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Results for “Adaptive Immunity”

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At least 577 records · Page 32Linked to original sources
PubMed2006

[Neutrophils induce the maturation and activation of immature dendritic cells during adaptive immune responses].

OBJECTIVE: To investigate whether polymorphonuclear neutrophilic leucocyte (PMN) can induce the maturation and activation of immature dendritic cells, thus promoting the Th1 immunity to microbial pathogens in vitro. METHODS: PMN isolated from mouse bone marrow were stimulated by lipopolysaccharide (LPS), and were cultured with immature DC (imDCs) isolated from mouse bone marrow for 18 hours. Then the analysis of DC surface markers CD40 and CD86 was done by flow cytometry, and ELISA was used to detect the levels of TNF-alpha and IL-12. Purified DC cocultured with LPS-PMN (PMN-DC) and imDC were incubated with fluorescein isothiocyanate conjugated OVA (FITC-OVA), and the phagocytic capacity of PMN-DC and imDC was assessed by flow cytometry. Splenic CD4(+) T cells from DO11.10 x C57BL/6 F1 hybrid mice were obtained, and then cultured with PMN-DC or imDC in the presence of OVA (323 - 339). The cells were double stained with anti-CD4-PE and 7-amino-actinomycin D. The cellular data were acquired for 56s with a flow cytometer and the assay of IFN-gamma and IL-4 was done by intracellular staining. RESULTS: LPS-PMN induced strong up-regulation of CD40 and CD86, and this capacity was remarkably inhibited after being neutralized by anti-TNF-alpha monoclonal antibody. LPS-PMN also stimulated imDCs to produce IL-12 and TNF-alpha. PMN-DCs demonstrated decreased phagocytic capacity compared with that of imDCs. Furthermore, the PMN-DC induced considerable DO11.10 T cell proliferation, and stimulated DO11.10 T cell to produce a large amount of IFN-gamma, but a relatively low amount of IL-4. CONCLUSION: LPS-PMN can induce the maturation and activation of imDCs, including the cytokine secretion, specific antigen presentation and Th1 differentiation, thus promoting the type I immunity to microbial pathogens.

Animals↗
PubMed2000

Competitive coexistence in antiviral immunity.

Adaptive immunity to viruses in vertebrates is mediated by two distinct but complementary branches of the immune system: the cellular response, which eliminates infected cells, and the humoral response, which eliminates infectious virus. This leads to an interesting contest, since the two responses compete, albeit indirectly, for proliferative stimuli. How can a host mount a coordinated antiviral campaign? Here we show that competition may lead to a state of "competitive coexistence" in which, counterintuitively, each branch complements the other, with clinical benefit to the host. The principle is similar to free-market economics, in which firms compete, but the consumer benefits. Experimental evidence suggests this is a useful paradigm in antiviral immunity.

Animals↗
PubMed2006

Aging and innate immunity.

Adaptive immunity undergoes severe deterioration with age and represents the main problem in the elderly. However, evidence accumulated over the last decade supports the hypothesis that aging also has a profound impact on innate immunity, which in turn markedly impacts the health and longevity of older people.

Aging↗
PubMedDate not supplied

Gene rearrangement in cells with natural killer activity and expression of the beta-chain of the T-cell antigen receptor.

The mammalian host defence system can be divided broadly into adaptive and non-adaptive immunity. Adaptive immunity is acquired and is mediated by B and T lymphocytes. Non-adaptive immunity is mediated in part by a small subclass of heterogeneous peripheral blood mononuclear cells. This population, termed null cells, consists of haematopoietic precursors and cells mediating natural killer (NK) activity and antibody-dependent cellular cytotoxicity (ADCC). NK cells are a class of non-adherent, non-phagocytic, rapidly cytotoxic lymphocytes which can efficiently lyse a wide variety of tumour cells, virally infected cells and immature cell types of normal origin. Despite the broad range of targets, only a limited number of specificities are thought to be involved in target-cell recognition. Morphologically, NK cells are large granular lymphocytes, but they have been shown to exhibit cell-surface markers characteristic of both T cells and monocytes, raising doubt over their lineage. The recent cloning of the beta-chain of the T-cell antigen receptor has now allowed us to investigate whether some NK cells are T-cell-related. We have examined rearrangement and expression of the beta-chain of the T-cell receptor in cloned murine NK cell lines and fresh murine NK cell populations, and our results support the hypothesis that a subpopulation of NK cells is related to T cells and provide basis for examining whether some NK activity is mediated by a small number of T-cell receptors.

Animals↗
PubMed2002

Gene therapy in transplantation.

Gene transfer and gene therapy represent a relatively new field that has grown and expanded enormously in the last 5-10 years. The application of gene transfer and gene medicines to transplantation is currently in its infancy. Consideration for gene medicines in transplantation requires delivery of vectors, either to the graft or to the immune system. Delivery of vectors to the graft provides a choice of potential immunologic targets including: costimulatory signals; inhibitory cytokines; adhesion molecules; and molecules relating to apoptosis. In addition, non-immunologic targets, that increase graft protective mechanisms by reducing ischemic and immunologic damage, represent significant targets for gene transfer. Delivery of vectors to the immune system includes potential targets to modify the immune system, and results in tolerance. Other considerations for gene therapy include the development of additional technologies, such as gene conversion or transgenesis coupled with xenotransplantation, which may provide genetically modified organs. Another important aspect of gene transfer relates to regulation of the transgene expression. A variety of issues concerning innate immunity, adaptive immunity, response to vector components, response to transgene products, and entry of vectors into the antigen presentation and processing pathway require further investigation and refinement of approaches. Lastly, regulatable promoters and the understanding of their interaction with individual cells, tissues and organs, and their interaction with innate and adaptive immunity, are of paramount importance to improving the efficacy and utility of gene transfer. There is no doubt that there is much exciting basic and translational science to be accomplished in the next decade in order to solve these potential barriers and advance gene medicines into the clinical realm in transplantation.

Abatacept↗
PubMed2000

STAT proteins and transcriptional responses to extracellular signals.

Signal transducer and activator of transcription (STAT) transcription factors are implicated in programming gene expression in biological events as diverse as embryonic development, programmed cell death, organogenesis, innate immunity, adaptive immunity and cell growth regulation in organisms ranging from slime molds to insects to man. Rapid progress has unearthed much about the activation of STATs by Janus kinases (JAKs) and other tyrosine kinases and their ability to interface with other signaling systems. Once inside the nucleus, the STATs bind to promoters and join other transcriptional activators in the regulation of gene expression.

Animals↗
PubMed2006

New cellular and molecular immune pathways in ischemia/reperfusion injury.

Ischemia/reperfusion injury (IRI) is a multi-factorial antigen-independent inflammatory condition that profoundly affects both early and long-term function of the allograft as suggested by both clinical and experimental data. In recent years, the acute phase of IRI has been increasingly viewed as part of the innate immune response. Identification of novel molecular pathways and new insights into the mechanisms of known mediators of IRI have established links among innate immunity, adaptive immune responses and organ regeneration, and thus long-term graft function. This review approaches these novel aspects of IRI in the context of solid organ transplantation, presenting data on new observations with kidney, liver and heart allografts.

Animals↗
PubMed2004

Future research directions in asthma: an NHLBI Working Group report.

Over the last 20 years, the prevalence of asthma has nearly doubled and now affects 8-10% of the population in the United States. Asthma also remains a major illness in terms of morbidity and suffering, and is the leading cause of hospitalizations in children under 15 years of age. Because asthma poses a lifelong burden to patients and society, efforts to increase the understanding of its pathogenesis are a key factor leading to its control and cure. Consequently, the National Heart, Lung, and Blood Institute (NHLBI) convened a Working Group of extramural experts, entitled "Future Research Directions in Asthma," on April 9-10, 2003, to identify research areas of greatest promise and opportunity in the field of asthma. The priority areas identified for research in asthma include: (1) innate immunity, adaptive immunity, and tolerance; (2) mechanisms and consequences of persistent asthma and asthma exacerbations; (3) airway remodeling: clinical consequences and reversibility (clinical relevance and resolution); (4) genetics/gene-environment interactions, pharmacogenetics; (5) intervention/prevention/therapeutics; and (6) vascular basis of asthma.

Asthma↗
PubMed2006

Cytokines as critical co-stimulatory molecules in modulating the immune response of natural killer cells.

Cytokines are involved in directing the activation of natural killer (NK) cells. NK cells are involved in the recognition of cells that have been altered; thus they do not recognize specific insults to the host, but when activated, are capable of destroying infected cells directly, as well as promoting the recruitment and response of the other components of the immune system by the release of cytokines and chemokines. It is these properties that have made NK cells a critical part of innate immunity and adaptive immunity, and they play a principal role linking innate and adaptive immunity by the recruitment of an adaptive immune response to an innate immune reaction.

Cytokines↗
PubMed2006

Regulatory T cells and innate immune regulation in tumor immunity.

Innate and adaptive immunity play important roles in immunosurveillance and tumor destruction. However, increasing evidence suggests that tumor-infiltrating immune cells may have a dual function: inhibiting or promoting tumor growth and progression. Although regulatory T (Treg) cells induce immune tolerance by suppressing host immune responses against self- or nonself-antigens, thus playing critical roles in preventing autoimmune diseases, they might inhibit antitumor immunity and promote tumor growth. Recent studies demonstrate that elevated proportions of Treg cells are present in various types of cancers and suppress antitumor immunity. Furthermore, tumor-specific Treg cells can inhibit immune responses only when they are exposed to antigens presented by tumor cells. Therefore, Treg cells at tumor sites have detrimental effects on immunotherapy directed to cancer. This review will discuss recent progress in innate immunity, Treg cells, and their regulation through Toll-like receptor (TLR) signaling. It was generally thought that TLR-mediated recognition of specific structures of invading pathogens initiate innate and adaptive immune responses through dendritic cells. New evidence suggests that TLR signaling may directly regulate the suppressive function of Treg cells. Linking TLR signaling to the functional control of Treg cells opens intriguing opportunities to manipulate TLR signaling to control both innate and adaptive immunity against cancer.

Animals↗
PubMed2005

Indoleamine 2,3 dioxygenase and regulation of T cell immunity.

Regulation of adaptive immune responses is critically important to allow the adaptive immune system to eradicate infections while causing minimal collateral damage to infected tissues, as well as preventing autoimmune disease mediated by self-reactive lymphocytes. Tumors and pathogens that cause persistent infections can subvert immunoregulatory processes to protect themselves from destruction by T cells, to the detriment of patients. A growing body of evidence supports the hypothesis that specialized subsets of dendritic cells expressing indoleamine 2,3 dioxygenase (IDO), which catalyzes oxidative catabolism of tryptophan, play critical roles in regulation of T cell-mediated immune responses. IDO-dependent T cell suppression by dendritic cells suggests that biochemical changes due to tryptophan catabolism have profound effects on T cell proliferation, differentiation, effector functions, and viability. This has critical implications for immunotherapeutic manipulations designed for patients with cancer and chronic infectious diseases. In this review, I focus on dendritic cells that can express IDO, and which acquire potent T cell regulatory functions as a consequence.

Animals↗
PubMed2004

[Host defense mechanisms against Salmonella infection].

Salmonella is one of the gram negative intracellular pathogens. The immune response to Salmonella includes innate immunity and adaptive immunity. The intestinal epithelium, neutrophil, macrophage, dendritic cell, NK cell, NK T cell and gammadelta T cell take important part in former process, and antigen specific T cell and B cell take part in the later process. Macrophages and dendritic cells increase in number early after Salmonella infection and produce variety of cytokines. Especially, IL-12, IL-15 and IL-18 play important roles in protection against Salmonella infection, proliferation of NK cell, NKT cell and gammadelta T cell, producing IFN-gamma, in addition, IL-12 and IL-18 induce IFN-gamma production by Th1 cells and adaptive immune response.

Animals↗
PubMed2006

[Toll-dependent and toll-independent innate antiviral immunity].

Until recently, adaptive immunity and cytotoxic T cells were considered as the only essential components of the antiviral defence arsenal. Additional data that do not rule out the crucial role of these cells in the clearance of viral pathogens have, however, recently emerged. They indicate that innate immune cells such as macrophages, dendritic cells, gammadelta T cells as well as natural killer (NK) cells play a primordial role in this mechanism. It is now well established that innate immune cells can detect various pathogens (bacteria, viruses, fungi or parasites) very rapidly and respond to their presence through the activation of specific receptors. Once activated, these molecules trigger several signalling cascades that culminate in the establishment of very potent defence mechanisms. In addition, cytokines produced during this initial response are essential for the activation of the adaptive immune response which will add specificity and memory to the system. Among the innate immune receptors, attention has focused on the Toll-like receptors (TLR) and many reports indicate that some of the TLRs are clearly involved in defence against viral pathogens. However, new molecules, acting independently from any TLR, have recently been discovered. They define a second antiviral pathway which is presently the subject of intense research. In this article, we will review the role of the different molecules involved in each pathway within the framework of innate antiviral defence.

DEAD Box Protein 58↗