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Results for “Adaptive Immunity”

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At least 469 records · Page 26Linked to original sources
PubMed2006

Trichostatin-A enhances adaptive immune responses to DNA vaccination.

BACKGROUND: The efficacy of DNA vaccines to date has overall been disappointing, especially in large animal models and in humans, which might be partially explained by the chromatinization of the administered foreign DNA. Trichostatin-A (TSA) is a specific inhibitor for histone deacetylase (HDAC) and a gene expression enhancer in in vitro DNA viral infection, including herpes simplex type 1 (HSV-1) and cytomegalovirus (CMV). OBJECTIVES: We sought to determine if increasing antigen expression of DNA vaccines through inhibition of HDAC-induced chromatin silencing using TSA would enhance DNA vaccine efficacy in vivo. STUDY DESIGN: A luciferase assay was used to detect effects of TSA on different promoters in vitro. The effects of TSA on DNA vaccination of mice were determined by neutralization assays for antibody production and interleukin staining for detection of specific T cell responses. RESULTS: Mice receiving TSA in combination with a DNA vaccine exhibited higher antibody responses to the vaccine than mice not given TSA. Co-administration of TSA also enhanced specific CD8 T cells response. CONCLUSION: Drugs such as TSA that reduce initial gene silencing by preventing histone deacetylation can increase immune responses to DNA vaccination.

Animals↗
PubMed2006

Acute psychological stress alerts the adaptive immune response: stress-induced mobilization of effector T cells.

Influences of psychological stress on the acquired immune system have not consequently been investigated. We found acute psychological stress to cause an increase in CD56+ and CCR5+ effector T cells in the peripheral blood of healthy human subjects (N=22), while skin-homing CLA+ T cells decreased. At the same time, we observed a stress-induced decrease in CD45RA+/CCR7+ naive and CD45RA-/CCR7+ central memory T cells, while CD45RA-/CCR7- effector memory and CD45RA+/CCR7- terminally differentiated T cells increased. This T cell redistribution translated into an increase in T cells expressing perforin/granzyme B and in Epstein-Barr virus-specific, cytomegalovirus-specific and influenza virus-specific CD8+ T cells. Thus, acute stress seems to promote the retention of less mature T cells within lymphoid tissue or skin while effector-type T cells are mobilized into the blood in order to be able to rapidly migrate into peripheral tissues.

Acute Disease↗
PubMed2006

Gene-environment interactions in multiple sclerosis: innate and adaptive immune responses to human endogenous retrovirus and herpesvirus antigens and the lectin complement activation pathway.

Aspects of gene-environment interactions in multiple sclerosis (MS) were analysed in serum samples from 46 MS families (25 sporadic MS cases and 42 familial MS cases): antibodies to the MS-associated human endogenous retrovirus HERV-H, and levels of three components in the innate pathogen-associated molecular pattern recognition: mannan-binding lectin (MBL), and MASP-2 and MASP-3. For representative MS families, we also determined herpesvirus serology for HSV-1, VZV, and EBV; and tissue typed for HLA-B, and HLA DR and DQ. In MS, a significant correlation between elevated immune reactivity to HERV-H Env and disease activity was demonstrated, as were indications of a protective effect of high MBL and MASP-3 levels. The HLA alleles B*07, DRB*02, and DQB1*06 were commonly present together in the MS families, both in MS patients, and in unaffected family members. Our results support that HERV-H and the antiviral immune response may play a role in MS development, and also underline the tenuous nature of specific genetic contributions to this complex disease.

Adult↗
PubMed2006

Yersinia's stratagem: targeting innate and adaptive immune defense.

In contrast to Salmonella and Shigella, enteropathogenic Yersinia species are extracellular multiplying Gram-negative bacteria. This life style requires a sophisticated anti-host strategy, which is implemented by the Yersinia virulence plasmid. This plasmid encodes the type 3 secretion system (injectisome), at least six microinjected anti-host effector proteins, a trimeric coiled coil outer membrane protein (Yersinia adhesin) with cell adhesin and protective functions against complement and defensins, and the released V antigen, which has Toll-like receptor 2 agonist activity.

Adhesins, Bacterial↗
PubMed2006

Human host genetic factors in nontuberculous mycobacterial infection: lessons from single gene disorders affecting innate and adaptive immunity and lessons from molecular defects in interferon-gamma-dependent signaling.

Mendelian defects in interferon-gamma (IFN-gamma) signaling most commonly lead to infection with nontuberculous mycobacteria. Mutations have been identified in the genes encoding IFN-gamma-receptor-1, IFN-gamma-receptor-2 and Stat-1. Partial and complete deficiencies in signaling are found, leading to parallel clinical, pathological, and cellular phenotypes. These rare defects have led to better molecular and mechanistic understanding of the role of IFN-gamma in the human immune system.

Animals↗
PubMed2006

Human host genetic factors in mycobacterial and Salmonella infection: lessons from single gene disorders in IL-12/IL-23-dependent signaling that affect innate and adaptive immunity.

Interleukin (IL)-12/IL-23 signal transduction-deficient individuals with genetic defects in IL12RB1 or IL12B often suffer from unusual mycobacterial and Salmonella infections. Here we discuss recent questions that have arisen from clinical observations that cast doubt on the necessity of IL-12/IL-23 signaling in controlling infections with intracellular bacteria. Alternative IL-12/IL-23-dependent, interferon-gamma-independent pathways of immunity to intracellular bacteria are also discussed.

Genetic Predisposition to Disease↗
PubMed2004

Innate and adaptive immune requirements for induction of autoimmune demyelinating disease by molecular mimicry.

Molecular mimicry is the main postulated mechanism by which infectious agents induce autoimmune disease. A number of animal models have been utilized to establish a link between molecular mimicry and autoimmunity. However, a model of infectious disease whereby a natural pathogen expressing a known mimic epitope can induce autoimmunity to a known self-antigen leading to clinical autoimmune disease is still lacking. We have engineered a recombinant Theiler's murine encephalomyelitis virus (TMEV) to express an encephalitogenic myelin proteolipid protein PLP139-151 epitope (PLP-TMEV) and a PLP139-151 mimic peptide naturally expressed by Haemophilus influenzae (HI-TMEV). Infection of mice with either PLP-TMEV or HI-TMEV induces early-onset disease that is associated with the activation of cross-reactive PLP139-151-specific immunopathologic CD4+ Th1 cells. Based on results from this model, we hypothesize, due to the considerable degeneracy in the T cell repertoire, that induction of full-blown autoimmune disease via molecular mimicry is a tightly regulated process requiring multiple factors related to the pathogen expressing the potential mimic epitope. In this review, we will discuss how various factors related to the infectious environment control whether or not autoimmune disease is initiated. Contributing factors include the nature of the innate immune response to the pathogen which determines the immunopathologic potential of the induced cross-reactive T cells, the capacity of the mimic epitope to be processed and presented from its natural flanking sequences in the pathogen-encoded protein, the site(s) of the primary infection in the host and the ability of the pathogen to persist, and the potential requirement for multiple infections with the same or different pathogens.

Animals↗
PubMed2004

Modulation of adaptive immune responses by sphingosine-1-phosphate.

Sphingosine-1-phosphate (S1P) has long been recognized as a mediator of a variety of cell functions. A growing body of evidence has accumulated demonstrating its role in cell migration and as a mediator of growth factor-induced events. In recent years, it has become apparent that S1P also mediates many cytokine and chemokine functions. Cells of the immune system function and migrate in response to a complex network of cytokines and chemokines, and the outcome is determined by the interplay of the effects of these molecules on the target cell. S1P may be a bona fide component of these networks and influence the responses of cells to these immune modulators.

Animals↗
PubMed2006

Intestinal IgA synthesis: a primitive form of adaptive immunity that regulates microbial communities in the gut.

Our intestine is colonized by an impressive community of bacteria, that has profound effects on the immune functions. The relationship between gut microbiota and the immune system is one of reciprocity: bacteria have important contribution in nutrient processing and education of the immune system and conversely, the immune system, particularly gut-associated lymphoid tissues (GALT) plays a key role in shaping the repertoire of gut microbiota. In this review we discuss new insights into the role of IgA in the maintenance of immune homeostasis and the reciprocal interactions between gut B cells and intestinal bacteria.

B-Lymphocytes↗
PubMed2006

Rehabilitation of adaptive immunity and regeneration of beta cells.

Type 1 Diabetes (T1D) is an autoimmune disease resulting from the destruction of pancreatic insulin-producing beta cells that most frequently occurs in genetically predisposed children. Recent observations illustrating the regenerative capability of the endocrine pancreas in addition to advances in stem cell and gene therapy technologies enable the exploration of alternatives to allogeneic islet transplantation. Living-cell-mediated approaches can abrogate autoimmunity and the consequent destruction of beta cells without the need for immunosuppressive drugs. Such approaches can be used as a foundation for new protocols that more easily translate to the clinical setting. The twin goals of controlling autoimmune disease and promoting stable regeneration of insulin-producing beta cells should be considered the cornerstones of the successful development of a cure for this chronic disease.

Animals↗
PubMed2004

Differential regulation of innate and adaptive immune responses in viral encephalitis.

Viral encephalitis is a global health concern. The ability of a virus to modulate the immune response can have a pivotal effect on the course of disease and the fate of the infected host. In this study, we sought to understand the immunological basis for the fatal encephalitis following infection with the murine coronavirus, mouse hepatitis virus (MHV)-JHM, in contrast with the more attenuated MHV-A59. Distinct glial cell cytokine and chemokine response patterns were observed within 3 days after infection, became progressively more polarized during the course of infection and with the infiltration of leukocytes. In the brain, MHV-JHM infection induced strong accumulation of IFNbeta mRNA relative to IFNgamma mRNA. This trend was reversed in MHV-A59 infection and was accompanied by increased CD8 T cell infiltration into brain compared to MHV-JHM infection. Increased apoptosis appeared to contribute to the diminished presence of CD8 T cells in MHV-JHM-infected brain with the consequence of a lower potential for IFNgamma production and antiviral activity. MHV-JHM infection also induced sustained mRNA accumulation of the innate immune response products interleukin (IL)-6 and IL-1. Furthermore, high levels of macrophage-inflammatory protein (MIP)-1alpha, MIP-1beta, and MIP-2 mRNA were observed at the onset of MHV-JHM infection and correlated with a marked elevation in the number of macrophages in the brain on day 7 compared to MHV-A59 infection. These observations indicate that differences in the severity of viral encephalitis may reflect the differential ability of viruses to stimulate innate immune responses within the CNS and subsequently the character of infiltrating leukocyte populations.

Animals↗
PubMed2005

The atheroprotective effect of 17beta-estradiol depends on complex interactions in adaptive immunity.

Estradiol prevents fatty streak formation in chow-fed atherosclerosis-prone apolipoprotein E (ApoE)-deficient mice. We previously reported that fatty streak development of immunodeficient ApoE(-/-)/recombination activating gene 2 (RAG-2(-/-)) double-deficient mice was insensitive to estradiol. In the present work, we demonstrate that the reconstitution of ApoE(-/-)/RAG-2(-/-) with bone marrow from immunocompetent ApoE(-/-)/RAG-2(+/+) mice restores the protective effect of estradiol on fatty streak constitution. We extended this demonstration to the model of low-density lipoprotein receptor-deficient mice, establishing the obligatory role of mature lymphocytes in this process. We then investigated whether the protective effect of estradiol was mediated by a specific lymphocyte subpopulation by studying the hormonal effect on fatty streak constitution in recently developed models of ApoE(-/-) mice deficient in selective T-lymphocyte subsets (either TCRalphabeta+, CD4+, CD8+, or TCRgammadelta+ lymphocytes) or B lymphocytes. In all these specifically immunodeficient mice, estradiol administration to ovariectomized mice conferred protection as in immunocompetent ApoE(-/-) mice, clearly demonstrating that no single lymphocyte subpopulation was specifically required for this effect. These results point to additional lymphocyte-dependent mechanisms such as modulating the interactions among lymphocytes and between lymphocytes and endothelial and/or antigen-presenting cells.

Animals↗
PubMed2002

Adapting immunity with subunit vaccines: case studies with group A Streptococcus and malaria.

Although vaccines have widely been regarded as the most cost-effective way to improve public health, for some organisms new technological advances in vaccine design and delivery, incurring additional developmental costs, will be essential. These organisms are typically those for which natural immunity is either slow to develop or does not develop at all. Clearly, such organisms have evolved strategies to evade immune responses and innovative approaches will be required to induce a type of immune response which is both different to that which develops naturally and is effective. This article describes some approaches to develop vaccines for two such organisms (malaria parasites and Streptococcus pyogenes (group A Streptococcus)) that are associated with widespread mortality and morbidity, mostly in the poorest countries of the world. At this stage, the challenges are primarily scientific, but if these hurdles are surmounted then the challenges will become financial ones--developing much needed vaccines for people least able to afford them.

Animals↗
PubMed2001

Characterization of the innate and adaptive immunity to Salmonella enteritidis PT1 infection in four broiler lines.

Four broiler lines were inoculated orally with Salmonella enteritidis phage type 1 at the age of 7 days (experiment A: lines 1 and 2) and at the age of 1 day (experiment B: lines 3 and 4). At various days post-infection chickens were sacrificed and the number of Salmonella in the caeca, liver, and spleen were determined. Furthermore, phagocytic activity, cellular immune responses, and humoral responses were determined using, respectively, single-cell suspensions of spleen or intestine and serum. In both experiments, similar trends were seen. Increased numbers of S. enteritidis were found in the caeca of lines 1 and 3, whereas at the same time a decreased colonization was found in the spleen and in the liver, as compared to lines 2 and 4. In the latter two lines, the phagocytic activity of the phagocytes was higher and the humoral responses were lower. Observations from this study suggest that lower activity of phagocytes and higher humoral activity prevent systemic S. enteritidis infection.

Animals↗