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Results for “Adaptive Immunity”

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At least 487 records · Page 27Linked to original sources
PubMed1999

Innate and adaptive immune responses can be beneficial for CNS repair.

The limitation of immune responsiveness in the mammalian CNS has been attributed to the intricate nature of neuronal networks, which would appear to be more susceptible than other tissues to the threat of permanent disorganization when exposed to massive inflammation. This line of logic led to the conclusion that all forms of CNS inflammation would do more harm than good and, hence, the less immune intervention the better. However, mounting evidence indicates that some forms of immune-system intervention can help to protect or restore CNS integrity. We have shown that the innate immune system, represented by activated macrophages, can facilitate the processes of regeneration in the severed spinal cord. More recently, we found that autoimmune T cells that are specific for a component of myelin can protect CNS neurons from the catastrophic secondary degeneration, which extends traumatic lesions to adjacent CNS areas that did not suffer direct damage. The challenge, therefore, is to learn how to modify immune interactions in the traumatized CNS in order to promote its post-injury maintenance and repair.

Animals↗
PubMed1999

A knockout approach to understanding CD8+ cell effector mechanisms in adaptive immunity to Listeria monocytogenes.

In the described experimental approach, we use an attenuated LM strain to evoke LM specific CD8+ T cell responses. In this fashion, we can immunize immunocompromised gene knockout mice, that would succumb to low level infection with virulent LM. We then generate antigen matched, LM-specific CD8+ T cell lines from wild-type and gene knockout mice, and compare their capacity to provide immunity to LM infection in vivo. To date, our results demonstrate that CD8+ T cell-derived IFN-gamma and TNF are not required effector functions. Perforin deficiency has an impact on CD8+ T cell immunity but our studies provide strong evidence for the existence of perforin independent pathways of CD8+ T cell immunity to LM. To assess the potential for redundancy in effector mechanisms, we have generated mice deficient in both perforin and IFN-gamma and are developing mice deficient in perforin and TNF. By removing the major CD8+ T cell effector mechanisms, singly and in combination, we will eventually determine whether immunity to LM can be provided by redundant effector pathways or if novel effector mechanisms exist beyond our current knowledge. The generation of MHC matched, single and double knockout mice, will also aid in continuing studies to analyze the role of these molecules in resistance to in vivo infection.

Animals↗
PubMed1981

Adaptive immunity of the tympanic membrane.

In a previous experiment an antiserum was developed in the rabbit from the lamina propria of the tympanic membrane of the guinea pig. In the present study 18 Hartley guinea pigs were used in an in vivo experiment in which the antiserum (RAGTM IgG) served passively to immunize the animals subjected to various forms of trauma to the right tympanic membrane. Two groups (18 animals) immunized with normal rabbit IgG or normal saline served as controls. The left tympanic membrane remained untouched in all groups and served as an internal control. Various forms of trauma (infection, cauterization, section), various times (one to 21 days), and diverse techniques of staining (immunofluorescence, complement, and immunoperoxidase) were studied. The results indicate that the combination of trauma and sensitization in the first group evokes a particular response in the lamina propria of the tympanic membrane in immunized animals (RAGTM IgG). The form of trauma does not influence the results, but time seems to be an important factor. This work addresses several questions concerning the possible role of the combination of trauma and sensitization in conditions that involve the tympanic membrane and middle ear clinically.

Animals↗
PubMed1998

Linkages of innate and adaptive immunity.

The innate immune system is activated by pathogens or environmental antigens following their binding by recognition molecules such as mannan-binding lectin, C-reactive protein and the mannose receptor. Natural antibody, which represents a collection of germline-encoded antigen recognition molecules, is also important in recognition of pathogens and activation of the innate immune system via the classical pathway of complement activation. The major source of natural antibody is CD5+ B-1 cells which differ from conventional B cells (B-2 cells) firstly because they are thought to require contact with antigen for expansion and maintenance and secondly because in general they do not appear to undergo somatic hypermutation. We review results which support an important role for complement in maintenance of B-1 cells, the effect being mediated by B cell expression of complement receptors CD21 and CD35. We propose that complement and natural antibody are interdependent: clonal selection and expansion of CD5+ B-1 cells is dependent on contact with antigen coated by the complement component C3d, while efficient recognition of pathogens and activation of complement is dependent in a large part on natural antibody. This hypothesis is supported by the finding that mice deficient in CD21 and CD35 have a reduced number of CD5+ B-1 cells and are missing specificities for certain antigens commonly found in wild-type mice, such as lipopolysaccharide, Escherichia coli surface antigens and neoepitopes expressed on hypoxic intestinal endothelium.

Animals↗
PubMed2003

Innate and adaptive immune responses to an intracellular bacterium, Francisella tularensis live vaccine strain.

The immune response to intracellular bacterium, Francisella tularensis, which causes tularemia and is proposed to be a potential bioterrorism pathogen, has been studied in mice using the attenuated live vaccine strain (LVS). Here we review this infection model, which provides a convenient means of studying protective immune mechanisms not only for Francisella, but also for the large and important class of intracellular pathogens.

Animals↗
PubMed2002

Interactions between bacterial CpG-DNA and TLR9 bridge innate and adaptive immunity.

The astounding adjuvanticity and Th1-polarizing immunobiology of bacterial CpG-DNA and mimicking CpG-oligonucleotides continue to mirror promising therapeutic potential. The past year has witnessed some particularly impressive progress in knowledge of its molecular mode of action. Accordingly, CpG-DNA acts as a "pathogen-associated" molecular pattern that is recognized by TLR9 expressed, in particular, by dendritic cells. Interactions between CpG-DNA and TLR9 rapidly activate antigen-presenting dendritic cells through the ancient Toll/IL-1-receptor signaling pathway to upregulate co-stimulatory molecules and to produce Th1-polarizing cytokines, such as interleukin-12 and interleukin-18. Thus, interactions between CpG-DNA and TLR9 effectively bridge innate and acquired immunity.

Animals↗
PubMed2003

Defensin-induced adaptive immunity in mice and its potential in preventing periodontal disease.

The severity of periodontal disease is dependent on a combination of host, microbial agent and environmental factors. One strong correlate related to periodontal disease pathogenesis is the immune status of the host. Here we show that human neutrophil peptide (HNP) defensins or human beta-defensins (HBD), co-administered intranasally with the antigen ovalbumin (OVA), induce unique immune responses that if used with microbial antigens may have the potential to hinder the pathogenesis of periodontal disease. C57BL/6 mice were immunized intranasally with phosphate buffered saline (PBS) containing 1 micro g HNP-1, HNP-2, HBD1 or HBD2 with and without 50 microg OVA. At 21 days, isotypes and subclasses of OVA-specific antibodies were determined in saliva, serum, nasal wash, bronchoalveolar lavage fluid, and fecal extracts. OVA-stimulated splenic lymphoid cell cultures from immunized mice were assessed for interferon (IFN)-gamma, Interleukin (IL)-4 and IL-10. In comparison with mice immunized with only OVA, HNP-1 and HBD2 induced significantly higher (P < 0.05) OVA-specific serum IgG, lower, but not significant, serum IgM and significantly lower (P < 0.05) IFN-gamma. In contrast, HNP-2 induced low OVA-specific serum IgG and higher, but not significant, serum IgM. HBD1 induced significantly higher (P < 0.05) OVA-specific serum IgG, higher, but not significant, serum IgM, and significantly higher (P < 0.05) IL-10. The elevated serum IgG subclasses contained IgG1 and IgG2b.

Adjuvants, Immunologic↗
PubMed2004

Chronic pneumonia despite adaptive immune response to Mycobacterium bovis BCG in MyD88-deficient mice.

To assess the role of Toll-like receptor (TLR) signalling in host response to mycobacterial infection, mice deficient in the TLR adaptor molecule myeloid differentiation factor 88 (MyD88) were infected with the vaccine strain Mycobacterium bovis (BCG), and the immune response and bacterial burden were investigated. Macrophages and dendritic cells from MyD88-deficient mice stimulated in vitro with BCG mycobacterial antigens produced very low levels of proinflammatory cytokines, while the expression of costimulatory molecules such as CD40 and CD86 was preserved. Upon systemic infection with BCG (2 x 10(6) CFU i.v.) MyD88-deficient mice developed confluent chronic pneumonia with two log higher CFU than wild-type mice. Interestingly, the infection was controlled in liver and spleen and there was efficient systemic T-cell priming with high IFNgamma production by CD4+ splenic T cells in MyD88-deficient mice. Lung infiltrating cells showed IFNgamma production by pulmonary CD4+ T cells upon specific restimulation, and a reduced capacity to produce nitric oxide and IL-10. In summary, despite the dramatic reduction of the innate immune response, MyD88-deficient mice were able to mount an efficient T-cell response to mycobacterial antigens, which was however insufficient to control infection in the lung, resulting in chronic pneumonia in MyD88-deficient mice.

Adaptor Proteins, Signal Transducing↗
PubMed2003

Impairment of dendritic cells and adaptive immunity by anthrax lethal toxin.

Anthrax poses a clear and present danger as an agent of biological terrorism. Infection with Bacillus anthracis, the causative agent of anthrax, if untreated can result in rampant bacteraemia, multisystem dysfunction and death. Anthrax lethal toxin (LT) is a critical virulence factor of B. anthracis, which occurs as a complex of protective antigen and lethal factor. Here we demonstrate that LT severely impairs the function of dendritic cells--which are pivotal to the establishment of immunity against pathogens--and host immune responses by disrupting the mitogen-activated protein (MAP) kinase intracellular signalling network. Dendritic cells exposed to LT and then stimulated with lipopolysaccharide do not upregulate co-stimulatory molecules, secrete greatly diminished amounts of proinflammatory cytokines, and do not effectively stimulate antigen-specific T cells in vivo. Furthermore, injections of LT induce a profound impairment of antigen-specific T- and B-cell immunity. These data suggest a role for LT in suppressing host immunity during B. anthracis infections, and represent an immune evasion strategy, where a microbe targets MAP kinases in dendritic cells to disarm the immune response.

Adoptive Transfer↗