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At least 253 records · Page 14Linked to original sources
PubMed2000

[Dynamic observation and clinical significance of integrated traditional Chinese and Western medicine on interleukin-2 system, T cell and erythrocyte immune system in patients of lung cancer].

OBJECTIVE: To study the dynamic changes and its clinical significance of integrated traditional Chinese and western medicine (TCM-WM) on IL-2 system, T cell and erythrocyte immune system in patients of lung cancer. METHODS: Forty-eight cases with lung cancer were randomly divided into two groups: TCM-WM group (group I) and the chemotherapy group (group II); and 20 healthy subjects were simultaneously compared. The relevant immune indices, clinical symptoms and signs, changes of solid tumor and living quality were dynamically observed. RESULTS: (1) The serum IL-2 level of lung cancer patients were significantly lower, while sIL-2R level higher than that of the healthy subjects. And they were raised and lowered respectively after treatment, especially in the group I, but different from the control group yet. And there were highly negative correlation between IL-2 and sIL-2R levels. (2) The percentage of CD3, CD4 and the ratio CD4/CD8 were decreased markedly in both groups, except CD8 which was increased markedly. And the percentage of RBC-C3b RR was obviously lower, while that of RBC-ICR was obviously higher. But the above-mentioned indices could be improved after treatment, especially in the group I, and there were highly positive correlation between CD4/CD8 ratio and RBC-C3bRR. (3) After treatment, all above-mentioned indices were changed significantly to their corresponding opposites. However, in regard to the degree of improvement, the patients of group I were in a better position than those of group II. At the same time, improvement of their clinical symptoms and signs, change of solid tumor and living quality also showed advantageous. CONCLUSION: The therapeutic superiority of TCM-WM on lung cancer may be related with the modulation on immune function. Thus we can say that the effect of TCM-WM is better than that of chemotherapy alone.

Adenocarcinoma↗
PubMed1989

Immune system control of rat and rabbit colonic electrolyte transport. Role of prostaglandins and enteric nervous system.

The role of the immune system in controlling intestinal electrolyte transport was studied in rat and rabbit colon in Ussing chambers. A phagocyte stimulus, the chemotactic peptide FMLP, and a mast cell stimulus, sheep anti-rat IgE, caused a brief (less than 10 min) increase in short-circuit current (Isc). Products of immune system activation, platelet-activating factor (PAF) and reactive oxygen species (ROS), caused a sustained, biphasic increase in the Isc. Ion replacement and flux studies indicated that these agonists stimulated electrogenic Cl secretion and inhibited neutral NaCl absorption; responses that were variably inhibited by the cyclooxygenase blockers indomethacin and piroxicam. Lesser degrees of inhibition by nordihydroguaiaretic acid could be accounted for by decreased prostaglandin synthesis rather than by lipoxygenase blockade. Tetrodotoxin, hexamethonium, and atropine also inhibited immune agonist-stimulated Isc, but had no effect on immune agonist-stimulated production of PGE2 or PGI2. These results indicate that immune system agonists alter intestinal epithelial electrolyte transport through release of cyclooxygenase products from cells in the lamina propria with at least 50% of the response being due to cyclooxygenase product activation of the enteric nervous system. The immune system, like the enteric nervous system and the endocrine system, may be a major regulating system for intestinal water and electrolyte transport in health and disease.

Animals↗
PubMed2002

Regional manifestations and control of the immune system.

Although immune responses are generally considered to be systemic, local events such as interaction of complement products with blood vessels and with inflammatory cells play a pivotal role in determining the nature and manifestations of immune responses. This paper will discuss how blood vessel physiology and immunity influence one another to reach homeostasis upon exposure to an infectious agent. We review new insights into the mechanisms by which the microenvironment of tissues protects against microbial invasion yet facilitates migration of leukocytes and 'decides' whether immunity or tolerance ensues and whether, in the face of immunity, protective responses or tissue injury ensues. These 'decisions' are made based on interaction of components of normal tissues such as proteoglycans and injured tissues such as cell-associated cytokines with receptors on immune cells and blood vessels.

Animals↗
PubMed1998

Chemical sensitivity and the immune system: a paradigm to approach potential immune involvement.

This paper approaches the issue of chemical sensitivity and the immune system though a consideration of established environmentally-induced immune alterations which have particular relevance to the broader topic of chemical sensitivity. Additionally, the report discusses the potential problems associated with prior narrow evaluation strategies for the assessment of environmentally-induced inflammation. A combined approach to assessment drawing upon biomarkers of both the immune and neurological systems is suggested. Such an approach recognizes the key roles which mediators of these two systems play in facilitating host inflammatory responses. The paper concludes with a discussion of the types of specific immune alterations which, from a mechanistic perspective, are likely to be involved with any linkage of chemical sensitivity to the immune system.

Environmental Exposure↗
PubMed2003

[Relationships between the brain and the immune system].

The concept that the brain can modulate activity the immune system stems from the theory of stress. Recent advances in the study of the inter-relationships between the central nervous system and the immune system have demonstrated a vast network of communication pathways between the two systems. Lymphoid organs are innervated by branches of the autonomic nervous system. Accessory immune cells and lymphocytes have membrane receptors for most neurotransmitters and neuropeptides. These receptors are functional, and their activation leads to changes in immune functions, including cell proliferation, chimiotactism and specific immune responses. Brain lesions and stressors can induce a number of changes in the functioning of the immune system. All these changes are not necessarily mediated by the neuroendocrine system. They can also be dependent on autonomic nerve function. The communication pathways that link the brain to the immune system are normally activated by signals from the immune system, and they serve to regulate immune responses. These signals originate from accessory immune cells such as monocytes and macrophages and they are represented mainly by proinflammatory cytokines. Proinflammatory cytokines produced at the periphery act on the brain via two major pathways: (1) a humoral pathway allowing pathogen specific molecular patterns to act on Toll-like receptors in those brain areas that are devoid of a functional blood-brain barrier, the so-called circumventricular areas; (2) a neural pathway, represented by the afferent nerves that innervate the bodily site of infection and injury. In both cases, peripherally produced cytokines induce the expression of brain cytokines that are produced by resident macrophages and microglial cells. These locally produced cytokines diffuse throughout the brain parenchyma to act on target brain areas so as to organise the central components of the host response to infection (fever, neuroendocrine activation, and sickness behavior).

Animals↗
PubMed1992

Immune system of the spontaneously hypertensive rat. I. Sympathetic innervation.

Extensive bidirectional interactions are believed to exist between the sympathetic nervous system and the immune system. The spontaneously hypertensive rat (SHR) is known to possess both increased sympathetic nervous system activity with increased tissue catecholamine levels in several peripheral organs and a moderate T lymphocyte immune deficiency. We examined the development of innervation in both primary (thymus) and secondary (spleen) organs of the immune system of the SHR compared to immunocompetent Wistar-Kyoto (WKY), Fisher 344 (F-344), and Long Evan (LE) rats from birth through 24 weeks. Using glyoxylic acid-induced histofluorescence to visualize monoaminergic nerve fibers, coded specimens were examined and morphologically evaluated for the extent and distribution of innervation. The innervation of the SHR thymus was significantly increased at 2 and 12 weeks of age over the other strains. Unlike the control strains, splenic innervation in SHR was delayed until 2 weeks of age when it suddenly became exuberant. At 12 weeks, the innervation of the SHR spleen was increased over all control strains. By 24 weeks the innervation had regressed to a level comparable to the levels of the other rat strains in these tissues. During the suckling period, the size (weight) of the WKY spleen was larger and the level of innervation was decreased compared to the other strains. These strain-related differences in the development of sympathetic innervation of thymus and spleen likely reflect the complex, bidirectional interplay between the nervous and the immune systems.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1997

Murine silver-induced autoimmunity: silver shares induction of antinucleolar antibodies with mercury, but causes less activation of the immune system.

BACKGROUND: Mercury and silver induce antinucleolar autoantibodies (ANoA) targeting the 34-kDa nucleolar protein fibrillarin in susceptible mouse strains. Mercury has the ability to cause a general activation of the immune system, but antigen-specific mechanisms following direct or indirect interaction between mercury and fibrillarin are now believed to play a crucial role in the autoimmune pathogenesis. Our previous studies showed that silver neither induced the systemic immune complex deposits nor the increase of serum immunoglobulins seen after mercury treatment. The main objective of this study was to examine the relation between activation of the immune system and the induction of ANoA. METHODS: During 4 weeks of subcutaneous silver nitrate injections into mice of the susceptible A.SW and SJL strains and the resistant A.TL strain, the number of T and B cells as well as the expression of cell surface activation and proliferation markers were monitored by flow cytometry. The number of cytoplasmic Ig+ splenocytes was determined by direct immunofluorescence technique on slides, and serum Ig levels as well as anti-ssDNA anti anti-DNP antibodies were determined by ELISA. Serum ANoA were monitored by the indirect immunofluorescence technique. RESULTS: Silver caused in the susceptible strains a weaker and later activation and proliferation of T and B cells than mercury, and no significant polyclonal B cell activation. In contrast, the ANoA titer was not different from that seen in mercury-treated mice of the same strains. Silver-treated mice of the A.TL strain showed neither activation of the immune system nor ANoA. CONCLUSIONS: Despite being as effective as mercury inducing ANoA, silver caused only a slight activation of the immune system. This demonstrates that the massive activation of the immune system in mercury treatment is not necessary for the induction of ANoA, and indicates that (auto)antigen-specific mechanisms are likely to play a key role in mercury- and silver-induced murine autoimmunity.

Animals↗
PubMed1997

Microorganisms and their interaction with the immune system.

Microorganisms interact with the immune system in multiple ways. In an interaction between a microorganism and its host, the defense of the host does not go unchallenged. Microorganisms have for decades been suspected of possessing the capabilities of hiding from and escaping the consequences of immune surveillance. Escape mechanisms like antigenic variation, latency, and genomic integration can best be described as passive mechanisms for avoiding interaction with the host immune system, to differentiate them from the more engaging and host-directed active mechanisms of interaction. Studies of the mechanism of direct entry of viruses (HIV, measles, and enteroviruses), bacteria (streptococci and staphylococci), and parasites (Leishmania and plasmodium) into immune cells like CD4+ T cells or macrophages, as reported very recently, indicate an even more aggressive mode of interaction. This aggressive mechanism of interaction with the components of the host immune system allows the microbe not only to block the normal function of immune components on the surface of immune cells from functioning, but also to obliterate a vital immune function, cellular immunity, causing immunosuppression, e.g. the depletion of CD4+ T cells due to the entry and replication of HIV. Collectively, microorganisms have evolved various mechanisms by which they can actively block almost any cellular, humoral, or systemic immune response. One general feature of the proteins that assist microorganism to immunomodulate and actively evade host defense is their structural and therefore functional similarity to the host proteins, which they effectively mimic. Understanding the different mechanisms by which microorganisms interact with the immune system can impact the design of live vaccines as well as the development of novel therapeutic immunomodulators that can provide medicine with powerful new tools to manage immune disorders, allograft rejection, remote multiple organ failure resulting from trauma, autoimmune diseases, etc.

Animals↗
PubMed1979

Comparison of intratracheal and intravenous inoculation of sheep erythrocytes in the induction of local and systemic immune responses.

The interdependence of the local and systemic immune systems in the development of the immune responses relating to the lung was evaluated. Hamsters were inoculated with 10(9) sheep erythrocytes (SRBC) via local (intratracheal) or systemic (intravenous) routes of immunization. The local immune response was quantitated by the specific antibody-forming cell (sAFC) response in the pulmonary draining lymph nodes (pdLNC). sAFC in the spleens and serum hemagglutination titers evaluated the systemic immune response. The local inoculation of antigen was superior for induction of the maximal numbers of immunoglobulin M (IgM) and non-IgM sAFC in the pdLNC at 4 days post-immunization. However, the local response coould be enhanced by a concomitant splenic response. The local route of inoculation did not consistently induce an sAFC response in the spleen, but when the spleen was involved, two unique observations were recorded regarding the IgM response: (i) an approximate twofold increase in the numbers of sAFC was seen in the pdLNC on day 7 post-inoculation in animals that had a splenic sAFC response; and (ii) the appearance of an early (day 4) serum IgM hemagglutination titer was observed in the animals with a splenic sAFC response. However, the appearance of IgG serum hemagglutination titers was independent of the indirect sAFC response in the spleen but correlated with the appearance of indirect sAFC response in the pdLNC. As expected, intravenous inoculation of antigen was superior for inducing a systemic IgM response. We concluded that the local and systemic immune responses are related and interdependent in providing immune reactivity related to the lung. Whereas the systemic response enhanced both the serum IgM titer and the specific IgM antibody-forming cell response in the draining nodes, we observed that the local response was sufficient for the IgG serum hemagglutination titer even in the absence of a splenic sAFC response.

Animals↗
PubMed2000

Special feature for the Olympics: effects of exercise on the immune system: neuropeptides and their interaction with exercise and immune function.

It is known today that the immune system is influenced by various types of psychological and physiological stressors, including physical activity. It is well known that physical activity can influence neuropeptide levels both in the central nervous system as well as in peripheral blood. The reported changes of immune function in response to exercise have been suggested to be partly regulated by the activation of different neuropeptides and the identification of receptors for neuropeptides and steroid hormones on cells of the immune system has created a new dimension in this endocrine-immune interaction. It has also been shown that immune cells are capable of producing neuropeptides, creating a bidirectional link between the nervous and immune systems. The most common neuropeptides mentioned in this context are the endogenous opioids. The activation of endogenous opioid peptides in response to physical exercise is well known in the literature, as well as the immunomodulation mediated by opioid peptides. The role of endogenous opioids in the exercise-induced modulation of immune function is less clear. The present paper will also discuss the role of other neuroendocrine factors, such as substance P, neuropeptide Y and vasoactive intestinal peptide, and pituitary hormones, including growth hormone, prolactin and adrenocorticotrophin, in exercise and their possible effects on immune function.

Animals↗
PubMed1999

Binding specificity of hydrolytic catalytic antibody: lessons from the diverse immune system.

The diverse immune system has the potential to provide numerous antibodies that catalyze a great variety of reactions and exhibit diversity in mechanism and substrate specificity. However, to find such an antibody is not practical, unless we understand the immune response precisely and utilize it. We applied an alternative screening methodology based on the binding specificity of antibodies for the structure of the transition-state analog p-nitrophenyl phosphonate in order to study the built-in diversity of the immune response. This study uncovered the unpredictable binding and substrate specificity of catalytic antibodies derived from the diverse immune response.

Animals↗
PubMed2005

Animal models of arthritis caused by systemic alteration of the immune system.

Animal models are instrumental in understanding the etiology and pathogenetic mechanisms of rheumatoid arthritis. Several new mouse models have either been produced, including transgenics, gene-knockouts, and gene knock-ins, or established as a spontaneous disease due to natural gene mutations. These models are suitable for addressing the roles of T cells, autoantibodies, cytokines and innate immunity in the development and progression of rheumatoid arthritis. In particular, they now provide insights into how systemic alterations of the immune system result in a local development of chronic arthritis that leads to joint destruction.

Animals↗
PubMed1998

Functional properties of CD4+ CD28- T cells in the aging immune system.

The aging immune system is characterized by a progressive decline in the responsiveness to exogenous antigens and tumors in combination with a paradoxical increase in autoimmunity. From a clinical viewpoint, deficiencies in antibody responses to exogenous antigens, such as vaccines, have a major impact and may reflect intrinsic B cell defects or altered performance of helper T cells. Here we describe that aging is associated with the emergence of an unusual CD4 T cell subset characterized by the loss of CD28 expression. CD28 is the major costimulatory molecule required to complement signaling through the antigen receptor for complete T cell activation. CD4+ CD28- T cells are long-lived, typically undergo clonal expansion in vivo, and react to autoantigens in vitro. Despite the deficiency of CD28, these unusual T cells remain functionally active and produce high concentrations of interferon-gamma (IFN-gamma) and interleukin-2 (IL-2). The loss of CD28 expression is correlated with a lack of CD40 ligand expression rendering these CD4 T cells incapable of promoting B cell differentiation and immunoglobulin secretion. Aging-related accumulation of CD4+ CD28- T cells should result in an immune compartment skewed towards autoreactive responses and away from the generation of high-affinity B cell responses against exogenous antigens. We propose that the emergence of CD28-deficient CD4 T cells in the elderly can partially explain age-specific aberrations in immune responsiveness.

Aging↗
PubMed2002

Total-body irradiation with high-LET particles: acute and chronic effects on the immune system.

Although the immune system is highly susceptible to radiation-induced damage, consequences of high linear energy transfer (LET) radiation remain unclear. This study evaluated the effects of 0.1 gray (Gy), 0.5 Gy, and 2.0 Gy iron ion (56Fe(26)) radiation on lymphoid cells and organs of C57BL/6 mice on days 4 and 113 after whole body exposure; a group irradiated with 2.0 Gy silicon ions (28Si) was euthanized on day 113. On day 4 after 56Fe irradiation, dose-dependent decreases were noted in spleen and thymus masses and all major leukocyte populations in blood and spleen. The CD19(+) B lymphocytes were most radiosensitive and NK1.1(+) natural killer (NK) cells were most resistant. CD3(+) T cells were moderately radiosensitive and a greater loss of CD3(+)/CD8(+) T(C) cells than CD3(+)/CD4(+) T(H) cells was noted. Basal DNA synthesis was elevated on day 4, but response to mitogens and secretion of interleukin-2 and tumor necrosis factor-alpha were unaffected. Signs of anemia were noted. By day 113, high B cell numbers and low T(C) cell and monocyte percents were found in the 2.0 Gy 56Fe group; the 2.0 Gy 2)Si mice had low NK cells, decreased basal DNA synthesis, and a somewhat increased response to two mitogens. Collectively, the data show that lymphoid cells and tissues are markedly affected by high linear energy transfer (LET) radiation at relatively low doses, that some aberrations persist long after exposure, and that different consequences may be induced by various densely ionizing particles. Thus simultaneous exposure to multiple radiation sources could lead to a broader spectrum of immune dysfunction than currently anticipated.

Animals↗
PubMed1983

[Useful stimulation of the immune system].

'Useful stimulation of the immune system is that type of stimulation which results in an immune response (particularly in the mucosae) that will reduce possible pathological effects following exposure to pathogenic organisms and/or toxins over prolonged periods'. Stimulation of the immune system, such as follows a 'natural supply' of antigen at the side of the mucosa and the question whether, on the whole, vaccination will result in useful stimulation of the immune system, are briefly discussed against the background of this definition. A number of instances are cited to illustrate differences and similarities between 'natural' stimulation and stimulation produced by vaccination. Finally, speculations on the use of a more natural system of vaccination are engaged in, a system which utilizes the predictable presence of antigen at the side of the mucosa in conjunction with generalized stimulation of the immune system by administration of adjuvants not including antigen.

Adjuvants, Immunologic↗
PubMed2006

Biology of longevity: role of the innate immune system.

Genetic factors play a relevant role in the attainment of longevity because they are involved in cell maintenance systems, including the immune system. In fact, longevity may be correlated with optimal functioning of clonotypic and natural immunity. The aging of the immune system, known as immunosenescence, is the consequence of the continuous attrition caused by chronic antigenic overload. The antigenic load results in the progressive generation of inflammatory responses involved in age-related diseases. Most of the parameters influencing immunosenescence appear to be under genetic control, and immunosenescence fits with the basic assumptions of evolutionary theories of aging, such as antagonistic pleiotropy. In fact, by neutralizing infectious agents the immune system plays a beneficial role until reproduction and parenting. However, by determining chronic inflammation, it can be detrimental later in life, a period largely unforeseen by evolution. In particular, the data coming from the long-lived male population under study show that genetic polymorphisms responsible for a low inflammatory response might result in an increased chance of long lifespan in an environment with a reduced pathogen burden. Such a modern and healthy environment also permits a lower grade of survivable atherogenic inflammatory response.

Aged, 80 and over↗
PubMed1989

[Sex steroids and the immune system].

Endocrine and immune system are strongly correlated. Hormonal contraceptive drugs influence humoral, cellular and mucosal immunity in different kind and in dependency of the relationships between estrogens and gestagens. At present most authors support the opinion that estrogens are responsible for immunosuppressive features. This review summarizes experimental and clinical reports.

Antibody Formation↗
PubMed1998

Differences in immune responses induced by oral and rectal immunizations with Salmonella typhi Ty21a: evidence for compartmentalization within the common mucosal immune system in humans.

Based on the concept of the common mucosal immune system, immunization at various inductive sites can induce an immune response at other, remote mucosal surfaces. The immune responses elicited through rectal and oral routes of antigen delivery were compared with respect to (i) measurement of antibody responses in serum and various external secretions of the vaccinees and (ii) characterization of the nature and homing potentials of circulating antibody-secreting cells (ASC). Specific ASC appeared in the circulation in 4 of 5 volunteers after oral and 9 of 11 volunteers after rectal immunization with Salmonella typhi Ty21a. The kinetics, magnitude, and immunoglobulin isotype distribution of the ASC responses were similar in the two groups. In both groups, almost all ASC (99 or 95% after oral or rectal immunization, respectively) expressed alpha4 beta7, the gut homing receptor (HR), whereas L-selectin, the peripheral lymph node HR, was expressed only on 22 or 38% of ASC, respectively. Oral immunization elicited a more pronounced immune response in saliva and vaginal secretion, while rectal immunization was more potent in inducing a response in nasal secretion, rectum, and tears. No major differences were found in the abilities of the two immunization routes to induce a response in serum or intestinal secretion. Thus, the rectal antigen delivery should be considered as an alternative to the oral immunization route. The different immune response profiles found in various secretions after oral versus rectal antigen administration provide evidence for a compartmentalization within the common mucosal immune system in humans.

Administration, Oral↗