by inflammatory meningeal lesions, stroke and epileptic seizures. Antigenic material may penetrate the barrier and enter the nerve tissue. The phagocytic cells in the central nervous system are mainly of haematogenous origin. The number of such cells in the brain is very low. There are also few lymphocytes under normal circumstances. These cells circulate from the blood, through the vessel walls and into the perivascular spaces, along the perivascular channels and to the CSF and back to the blood. This circulation may increase enormously during inflammatory conditions. In multiple sclerosis, the number of T-lymphocytes in the CSF is increased, corresponding to a preponderance of T-lymphocytes in the perivascular cell infiltrates in and around the lesions. Thus, the individual elements of the immune system are all present in the brain, which is only partially immunologically privileged. The mechanisms underlying the brain's immunological privilege may be of a non-immunological nature. As yet there are only few data which indicate that auto-immunity is a prominent feature in diseases of the human brain. The central nervous system also exerts a modulating influence upon the immune response. This may take place both by secretion of hormones and by a nervous/neurotransmitter influence upon the immune system.

Autoimmune Diseases↗
PubMed2001

Continuing education of the immune system--dendritic cells, immune regulation and tolerance.

T cells, as they develop in the thymus come to express antigen receptors. The specificity of these receptors cannot be predicted and must include many with potential anti-self reactivity. Those that encounter self-antigens, in association with self-MHC (major histocompatibility complex), with high affinity are inactivated and do not leave the thymus. Not all self-antigens however are expressed in the thymus and thus many potentially self-reactive T cells enter the periphery. It poses therefore a fundamental immunological question: how peripheral self-tolerance is maintained in health? Dendritic cells (DC) play a central role in the activation of T cells, especially naïve T cells. Their importance in initiating immune responses against pathogens has been well established. However, DC represent complex populations of cells. Recent advances in our knowledge including molecular understanding of DC/T cell interactions have begun to reveal another important dimension of DC functions in the periphery, being not only initiators but also regulators of the immune system. This review summarises recent findings on the roles of DC in the regulation of immune responses and the maintenance of peripheral tolerance, in an attempt to explain how break down of this may lead to immunopathologies and autoimmunity. The concept of a regulatory DC and its possible role in the generation of T regulatory cells in health and in diseases are also discussed. Based on these, the need for a "continuing education" of the immune system throughout one's life, in which DC are again the "tutors", is postulated.

Animals↗
PubMed2006

An immune edited tumour versus a tumour edited immune system: Prospects for immune therapy of acute myeloid leukaemia.

Cell based therapies for acute myeloid leukaemia (AML) have made significant progress in the last decade benefiting the prognosis and survival of patients with this aggressive form of leukaemia. Due to advances in haematopoietic stem cell transplantation (HSCT) and particularly the advent of reduced intensity conditioning (RIC), the scope of transplantation has now extended to those patients previously ineligible due to age and health restrictions and has been associated with a decrease in transplant related mortality. The apparent graft versus leukaemia (GvL) effect observed following HSCT demonstrates the potential of the immune system to target and eradicate AML cells. Building on previously published pre-clinical studies by ourselves and others, we are now initiating a Phase I clinical study in which lentiviral vectors are used to genetically modify AML cells to express B7.1 (CD80) and IL-2. By combining allogeneic HSCT with immunisation, using the autologous AML cells expressing B7.1 and IL-2, we hope to stimulate immune eradication of residual AML cells in poor prognosis patients that have achieved donor chimerism. In this report we describe the background to cell therapy based approaches for AML, and discuss difficulties associated with the deployment of a chronically stimulated, hence exhausted/depleted immune system to eradicate tumour cells that have already escaped immune surveillance.

Acute Disease↗
PubMedDate not supplied

Critical windows in development of the rodent immune system.

The immune system of rodents, like that in humans, develops from a population of pluripotential hematopoietic stem cells (HSC) that are generated early in gestation from uncommitted mesenchymal stem cells in the intraembryonic splanchnoplure surrounding the heart. This early population of HSC gives rise to all circulating blood cell lineages, including cells of the innate and acquired immune system. To access the impact of chemical exposure on the developing immune system and establish developmental windows of potential vulnerability to these exposures, it is essential to first consider the anatomical development of hematopoietic and lymphopoietic tissues and the sequence of appearance of cells that give rise to the immune system. This is particularly true in embryonic development because, after they initially appear in intraembryonic mesenchyme early in gestation, HSC migrate through an orderly series of tissues before establishing residence in the bone marrow and thymus. The effect of exposure to chemical insults in utero, then, may differ depending on the specific timing of exposure and anatomical location of hematopoiesis. Mechanisms and consequences of developmental immunotoxicity in experimental animals will need to be considered in that context. This review presents an overview of developmental hematopoiesis and a working hypothesis of critical developmental windows of vulnerability of this developmental system to toxic insult by chemical exposure.

Age Factors↗
PubMed2006

The role of galactosyltransferases in cell surface functions and in the immune system.

The immune system relies on cellular communication and often on the recognition of carbohydrates by mammalian lectins. Galactose (Gal)-containing structures are involved in both the innate and adaptive immune systems. Gal is a ligand for Gal/N-acetylgalactosmine (GalNAc) receptors and galectins, and is part of the scaffold structure that synthesizes oligosaccharide ligands for selectins, siglecs and other lectins of the immune system. Gal residues are added to glycoproteins and glycolipids by members of a large family of galactosyltransferases. The expression of many of these enzymes is regulated by the action of cytokines, and becomes altered in various disease states. Specific galactosyltransferases have been shown to control cell adhesion and leukocyte functions. Antibodies need to be galactosylated for normal function, and undergalactosylated immunoglobulin (Ig) is associated with rheumatoid arthritis, while Gal is lacking in the IgA of patients with IgA nephropathy. Interactions involving Gal play important roles in host defenses; they can also result in serious pathophysiology. Galactosyltransferases represent potential targets for the control of cell growth and apoptosis, inflammation and infections.

ABO Blood-Group System↗