Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Immune System”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 109 records · Page 6Linked to original sources
PubMed1990

Secretory immune system of the female reproductive tract. II. Local immune system in normal and infected fallopian tube.

The existence of a secretory immune system in the female genital tract has been demonstrated by the predominance of immunoglobulin (Ig)A-producing plasma cells in human fallopian tube, uterine cervix, and vagina. Epithelium lining fallopian tubes expresses a receptor for IgA, secretory component (SC), and thus resembles other secretory tissues such as intestine, mammary, lacrimal, and salivary glands. The present study extends the characterization of the local immune system in the fallopian tube and assesses its response to infection. We examined normal and infected fallopian tubes from surgical specimens, obtained at tubal ligation and abdominal hysterectomy, for the presence of Ig-producing cells, T cells, and natural killer cells. All tubular segments contained a predominance of IgA plasma cells in the subepithelial lamina propria. The epithelial cells were strongly positive for SC. Luminal contents stained positively for IgA, SC, and J chain, suggesting that this material contained secretory IgA. Submucosal plasma cells of IgM and IgG classes were less frequent than IgA. T cells were present in numbers approximately twofold greater than plasma cells in normal fallopian tubes. T-suppressor (CD8+) cells, which may function in the induction of immune tolerance, were present in the intraepithelial spaces. Infected segments of fallopian tubes demonstrated six- to tenfold increased numbers of plasma cells of all classes. These data suggest that a local immune system is functioning in the human fallopian tube and may provide a first line of defense against tubal infection and the prevention of tubal factor infertility.

Epithelium↗
PubMed1992

How human immunodeficiency virus ravages the immune system.

The immune system of individuals infected with human immunodeficiency virus is affected in two distinct ways: by loss of CD4+ cells and by loss of T-helper-cell function. Neither of these processes is yet fully understood. Research during 1991 that investigated the interaction between human immunodeficiency virus and the immune system has raised as many questions as it answered. Nevertheless, many of the issues raised are relevant to mechanisms responsible for the ravaging of the immune system by human immunodeficiency virus.

Acquired Immunodeficiency Syndrome↗
PubMed1996

Lectin-carbohydrate interaction in the immune system.

The immune system consists of various types of cells and molecules that specifically interact with each other to initiate the host defense mechanism. Recent studies have shown that carbohydrates and lectins (carbohydrate-binding proteins) play an essential role in mediating such interactions. Both lectins and carbohydrates are widely distributed in the mammalian tissues as well as in microorganisms. Carbohydrates, due to their chemical nature, can potentially form structures that are more variable than proteins and nucleic acids. Lectins can exist in either soluble or cell-associated form, and although overall structures vary, invariably possess carbohydrate-recognition domains (CRD) with various specificities. The interaction between lectins and carbohydrates have been shown to be involved in such activities as opsonization of microorganisms, phagocytosis, cell adhesion and migration, cell activation and differentiation, and apoptosis. The number of lectins identified in the immune system is increasing at a rapid pace. The development in this area has opened a new aspect in studying the immune system, and at the same time, provided new therapeutic routes for the treatment and prevention of disease.

Animals↗
PubMed2005

An immunoglobulin C kappa-reactive single chain antibody fusion protein induces tolerance through receptor editing in a normal polyclonal immune system.

Understanding immune tolerance mechanisms is a major goal of immunology research, but mechanistic studies have generally required the use of mouse models carrying untargeted or targeted antigen receptor transgenes, which distort lymphocyte development and therefore preclude analysis of a truly normal immune system. Here we demonstrate an advance in in vivo analysis of immune tolerance that overcomes these shortcomings. We show that custom superantigens generated by single chain antibody technology permit the study of tolerance in a normal, polyclonal immune system. In the present study we generated a membrane-tethered anti-Igkappa-reactive single chain antibody chimeric gene and expressed it as a transgene in mice. B cell tolerance was directly characterized in the transgenic mice and in radiation bone marrow chimeras in which ligand-bearing mice served as recipients of nontransgenic cells. We find that the ubiquitously expressed, Igkappa-reactive ligand induces efficient B cell tolerance primarily or exclusively by receptor editing. We also demonstrate the unique advantages of our model in the genetic and cellular analysis of immune tolerance.

Animals↗
PubMed1995

Induction of genes during apoptosis: examples from the immune system.

The immune system provides many examples of cell populations that are susceptible to the induction of apoptosis. Self-reactive immature cells are deleted by triggering apoptosis. Additionally, mature peripheral lymphocytes are induced to undergo apoptosis, particularly when hyperactivated. In the past few years, several genes have been linked to cell death in lymphoid cells. However, only a handful of these genes has been shown to be required for cell death to occur in the immune system. This review focuses on signals known to mediate apoptosis in the immune system and those genes demonstrated to be required for the induction of cell death.

Animals↗
PubMedDate not supplied

[Psychoimmunology. II. The neuroendocrine system and the immune system in autism and schizophrenia].

In this paper the Authors report on the immunologic alterations in two psychiatric disease: schizophrenia and infantile autism. While a lot of researches have been concluded on the immunologic alterations in schizophrenia, only a few data on infantile autism are available. Based on data from international literature the Authors advance some hypotheses on the role possibly played by the immune system in the pathogenesis of schizophrenia and infantile autism.

Autistic Disorder↗
PubMed1994

Developmental regulation of gene expression for the MPTP delta isoforms in the central nervous system and the immune system.

MPTP delta is a murine transmembrane protein tyrosine phosphatase which has three isoforms, types A-C, differing in the structure of the extracellular regions. In this study, we examined MPTP delta isoform expression in the brain and the immune system at discrete developmental or differentiation stages. RT-PCR analysis demonstrated that another isoform, type D, is transcribed from the MPTP delta gene. In the brain, only type D was expressed until postnatal day 7 (P7), but after P14, all four isoforms were detected. In contrast, the spleen, thymus and all the hematopoietic cell lines examined express only types B and C isoforms. An in situ hybridization study showed that MPTP delta mRNA is diffusely expressed throughout the spleen, but its expression in the thymus is restricted to the medullary region.

Animals↗
PubMed2002

Reprogramming the immune system.

The immune system is organized so as to react to pathogens without risking damage to self. Harnessing those processes that prevent self-reactivity will have enormous potential in clinical medicine. This review outlines the efforts of this laboratory over the last 25 years to exploit tolerance so as to reprogram the immune system for therapeutic purposes.

Allergy and Immunology↗
PubMed2002

[1,25-dihydroxyvitamin D3: the endocrine system meets the immune system].

1,25(OH)2D3, the activated form of vitamin D, is well known for its effects on calcium and bone metabolism, but also non-classical effects on cells of the immune system were described, in vivo as well as in vitro. Structural analogues have been developed with less calcemic effects, but at least comparable immune effects. Our group showed that treatment with 1,25(OH)2D3 can protect the NOD mouse, the murine model for type 1 diabetes, from diabetes in primary, secondary and tertiary prevention. This effect is based on shifts in cytokine profiles (Thelper1 to Thelper2), that occur specifically for the autoantigens, and on enhanced sensitivity of the autoreactive T lymphocytes to apoptotic signals thus leading to a better elimination of these potentially dangerous cells. 1,25(OH)2D3 and its analogues can therefore be considered as interventions aimed at the prevention or treatment of human type 1 diabetes.

Animals↗
PubMed1985

Interactions between the gonadal steroids and the immune system.

The immune system is regulated by the gonadal steroids estrogen, androgen, and progesterone, but the circulating levels of these steroids can also be affected by immune system function. Such interactions appear to be mediated through the hypothalamic-pituitary-gonadal-thymic axis and depend on pituitary luteinizing hormone released by thymic factors under the control of the gonadal steroids.

Androgens↗
PubMedDate not supplied

[The nervous system and the immune system: the role of morphine and opioid peptides in the function of neutrophilic granulocytes].

Inhibition of human granulocyte chemotaxis towards casein was observed in the presence of mu and k receptor agonist, which per se exhibits chemokinetic activity. Naloxone was found to prevent both the opioid and opioid unrelated increase of granulocyte migration. Although opioid agonists with different receptors specificity were capable of strongly modifying human granulocyte migration, no conclusion can be drawn on the role of opioid receptors in regulating migration activity. The effects of morphine and opioid peptide on neutrophil aggregation and ATOP release were studied. Inhibition of human granulocyte aggregation and ATP release was observed in the presence of morphine in a naloxone stereoselective manner, whereas the opioid peptides were ineffective. The effect of DAGO, DADL and dynorphin 1-9 on granulocyte aggregation and ATP release were also evaluated, but these opioid peptides are unable to modify neutrophil function. Our studies confirm the role of mu receptors on modulation of polymorphonuclear granulocyte function and suggest a key role of opioid peptides in the regulation of some immune system functions. In comparative studies Ca++ (A 23,187) and dynorphin 1-9, per se, induced stimulation of arachidonic acid metabolites from granulocytes. In this regard dynorphin 1-9 may function as a mediator between the central nervous system and immunity.

Adenosine Triphosphate↗
PubMed1998

Avian macrophages: regulators of local and systemic immune responses.

Macrophages are key regulatory cells of the immune system involved in initiating and directing the innate and specific immune responses, the systemic acute phase response, tissue repair, and tissue remodeling. In the early stages of a challenge from invading microorganisms or from tissue injury, macrophages defend local and systemic homeostasis by initiating a complex series of cellular, biochemical, and behavioral events. These pathophysiological adjustments are mediated by an extensive variety of communication molecules, including: cytokines, cytokine inhibitors, endocrine hormones, eicosanoids, neurotransmitters, and reactive oxygen intermediates. The cytokines produced by macrophages (monokines) are not well characterized relative to their mammalian counterparts, but a variety of chemokine, pro-inflammatory, and colony-stimulating factor activities have been described. Although the sequence homology, and thus species cross-reactivity, between avian and mammalian cytokines is typically low, the functional characteristics appear to be generally similar. The pro-inflammatory cytokines are important initiators and regulators of the local immune response. They are also released in sufficient quantities during some infections to coordinate a systemic acute phase response that impacts the growth, reproduction, and well-being of poultry. An understanding of the mechanisms and molecules used by macrophages to regulate immune and inflammatory responses may permit the development of products, diets, or husbandry techniques to modulate immunity for the enhancement of the productivity of poultry.

Acute-Phase Reaction↗
PubMed1987

Use of bronchoalveolar lavage to compare local pulmonary immunity with the systemic immune response of Toxocara canis-infected mice.

Following infection of mice with larvae of the canine roundworm Toxocara canis, there is a persistent pneumonitis. Heretofore, nothing was known about the immunologic potential of the cells that constitute this inflammatory exudate. By performing bronchoalveolar lavage (BAL), enough inflammatory cells were obtained to compare the local pulmonary immune response to T. canis infection with the systemic immune response as reflected in the peripheral blood and spleen cells of the same mice. Groups of C57BL/6J female mice were given 100 infective ova and BAL, peripheral blood, and spleen cells collected on days 8, 11, 14, and 17 postinfection. The percentage of eosinophils in the BAL averaged about 80% and was four to five times as great as that in the peripheral blood at all times assayed. Use of concanavalin A (ConA)-elicited lymphocyte blastogenesis to evaluate T-lymphocyte activity revealed that BAL T-cell activity was low on day 8 and peaked on day 11. When the B-cell mitogen lipopolysaccharide was used in the assay, there appeared to be far less BAL cell reactivity compared with BAL T-cell activity. Both B- and T-cell responses of the BAL cells were only a fraction of the responses seen concurrently in spleen cells. Use of Toxocara exoantigens in the blastogenesis assay revealed that Toxocara exoantigens could elicit between 20 and 95% of the ConA response in BAL cells, while in spleen cells Toxocara exoantigens could only elicit 1 to 5% of the ConA response. These results suggest that BAL is a useful method for recovering local inflammatory cells that possess detectable immunologic activity. In the case of pulmonary toxocariasis, eosinophils account for the majority of the cells that are present, with most of the remaining cells being T. canis antigen-specific T lymphocytes.

Animals↗
PubMed1990

Intragonadal regulation of immune system functions.

Immune responses within the mammalian gonads, and in particular the testis, are deficient in spite of adequate lymphatic drainage and the presence of lymphocytes and MHC II+ macrophages. There is considerable evidence from in vivo and in vitro studies that this 'suppression' of the immune system may be due, at least in part, to localized inhibition or regulation of normal lymphocyte and/or macrophage functions within the gonads. In the testis, both steroidal and non-steroidal products of the Leydig cells, including androgens, endorphins, and inhibin-related proteins, have been implicated in mediating this activity. In turn, a number of immune cell cytokines affect steroidogenic cell function in vitro. The studies described in this paper indicated that [3H]-thymidine incorporation by adult rat thymocytes in vitro was inhibited by conditioned medium collected from short-term incubations of Percoll-purified adult rat Leydig cells, but stimulated by testicular interstitial fluid and by conditioned medium collected from short-term incubations of adult rat seminiferous tubules. The factors responsible for these effects on thymocyte function appeared to be of large molecular weight, as they were retained by ultrafiltration membranes with exclusion limits of 10,000 or 30,000 daltons. It is hypothesized that an 'immunosuppressive' mechanism, principally mediated by non-steroidal factors secreted by the steroidogenic cells of the gonadal interstitial tissue, exists within the gonads in order to prevent activation of the immune system by germ cell antigens and growth factors associated with germ cell proliferation and differentiation. This mechanism probably acts in parallel with normal antigen-specific tolerance mechanisms operating at the gonadal level. As immune responses to germ cells are believed to be a significant causative factor in infertility, particularly in men, this represents an important area for further study.

Animals↗
PubMed1999

The central effectors of cell death in the immune system.

The immune system relies on cell death to maintain lymphoid homeostasis and avoid disease. Recent evidence has indicated that the caspase family of cysteine proteases is a central effector in apoptotic cell death and is absolutely responsible for many of the morphological features of apoptosis. Cell death, however, can occur through caspase-independent and caspase-dependent pathways. In the case of cells that are irreversibly neglected or damaged, death occurs even in the absence of caspase activity. In contrast, healthy cells require caspase activation to undergo cell death induced by surface receptors. This review summarizes the current understanding of these two pathways of cell death in the immune system.

Animals↗
PubMed1984

Physiological and pathological influences of central nervous system on the immune system: a critical appraisal.

There is considerable evidence of intricate links between central nervous and immune systems. This paper makes a critical assessment of these relationships. Recent experimental data on hypothalamic influences on Natural Killer activity in mice have been presented and the problems met with in defining causal nexuses discussed. Some information on immune reactivity in patients with mental disorders has briefly been reviewed.

Animals↗