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 289 records · Page 16Linked to original sources
PubMedDate not supplied

Corticotropin-releasing hormone: interactions with the immune system.

Communication between the neuroendocrine and immune systems is crucial to host defence in both health and disease. Stress adversely interferes with the function of the immune system but the mechanism of such stress-induced immunosuppression is not well understood. Corticotropin-releasing hormone (CRH) is a 41-amino residue peptide which primarily stimulates ACTH secretion. In addition, CRH integrates a series of responses during the stress response. Over the last few years increasing evidence has suggested that CRH, the major stress-integrating peptide, may also directly modulate immune system function. Thus, recent data have demonstrated that CRH acts centrally as an immunosuppressant agent independent of circulating glucocorticoids. This central immunosuppressive effect of CRH is mediated at least partly via the central stimulation of sympathetic outflow. At a peripheral level, the presence of CRH and CRH receptors within cells of the immune system, and its complex effects directly on immune function, suggest that CRH is intimately associated with communication between the neuroendocrine and immune systems.

Adaptation, Physiological↗
PubMed1994

Sympathetic nervous system modulation of the immune system. II. Induction of lymphocyte proliferation and migration in vivo by chemical sympathectomy.

We have used chemical sympathectomy with 6-hydroxydopamine (6-OHDA) in adult mice to study the role of the sympathetic nervous system (SNS) in regulating cellular proliferation and migration in lymphoid organs. Following sympathectomy, an increase in inguinal and axillary lymph node (LN) weight and cellularity was observed. This increase paralleled increased cellular proliferation in vivo, as measured by uptake of [125I]deoxyuridine (125IUdR). Transient increases in cellular proliferation also were observed in spleen and bone marrow following sympathectomy. Administration of desipramine prior to 6-OHDA to prevent sympathectomy resulted in control levels of proliferation. beta-Adrenoceptor blockade just prior to or following 6-OHDA treatment did not alter the enhanced proliferation. Migration of normal 51Cr-labelled lymphocytes into inguinal and axillary LN was enhanced in sympathectomized recipients. Conversely, cells from sympathectomized animals showed diminished migration to these LN upon transfer into intact recipients. These results demonstrate that depletion of NA innervation alters cellular proliferation and lymphocyte migration in primary and secondary lymphoid organs.

Animals↗
PubMed1979

Virus induced diabetes and the immune system. II -- Evidence for an immune pathogenesis of the acute phase of diabetes.

The infection of normal DBA2 and BALB/C nu/ + mice with 2 X 10(2,6) TCID50 of the M variant of the EMC virus induced pathological mean glucose values of 426 +/- 99 mg/100 ml in DBA2 mice and 292 +/- 130 mg/100 ml in BALB/C nu/ + mice on day five following infection. As diabetic animals died afterwards, mean glucose values decreased in the surviving animals on day seven and fourteen. The infected immunodeficient BALB/C nu/nu mice with thymus aplasia did not show abnormal mean glucose values or higher standard deviation of the means (114 +/- 37 mg/100 ml) when compared to uninfected controls (117 +/- 23 mg/100 ml). This demonstrates that a complete thymus-dependent immune system seems to be necessary for the development of the acute stage of virus-induced diabetes in the mouse.

Animals↗
PubMed1979

Secretory immune system of rabbit ocular adnexa.

A distinct system of immunity in a variety of animals is located subjacent to epithelial surfaces and is typified by the predominance of immunoglobulin A (IgA) and secretory component (SC) in various external secretions, including tears. The present study examined normal rabbit lacrimal gland, conjunctiva, and cornea for the presence of immunoglobulin and SC. IgA-staining plasma cells predominated within lacrimal gland and conjunctival stroma, and SC was found in the epithelial cells of both these tissues but not within corneal epithelium. These observations are consistent with findings for other secretory sites in both rabbits and humans and establish lacrimal gland and conjunctiva as integral parts of the rabbit secretory immune system.

Animals↗
PubMed1994

[Bidirectional communication between neural and immune systems].

The brain and the immune system communicate with each other by sharing the signal molecules and receptors. While the brain modulates immunity through the neuroendocrine and autonomic nervous controls, the immune system signals the brain by means of cytokines. This paper gives a brief review on our recent findings on (1) the central neural circuits involved in the stress-induced immunosuppression, (2) the roles of the sympathetic nerve innervating the spleen as a communicating channel from brain to immune system, and (3) the role of the organum vasculosum lamina terminalis region as a site of blood-brain signal transduction. Particularly, we have revealed that an inescapable stress elicits an activation of brain opioid systems which leads to an enhanced activity of the splenic sympathetic nerve through the brain CRF system and thereby suppresses the splenic natural killer cytotoxicity by beta-adrenergic mechanisms.

Animals↗
PubMed1980

The immune system development and function.

The immune system in its four components T cells, B cells, complement and phagocytes is vital for the defense of the organism against foreign substances or antigens. Elimination of an antigen involves the interaction of the four complements of the immune system with antigen and with each other. The final common pathway is the breakdown of the antigen by the intracellular machinery of the phagocytic cell. The maintenance of the self depends on the integrity of the immune system. Whenever this integrity is breached (by aging, congenital immune deficiency, cytotoxic drugs, irradiation, infiltrative disease...) the organism becomes prone to uncontrolled invasion by antigens (viruses, bacteria, fungi, neoplasms) and its survival is threatened.

Complement System Proteins↗
PubMed1998

Modulation of intestinal immune system by dietary fat intake: relevance to Crohn's disease.

Gut-associated lymphoid tissue is the major inductive site of the mucosal immune system, which is functionally independent of the systemic immune system. Both the amount and type of dietary fat modulate intestinal immune function. Absorption of long-chain fatty acids stimulates lymphocyte flux and lymphocyte blastogenesis in intestinal lymphatics. Long-chain fatty acid absorption also significantly enhances migration of T lymphocytes to Peyer's patches, possibly due to up-regulation of adhesion molecules, such as alpha4-integrin and L-selectin. Lipoproteins are involved in stimulation of lymphocyte function by both receptor-dependent and independent mechanisms. However, unsaturated fatty acids at higher concentrations have a suppressive effect on cell-mediated immunity via eicosanoid release, receptor affinity changes or interactions with intracellular signal transduction. Fat absorption also influences various other cells in the intestinal mucosa: increased cytokine release from intestinal epithelial cells follows long-chain fatty acid absorption. In Crohn's disease, elemental diets and total parenteral nutrition often induce remission, possibly by reducing antigenic load on activated immune cells in the intestine and, thus, down-regulating hyperreactive CD4 cells. Dietary oleic acid supplements caused an immunological reversal effect in the intestinal immune system of animals fed an elemental diet. An excess of long-chain fatty acids in an elemental diet, therefore, may negate its beneficial effect on gut-associated lymphoid tissues in Crohn's disease. In contrast, supplemental dietary fish oil apparently tends to prevent relapse of Crohn's disease. Because dietary fat intake is closely associated with immunological function of the intestinal mucosa, careful manipulation of dietary fat can be important in management of this disease.

Adjuvants, Immunologic↗
PubMed2000

Is there a role for the immune system in glaucomatous optic neuropathy?

Glaucoma and immunity are not traditionally perceived as being causally related. Recently, however, compelling observations have provided insight into a potential role for the immune system in the development of glaucomatous optic neuropathy. In this article, it is proposed that the role of the immune system in glaucoma is two-fold. In some patients, there is evidence that an autoimmune mechanism may be responsible for eliciting damage to the optic nerve, resulting in glaucomatous injury. Autoimmune damage to the optic nerve may occur directly by autoantibodies, or indirectly by way of a "mimicked" autoimmune response to a sensitizing antigen which, in turn, injuries retinal ganglion cells. We suggest that autoimmune-mediated glaucoma injury occurs most often, but not exclusively, in patients in whom the intraocular pressure has never been found to be elevated. A second role of the immune system in glaucoma is likely one of surveillance, in which signal pathways of the immune system regulate cell death in response to conditions that stress retinal neurons in glaucoma. These might include mechanical stress from high intraocular pressure, ischemia, excessive excitatory amino acids, or toxic products resulting from excessive nitric oxide synthase production in either neurons or glial fibers that surround the optic nerve as it exits the eye. In these cases, we propose that the immune system acts as an "arbiter" to help determine whether a neuronal cell will ultimately survive, or succumb to, those stressors that are perceived as injurious. It is conceivable that such surveillance and cell death regulation by the immune system is important in determining the fate of retinal neurons in both the more common "high-pressure" forms of glaucoma, such as primary open-angle glaucoma, and in cases in which the intraocular pressure appears within normal range.

Autoantibodies↗
PubMed1987

The ancestor of the adaptive immune system was the CAM system for organogenesis.

The adaptive immune system as we understand it is uniquely possessed by vertebrate species and by none other. Nevertheless, it is generally thought that this system represents the ultimate sophistication of much older cell-cell interaction mechanisms. In this paper, I have suggested that plasma membrane cell adhesion proteins that were involved in ontogenic organogenesis since time immemorial were the ultimate ancestor of the adaptive immune system. N-CAM of the chicken for neuronal organogenesis already possesses four beta 2-microglobulin-like domains and it is this domain from which the adaptive immune system sprang. The germ for this beta 2-microglobulin-like domain is already found in the cell adhesion protein of the slime mold straddling the border between unicellular and multicellular eukaryotes. A slightly different version of the above view has recently been expressed by my colleagues.

Amino Acid Sequence↗
PubMed2005

The innate immune system and HIV pathogenesis.

Innate immunity represents the first line of defense against microbial infections. The innate immune system is activated by conserved structures present on most pathogens and profoundly regulates subsequent adaptive immune responses. HIV is notorious for evading and disrupting the immune system. Although HIV directly targets and gradually destroys the adaptive immunity, it has become clear that the virus also perturbs the components of the innate immune system. In this paper, we review the role of two innate lymphocyte subsets, natural killer and natural killer T cells, that are disrupted during HIV infection.

Animals↗
PubMed2000

The sympathetic nerve--an integrative interface between two supersystems: the brain and the immune system.

The brain and the immune system are the two major adaptive systems of the body. During an immune response the brain and the immune system "talk to each other" and this process is essential for maintaining homeostasis. Two major pathway systems are involved in this cross-talk: the hypothalamic-pituitary-adrenal (HPA) axis and the sympathetic nervous system (SNS). This overview focuses on the role of SNS in neuroimmune interactions, an area that has received much less attention than the role of HPA axis. Evidence accumulated over the last 20 years suggests that norepinephrine (NE) fulfills the criteria for neurotransmitter/neuromodulator in lymphoid organs. Thus, primary and secondary lymphoid organs receive extensive sympathetic/noradrenergic innervation. Under stimulation, NE is released from the sympathetic nerve terminals in these organs, and the target immune cells express adrenoreceptors. Through stimulation of these receptors, locally released NE, or circulating catecholamines such as epinephrine, affect lymphocyte traffic, circulation, and proliferation, and modulate cytokine production and the functional activity of different lymphoid cells. Although there exists substantial sympathetic innervation in the bone marrow, and particularly in the thymus and mucosal tissues, our knowledge about the effect of the sympathetic neural input on hematopoiesis, thymocyte development, and mucosal immunity is extremely modest. In addition, recent evidence is discussed that NE and epinephrine, through stimulation of the beta(2)-adrenoreceptor-cAMP-protein kinase A pathway, inhibit the production of type 1/proinflammatory cytokines, such as interleukin (IL-12), tumor necrosis factor-alpha, and interferon-gamma by antigen-presenting cells and T helper (Th) 1 cells, whereas they stimulate the production of type 2/anti-inflammatory cytokines such as IL-10 and transforming growth factor-beta. Through this mechanism, systemically, endogenous catecholamines may cause a selective suppression of Th1 responses and cellular immunity, and a Th2 shift toward dominance of humoral immunity. On the other hand, in certain local responses, and under certain conditions, catecholamines may actually boost regional immune responses, through induction of IL-1, tumor necrosis factor-alpha, and primarily IL-8 production. Thus, the activation of SNS during an immune response might be aimed to localize the inflammatory response, through induction of neutrophil accumulation and stimulation of more specific humoral immune responses, although systemically it may suppress Th1 responses, and, thus protect the organism from the detrimental effects of proinflammatory cytokines and other products of activated macrophages. The above-mentioned immunomodulatory effects of catecholamines and the role of SNS are also discussed in the context of their clinical implication in certain infections, major injury and sepsis, autoimmunity, chronic pain and fatigue syndromes, and tumor growth. Finally, the pharmacological manipulation of the sympathetic-immune interface is reviewed with focus on new therapeutic strategies using selective alpha(2)- and beta(2)-adrenoreceptor agonists and antagonists and inhibitors of phosphodiesterase type IV in the treatment of experimental models of autoimmune diseases, fibromyalgia, and chronic fatigue syndrome.

Animals↗
PubMed1992

Bidirectional communication between the brain and the immune system.

There is now a substantial body of data available indicating that the brain, the nervous system, and the immune system are functionally connected. Consequently, environmental conditions of a psychosocial or physical nature may influence the body's defence. The magnitude of the change in immune reactivity is partly determined by the individual's evaluation of the psychological or physical stimulus. This is illustrated by pharmacological modification of perception resulting in more pronounced stress-induced immunomodulation. In man, it has been demonstrated that recently experienced life stress, particularly daily hassles, can codetermine the effect of an experimental stressor applied for a short period of time on the immune system. An intriguing finding relates to the synthesis and secretion of hormones and neuropeptides by immune cells. These chemical messengers act as autocrine or paracrine immunoregulatory molecules on the one hand, and as messengers for communication with the brain and peripheral nervous system on the other. Animal research indicates that this dialogue is of biological significance.

Animals↗
PubMed2002

Decoding the patterns of self and nonself by the innate immune system.

The innate immune system evolved several strategies of self/nonself discrimination that are based on the recognition of molecular patterns demarcating infectious nonself, as well as normal and abnormal self. These patterns are deciphered by receptors that either induce or inhibit an immune response, depending on the meaning of these signals.

Animals↗
PubMed1988

Immunological functions of the gut--role of the mucosal immune system.

This review summarizes recent information about immune responses in the intestinal mucosa with emphasis on the role of orally-administered antigens from the external environment. The intestinal mucosa provides an extensive surface for potential absorption of pathogenic environmental antigens, such as microbes, chemicals, and food. The intestinal mucosa is densely populated by IgA-producing plasma cells. The humoral immune responses to antigens in the intestinal mucosa are largely of the IgA class in secretory form (sIgA). This sIgA provides an immunological barrier to absorption of antigens on the mucosal epithelium and to penetration into the body. The cell-mediated immune mechanism is also equipped in the mucosal sites. In addition, the mucosal immune response induces hyporesponsiveness of nonmucosal (systemic) immune reactions, and the liver is an integral part of the mucosal immune system. Thus we consider that the mucosal immune system plays a central role in the maintenance of the homeostasis of the total immune system.

Animals↗
PubMed1995

Selective modulation of elements of the immune system by low molecular weight nucleosides.

To optimally modulate a system as complex as the immune system, one must ultimately control its elements individually. Up to this time, use of polyclonal immune stimulants has necessarily involved modulation of a block of immune functions, frequently including undesired activities as well as the activity of interest. We now report selective modulation of individual elements of the immune system by low molecular weight nucleosides, within the context of a fully functional immune system. Loxoribine (7-allyl-8-oxoguanosine) is a well characterized pleiotropic agonist of the immune system in a variety of species, including mouse and humans. In B-cells it binds to soluble cytoplasmic binding proteins, which upregulate transcription upon translocation to the nucleus. By altering specific portions of the loxoribine molecule, multiple distinct, bioactivity profiles have now been obtained. These include: 1) selective augmentation of antibody responses without effects on B-cell proliferation or NK-cell activity; 2) selective enhancement of NK-cell activity and B-cell proliferation in the absence of antibody responses; and 3) selective enhancement of NK-cell activity and antibody responses without B-cell proliferation. Predominant NK-cell responses with minimal B-cell activity of either type also can be generated. The pattern of cytokine mRNA transcription induced is consistent with the spectrum of cellular activities observed. Thus, it is possible to modulate selective activities of the immune system by relatively minor structural modifications of a broad-spectrum immunomodulator in an unseparated cell system.

Adjuvants, Immunologic↗
PubMed2003

Eosinophilic gastroenteritis: a problem of the mucosal immune system?

The gastrointestinal immune system is a major component of the mucosal barrier, which provides an appropriate immunologic homeostasis between host and numerous foreign antigens, including microbial and dietary antigens. However, under certain pathological circumstances created by disturbance of the immunologic balance, allergic responses associated with the gastrointestinal tract can be triggered by abnormal immune responses against selected food protein antigens. Among the several types of immune competent cells, eosinophils are generally considered to play a central role for the development of allergic diseases in gastrointestinal tissue. Although most research has been focused on the molecular and cellular understanding of eosinophils in the peripheral tissues and lung, recent studies elucidate the unique trafficking and regulation mechanisms of eosinophils in the gastrointestinal tissues. In this review, we summarize current findings in the regulatory mechanism of gastrointestinal eosinophils. Furthermore, several unique murine models for eosinophilic gastroenteritis, which can be applied for the elucidation of underlying mechanisms of eosinophil-mediated gastrointestinal allergy, and the development of new mucosal immune therapy for the control of food allergy are reviewed.

Animals↗
PubMed2003

Species comparison of anatomical and functional immune system development.

The components of the immune system have not been traditionally emphasized as potential target organs in standard developmental and reproductive toxicity (DART) protocols. A number of workshops have been organized in recent years to examine scientific questions that underlie developmental immunotoxicity tests, and the interpretation of results as they relate to human risk assessment. A key question that must be addressed is to determine the most appropriate species and strains to model the developing human immune system. The objective of this review is to compare the anatomical and functional development of the immune system in several species important to either preclinical studies for drug development or safety assessments for chemicals, with what is known in humans. The development of the immune system in humans will be compared to what is known in mice, rats, dogs and nonhuman primates.

Age Distribution↗
PubMed1998

Homeostasis and self-tolerance in the immune system: turning lymphocytes off.

The immune system responds in a regulated fashion to microbes and eliminates them, but it does not respond to self-antigens. Several regulatory mechanisms function to terminate responses to foreign antigens, returning the immune system to a basal state after the antigen has been cleared, and to maintain unresponsiveness, or tolerance, to self-antigens. Here, recent advances in understanding of the molecular bases and physiologic roles of the mechanisms of immune homeostasis are examined.

Animals↗