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Results for “immune defense”

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At least 19 recordsLinked to original sources

PubMed1999

Expression of a local immune defense system in the female genital tract. An immunohistochemical study.

UNLABELLED: The aim of this study was to investigate the presence of a local immunological defense mechanism of the secretory IgA class in the female genital tract. MATERIAL AND METHODS: We studied by a streptavidin-biotin method the secretory component (SC) and IgA distribution in paraffin-embedded sections of 90 formalin-fixed specimens. We studied 10 normal and 5 neoplastic cervical specimens, 20 normal, 10 hyperplastic endometrial specimens and 10 endometrial adenocarcinomas, 5 normal ovarian tubes and 30 ovarian epithelial neoplasms, serous and mucinous. A polyclonal SC and (Dako) and a mab IgA (Dako) was used and the reaction was scored from 1-3. RESULTS: Normal cervical mucosa and atrophic endometria were negative, while the basal portion of the endometrium, focally the proliferative glands, most of the secretory glands and most of the hyperplastic glands were positive for SC. IgA showed a similar distribution and a perivascular stromal reaction. Adenocarcinomas were positive for SC, but the intensity of the reaction was dependent on the differentiation of the tumors. Mucous and most serous neoplasms were negative for SC. IgA showed a similar reaction. CONCLUSION: There is evidence that the female genital tract has a local defensive immune system that may be hormone dependent. SC is a valuable marker of glandular differentiation.

Adenocarcinoma↗

PubMed2005

Passive and active components of neonatal innate immune defenses.

Innate immune defenses are crucial for survival in the first days and weeks of life. At birth, newborns are confronted with a vast array of potentially pathogenic microorganisms that were not encountered in utero. At this age, cellular components of the adaptive immune system are in a naive state and are slow to respond. Antibodies received from the dam are essential for defense, but represent a finite and dwindling resource. Innate components of the immune system detect pathogen-associated molecular patterns (PAMPs) on microorganisms (and their products) by means of pattern-recognition receptors (PRRs). Soluble mediators of the innate system such as complement proteins, pentraxins, collectins, ficolins, defensins, lactoferrin, lysozyme etc. can bind to structures on pathogens, leading to agglutination, interference with receptor binding, opsonization, neutralization, direct membrane damage and recruitment of additional soluble and cellular elements through inflammation. Cell-associated receptors such as the Toll-like receptors (TLRs) can activate cells and coordinate responses (both innate and adaptive). In this paper, accumulated knowledge of the receptors, soluble and cellular elements that contribute to innate defenses of young animals is reviewed. Research interest in this area has been intermittent, and the literature varies in quantity and quality. It is hoped that documentation of the limitations of our knowledge base will lead to more extensive and enlightening studies.

Animals↗

PubMed1985

Evaluation of in vivo and in vitro effectivity of immune defense against a spontaneously arising, nonlymphoid rat tumor. I. Analysis of natural immune defense.

Possible mechanisms of natural defense against a nonimmunogenic, nonlymphoid rat tumor were evaluated in vitro and examined for effectivity in vivo, using BSp6S, the subcutaneously grown transplantation line of a spontaneously arising fibrosarcoma in the BDX rat strain, which is highly susceptible to natural killer (NK) cells and macrophages (Mø). The role of nonspecific immune defense in vivo was demonstrated by eliminating NK cells by irradiation and Mø by silica treatment. Especially after depletion of NK cells a significant acceleration of tumor growth and a reduction in the number of cells required for tumor takes was observed. Activation of Mø by Corynebacterium parvum (CP) did lead to retardation of tumor growth; prevention of tumor growth was only achieved after inoculation of a marginal dose of tumor cells. Activation of NK cells was of minor influence. It is concluded that NK cells and Mø are the main influences on survival time, the effectiveness of NK cells being limited to early periods of tumor growth.

Animals↗

PubMed2004

Steroidal regulation of uterine immune defenses.

Progesterone suppresses uterine immune defenses and predisposes postpartum animals to nonspecific uterine infections. Progesterone can also suppress uterine eicosanoid synthesis. This effect of progesterone seems to be an important factor in the onset of uterine infections because eicosanoids can enhance uterine immune defenses. In fact, exogenous prostaglandin F(2alpha) (PGF(2alpha)), an eicosanoid that stimulates uterine PGF(2alpha) production, enhances uterine immune defenses and promotes the ability of ewes and sows to resolve uterine infections, even when progesterone is maintained at luteal phase concentrations. Prostaglandin F(2alpha) is also a proinflammatory molecule that stimulates the production of proinflammatory cytokines and may enhance uterine production of leukotriene B(4) (LTB(4)), which stimulates various neutrophil functions. Neutrophils seem to mount the initial response to bacteria that enter the uterus, and proinflammatory cytokines and LTB(4) enhance phagocytic activity of neutrophils. Even though there are clear associations among PGF(2alpha), LTB(4), proinflammatory cytokines, phagocytosis, and the ability of the uterus to resist or resolve infections, the mechanisms of action of exogenous PGF(2alpha) in mitigating the immunosuppressive effects of progesterone have not yet been defined. However, defining the PGF(2alpha) mechanisms should yield important new information that can be used to develop novel prevention and treatment strategies that do not rely on antibiotic and antimicrobial compounds for managing uterine infections.

Animals↗

PubMed1991

Assembly of macromolecular pores by immune defense systems.

Immune defence systems (complement, cytolytic lymphocytes) make use of transmembrane pores assembled from up to 20 soluble monomers in a highly regulated process to induce cell death. Inhibitors of pore formation have been found which protect blood, endothelial and epithelial cells from the destructive effect of complement lesions. Recently, a pore-forming protein showing immunological crossreactivity to complement C9 has been found in the protozoan parasite Trypanosoma cruzi, thereby extending this protein family and generalizing its means of generating non-selective membrane permeability.

Animals↗

PubMed2006

Contrasting adaptive immune defenses and blood parasite prevalence in closely related Passer sparrows.

Immune system components differ in their functions and costs, and immune defense profiles are likely to vary among species with differing ecologies. We compared adaptive immune defenses in two closely related species that have contrasting inflammatory immune responses, the widespread and abundant house sparrow (Passer domesticus) and the less abundant tree sparrow (Passer montanus). We found that the house sparrow, which we have previously shown mounts weaker inflammatory responses, exhibits stronger adaptive immune defenses, including antibody responses, natural antibody titers, and specific T-cell memory, than the tree sparrow. Conversely, tree sparrows, which mount strong inflammatory responses, also mount stronger nonspecific inflammatory T-cell responses but weaker specific adaptive responses. Prevalence of avian malaria parasite infections, which are controlled by adaptive immune defenses, was higher in the geographically restricted tree sparrow than in the ubiquitous house sparrow. Together these data describe distinct immune defense profiles between two closely related species that differ greatly in numbers and distributions. We suggest that these immunological differences could affect fitness in ways that contribute to the contrasting abundances of the two species in North American and Western Europe.

Analysis of Variance↗

PubMed2025

Trade-off between antibacterial immune defense and oogenesis progression in female Drosophila melanogaster.

Trade-offs between reproduction and immunity are common in animals, potentially due to preferential allocation of limiting resources. In Drosophila melanogaster, mating stimulates egg production but also triggers a rapid and persistent decrease in female immune defense. Proteins essential for both processes are produced in fat body tissue, which may result in competition for cellular resources that could drive a functional trade-off between reproduction and immune defense. We predicted that arrest of oogenesis prior to egg provisioning would alleviate postmating immune suppression because cellular stress would be relieved, but that postmating immune suppression would be observed in genotypes that fully provision eggs even if fertility is compromised. In the present study, we test these predictions by evaluating postmating immune competence in mated D. melanogaster mutants that arrest oogenesis either prior to, or subsequent to, vitellogenesis. Consistent with our prediction, we find that mated female immune defense is maintained when egg development is arrested prior to vitellogenesis. We find that progression through the vitellogenic stages of oogenesis results in postmating immune suppression, except in the case of a mutant with an egg-retention phenotype, where we infer that the failure to lay eggs results in feedback that inhibits subsequent egg development. We additionally show that elimination of yolk protein synthesis in the fat body and follicle cells of the ovary partially restores female immune capacity. Nevertheless, females that lack yolk protein genes still experience partially reduced immune capacity after mating, suggesting that other reproductive demands also suppress immune defense.

Animals↗

PubMed1988

Intestinal mucosal immune defense mechanisms.

The intestinal mucosal immune defense mechanisms involve both humoral and cellular immunity. The prominence of suppressor/cytotoxic T lymphocytes in the epithelial layer suggests that these interepithelial lymphocytes play a role in defense against infections within this layer. Secretory IgA is overwhelmingly the major humoral immune response along the gastrointestinal tract and along other mucosal surfaces (respiratory tract, mammary glands, salivary glands, and lacrimal glands). While the functions of secretory IgA are incompletely understood, it is clear that it prevents attachment of microorganisms and toxins (cholera toxin, shiga toxin, etc.) to the surface epithelial cells. Furthermore, secretory IgA may collaborate with eosinophils or killer lymphocytes to mediate cytotoxic reactions against enteropathogens. By learning more about the mucosal immune response, we should be able to understand the relationship between the lamina propria plasmacytosis in inflammatory bowel disease and the increased number of interepithelial lymphocytes that we see in gluten-sensitive enteropathy and the underlying pathogenic mechanisms.

Humans↗

PubMed2000

Drosophila Thor participates in host immune defense and connects a translational regulator with innate immunity.

Thor has been identified as a new type of gene involved in Drosophila host immune defense. Thor is a member of the 4E-binding protein (4E-BP) family, which in mammals has been defined as critical regulators in a pathway that controls initiation of translation through binding eukaryotic initiation factor 4E (eIF4E). Without an infection, Thor is expressed during all developmental stages and transcripts localize to a wide variety of tissues, including the reproductive system. In response to bacterial infection and, to a lesser extent, by wounding, Thor is up-regulated. The Thor promoter has the canonical NFkappaB and associated GATA recognition sequences that have been shown to be essential for immune induction, as well as other sequences commonly found for Drosophila immune response genes, including interferon-related regulatory sequences. In survival tests, Thor mutants show symptoms of being immune compromised, indicating that Thor may be critical in host defense. In contrast to Thor, Drosophila eIF4E is not induced by bacterial infection. These findings for Thor provide the first evidence that a 4E-BP family member has a role in immune induction in any organism. Further, no gene in the translation initiation pathway that includes 4E-BP has been previously found to be immune induced. Our results suggest either a role for translational regulation in humoral immunity or a new, nontranslational function for 4E-BP type genes.

Amino Acid Sequence↗

PubMed2002

Direct link between mhc polymorphism, T cell avidity, and diversity in immune defense.

Major histocompatibility complex (mhc)-encoded molecules govern immune responses by presenting antigenic peptides to T cells. The extensive polymorphism of genes encoding these molecules is believed to enhance immune defense by broadening the array of antigenic peptides available for T cell recognition, but direct evidence supporting the importance of this mechanism in combating pathogens is limited. Here we link mhc polymorphism-driven diversification of the cytotoxic T lymphocyte (CTL) repertoire to the generation of high-avidity, protective antiviral T cells and to superior antiviral defense. Thus, much of the beneficial effect of the mhc polymorphism in immune defense may be due to its critical influence on the properties of the selected CTL repertoire.

Adoptive Transfer↗

PubMedDate not supplied

IFN-treatment of B16-F1 versus B16-F10: relative impact on non-adaptive and T-cell-mediated immune defense in metastatic spread.

Treatment of tumor cells with interferon-gamma (IFN) frequently reduces their susceptibility towards NK cells and results in augmented expression of MHC antigens, which may increase immunogenicity of tumor cells. Depending on the relative strength of these opposing effects, i.e. escape from non-adaptive immune defense versus facilitated activation of T-cell-mediated defense, IFN-treatment may be beneficial or disadvantageous for the tumor-bearing host. This is demonstrated for the variants F1 and F10 of the B16 melanoma, which differ in metastasizing capacity. IFN-treatment of B16-F1 melanoma cells significantly reduced susceptibility towards non-adaptive immune defense, and increased metastasizing potential. On the other hand, H2K antigen expression was augmented by a factor of 50; concomitantly, lysability by CTL was increased, together with the number and expansion rate of cytotoxic T-cell precursors (CTLp) recruited after immunization with IFN-treated B16-F1. The benefit of increased antigenicity and immunogenicity outweighed the disadvantage or reduced susceptibility towards non-adaptive immune defense. B16-F10 cells were less susceptible to NK cells, expression of MHC antigens was found to be stronger and they were more immunogenic than B16-F1 cells. After IFN-treatment, susceptibility to non-adaptive immune defense was further reduced. Expression of MHC antigens as well as antigenicity and immunogenicity were only moderately augmented. As a consequence, the decreased susceptibility to non-adaptive immune defense was dominating in the tumor bearing host and could not be counterbalanced by immunization with IFN-treated B16-F10 cells. We interpret these data to show that a precise knowledge of the relative decrease in susceptibility to non-adaptive immune defense, the relative increase in MHC antigen expression, antigenicity and immunogenicity may allow a more precise prognosis of the influence of IFN on metastatic capacity in the B16 system, and eventually also in a clinical therapeutic regimen.

Animals↗

PubMed2005

Evolutionary ecology of insect immune defenses.

Evolutionary ecology seeks to understand the selective reasons for the design features of the immune defense, especially with respect to parasitism. The molecular processes thereby set limitations, such as the failure to recognize an antigen, response specificity, the cost of defense, and the risk of autoimmunity. Sex, resource availability, and interference by parasites also affect a response. In turn, the defense repertoire consists of different kinds of immune responses--constitutive or induced, general or specific--and involves memory and lasting protection. Because the situation often defies intuition, mathematical analysis is typically required to identify the costs and benefits of variation in design, but such studies are few. In all, insect immune defense is much more similar to that of vertebrates than previously thought. In addition, the field is now rapidly becoming revolutionized by molecular data and methods that allow unprecedented access to study evolution in action.

Animals↗

PubMed2003

The evolution of immune defense and song complexity in birds.

There are three main hypotheses that explain how the evolution of parasite virulence could be linked to the evolution of secondary sexual traits, such as bird song. First, as Hamilton and Zuk proposed a role for parasites in sexual selection, female preference for healthy males in heavily parasitized species may result in extravagant trait expression. Second, a reverse causal mechanism may act, if sexual selection affects the coevolutionary dynamics of host-parasite interactions per se by selecting for increased virulence. Third, the immuno-suppressive effects of ornamentation by testosterone or limited resources may lead to increased susceptibility to parasites in species with elaborate songs. Assuming a coevolutionary relationship between parasite virulence and host investment in immune defense we used measures of immune function and song complexity to test these hypotheses in a comparative study of passerine birds. Under the first two hypotheses we predicted avian song complexity to be positively related to immune defense among species, whereas this relationship was expected to be negative if immuno-suppression was at work. We found that adult T-cell mediated immune response and the relative size of the bursa of Fabricius were independently positively correlated with a measure of song complexity, even when potentially confounding variables were held constant. Nestling T-cell response was not related to song complexity, probably reflecting age-dependent selective pressures on host immune defense. Our results are consistent with the hypotheses that predict a positive relationship between song complexity and immune function, thus indicating a role for parasites in sexual selection. Different components of the immune system may have been independently involved in this process.

Age Factors↗

PubMed2005

Glucocorticoids produced during exercise may be necessary for optimal virus-induced IL-2 and cell proliferation whereas both catecholamines and glucocorticoids may be required for adequate immune defense to viral infection.

Prolonged, exhaustive exercise has been associated with impaired immune responsiveness and increased susceptibility to infection. We have shown that one bout of exercise to fatigue followed by viral challenge increases mortality. Stress hormones such as corticosteroids and catecholamines have been suggested as potential mediators of exhaustive exercise-induced immunosuppression. The purpose of this study was to determine whether the administration of pharmacological agents to block the effect of catecholamines or corticosteroids would minimize the immunosuppression associated with this type of exercise. Mice either exercised to fatigue or were exposed to control conditions, and mice received an i.p. injection of either nadolol (beta-adrenergic receptor antagonist), RU486 (glucocorticoid type II receptor antagonist), or vehicle. Fifteen minutes post-exercise, mice were exposed to viral infection (Herpes simplex virus; HSV) via an intranasal route, and cells were collected 3 days post-infection. The results showed that exercise suppressed HSV-specific cell proliferation, HSV-specific IL-2, and IFN-gamma, but did not alter these same immune parameters when the mitogen ConA was used to stimulate cells. In addition, exercise reduced NK cell cytotoxicity, alveolar cell TNFalpha, and peritoneal IL-1beta, but did not affect IL-10. The pharmacological blockade did not attenuate the exercise-associated immunosuppression. In fact, RU486 treatment exacerbated the exercise-induced decline in HSV-induced IL-2 production and cell proliferation. RU486 and nadolol treatment also tended to decrease IL-10, IFN-gamma, TNFalpha (nadolol only), and IL-1beta (RU486 only) in both exercise and control mice, suggesting that stress hormones may be necessary during infection for optimal responsiveness. These findings suggest that suppression of immune defenses during viral infection persists for at least 3 days post-exercise, and stress hormones may be essential for optimal immune defense to viral challenge, rather than detrimental.

Animals↗

PubMed1988

Interferon-gamma treatment of B16 melanoma cells: opposing effects for non-adaptive and adaptive immune defense and its reflection by metastatic spread.

The impact of interferon-gamma (IFN) treatment of tumor cells on non-adaptive and adaptive immune defense and its reflection by metastatic spread were evaluated using a weakly metastasizing variant of B16 melanoma (B16-FI). Treatment of B16-FI with IFN resulted in a decrease in binding structures for NK cells and concomitantly in augmented metastasizing capacity. In line with this, activation of NK cells and Mo, which led to reduction of metastatic nodes, was less efficient with IFN-treated B16-FI, while after elimination of non-adaptive immune defense, the number of metastases increased significantly, but irrespective of IFN treatment. On the other hand, IFN-treated B16-FI cells become more prone to killing by cytotoxic T-cells (CTL). This was due to increased lysability by CTL and to increased immunogenicity; i.e., a higher frequency of B16-specific CTL was observed after immunization with IFN-treated than with untreated B16-FI. The reverse phenomenon was observed with anomalous and/or lymphokine-activated killer cells (AK/LAK). The common cause of increased antigenicity and immunogenicity may reside in increased expression of class-I and de novo expression of class-II MHC antigens after IFN treatment. Increased antigenicity and immunogenicity of IFN-treated B16-FI was reflected by significant reduction of metastatic nodes, prolonged survival and increased TD100 in animals immunized with IFN-treated vs. untreated melanoma cells. Comparison of the divergent effects of IFN treatment on B16-FI melanoma cells showed that the benefit of increased antigenicity/immunogenicity clearly outweighed the disadvantage of reduced susceptibility to non-adaptive immune defense.

Animals↗

PubMed1986

Acquired resistance towards immune defense during metastatic progression represents a secondary phenomenon.

The role of natural immune defense in the control of metastatic spread of tumor cells was evaluated by adapting an s.c.-grown, antigenic, but non-immunogenic rat fibrosarcoma (Bsp6S) to ascitic growth (BSp6A) in the strain of origin (BDX), where peritoneal cells display a high level of NK and macrophage activity. Parallel tests were performed to determine whether tumor cells can selectively adapt to non-specific immune defense, i.e. whether antigenicity of the non-immunogenic tumor remains unaltered, and whether this is accompanied by metastatic progression. During adaptation to ascitic growth the tumor line gradually lost susceptibility to NK cells and macrophages. This was due to the appearance of an increasing number of resistant clones (BSp6S, none; BSp6A, 50% of clones), which had lost binding structures for NK cells and macrophages. No alteration could be observed in antigenicity of the BSp6A variant as revealed by clonal analysis using LD of CTL. Neither BSp6S nor BSp6A cells metastasized. When the ascitic variant was retransplanted s.c. (BSp6AS), susceptibility to NK cells and macrophages was further decreased, in the sense that all clones of the BSp6AS variant became resistant. Furthermore, the BSp6AS variant had lost some of the tumor-associated antigens (TAAs) found on BSp6S and A variants. More important, upon s.c. transplantation BSp6AS regularly metastasized to the draining LN, contrary to BSp6S and BSp6A. When locally growing tumors were excised, rats implanted with BSp6AS frequently died with metastatic tumor burdens in LNs and lung, while other animals survived after excision of BSp6S or BSp6A. The data indicate a correlation between resistance to lysis, morphology and metastatic capacity. But the initial loss of susceptibility to NK cells and macrophages during adaptation to ascitic growth, which can be considered as an escape mechanism, was not accompanied by increased metastatic capacity. Hence, we suppose that with respect to metastatic progression of the BSp6AS variant, resistance to lysis by loss of binding structures represents only a secondary, but not a causative, element.

Animals↗

PubMed2001

Immunoglobulin A secretion into pancreatic juice as a novel marker of local immune defense and exocrine pancreatic function.

The importance of secretory immunoglobulin A (IgA) of local immune defense in the gastrointestinal tract has gained increasing acceptance. Bacterial contamination is a major factor related to mortality in acute pancreatitis. However, very little is known about IgA in pancreatic juice. Pure pancreatic juice was collected from 40 patients undergoing pancreatoduodenectomy. The patients were divided into three groups according to the degree of preoperative pancreatic duct obstruction, as follows: normal, narrowed, and obstructed. IgA concentration, amylase activity, and daily volume of pancreatic juice were measured. Daily IgA secretion into pancreatic juice was constant during the early period after the operation. The concentration of IgA in the control group was 5 +/- 0.8 microg/ml, and IgA daily secretion was 1.2 +/- 0.2 mg/day. Pancreatic duct obstruction resulted in a marked decrease in both amylase and pancreatic juice secretion. The concentration of IgA, however, was markedly increased in the narrowed group (11.1 +/- 2.4 microg/ml) and the obstructed group (32.5 +/- 5.4 microg/ml). The concentration of amylase increased with the increase in pancreatic juice. Conversely, the concentration of IgA increased with the decrease in volume of pancreatic juice. Similarly, the increased in IgA concentrations positively correlated with the decrease in amylase activity. In conclusion, the mechanisms that modulate IgA secretion in the human pancreas are essentially different from those that modulate digestive enzyme and fluid secretion. IgA in pancreatic juice may play an important role in pathological conditions such as pancreatic duct obstruction. As such, the measurement of IgA in pancreatic juice may potentially be used as a new marker of local immune defense and exocrine pancreatic function.

Amylases↗

PubMed1981

[Presence of lymph-vascular anatomical units in dermoid cysts and the probable existence of a local immune defense system in various tissues].

Studies on tooth eruption in several ovarian dermoïd cysts showing the existence of immune defense gingival structures has allowed the presence of similar structures associated with respiratory and digestive differentiation zones to be observed. These structures are formed of histiocyto-plasmocyto-lymphocytes associated with capillary loops. The origin and histogenesis of those structures remains to be clarified but they suggest the probable existence of localised immune defense systems within certain tissues.

Cell Differentiation↗