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Results for “Adaptive Immunity”

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At least 973 records · Page 54Linked to original sources

PubMed2000

Do lampreys have lymphocytes? The Spi evidence.

It is generally accepted that living jawless vertebrates (lampreys and hagfishes) lack the capability of mounting an adaptive immune response. At the same time, however, there are reports describing histological evidence for the presence in agnathan tissues of lymphocytes, the key players in adaptive immunity. The question therefore arises whether the cells identified morphologically as lymphocytes are true lymphocytes in terms of their genetic developmental program. In this study, evidence is provided that the lampreys express a member of the purine box 1 (PU.1)/spleen focus-forming virus integration B (Spi-B) gene family known to be critically and specifically involved in the differentiation of lymphocytes in jawed vertebrates. The lamprey gene is expressed in the lymphocyte-like cells of the digestive tract and inexplicably also in the ovary.

Amino Acid Sequence↗

PubMedDate not supplied

TLR9 in health and disease.

Toll-like receptor 9 (TLR9) is specialized for the recognition of pathogenic nucleic acids. TLR9 is expressed in intracellular compartments where it responds specifically to pathogen DNA. Several factors contribute to the ability of TLR9 to discriminate between self and foreign DNA. Regulatory mechanisms of the innate and adaptive immune system exist that balance the immune responses mediated by TLR9. Short synthetic CpG oligodeoxynucleotides are used to induce controlled and directed TLR9-dependent stimulation and are effective immune modulators in preclinical and clinical studies. This review will summarize the interplay between TLR9-dependent opposing stimulatory and regulatory effects in innate and adaptive immunity.

Animals↗

PubMed2004

Crystallization and preliminary X-ray analysis of VCBP3 from Branchiostoma floridae.

VCBPs represent a family of proteins with highly diversified immunoglobulin-like variable regions in species thought to lack an adaptive immune system. These proteins are expected to reveal important structural and functional features that could be highly informative in projecting the evolutionary history of the adaptive immune response. Preliminary X-ray diffraction data from amphioxus (Branchiostoma floridae) VCBP3 crystals were collected to 2.4 A resolution and reduced to primitive trigonal space groups P3(1(2))21. Unit-cell parameters are a = b = 58.99, c = 79.21 A, alpha = beta = 90, gamma = 120 degrees . Two distinct crystallization conditions yielded crystals with similar morphologies and these crystals are isomorphous to each other.

Chitin↗

PubMed2003

Immuno-gene therapy with adenoviruses expressing fms-like tyrosine kinase 3 ligand and CD40 ligand for mouse hepatoma cells in vivo.

Introduction of genes encoding immuno-stimulatory cytokines into cancer cells is known to enhance antitumor immunity. CD40 ligand (CD40L, CD154) and fms-like tyrosine kinase 3 ligand (Flt3L) are recently identified cytokines, which have been demonstrated to stimulate antitumor immunity in several cancer models. However little is known about antitumor activity of Ftl3L and CD40L against hepatocellular carcinoma (HCC). In the present study, we constructed replication-defective adenoviruses expressing Flt3L and CD40L and examined their therapeutic efficacy on mouse HCC, MH134 cells. Subcutaneous injection of MH134 cells genetically engineered to express Flt3L and/or CD40L developed tumors in all the syngeneic immunocompetent mice, but tumor growth was significantly delayed as compared to control mice. Partial inhibition of this antitumor effect in athymic nude mice suggests that both innate and adaptive immunity appear to play a role. It was shown by immunodepletion of NK cells with anti-asialo-GM1 antibody that the effector cells involved in innate immunity are NK cells. In a therapeutic setting, however, injection of adenovirus expressing Flt3L or CD40L into pre-established MH134 tumors exhibited no efficacy. These data demonstrate that Flt3L and CD40L induce significant, but only weak, antitumor immunity against MH134 cells presumably through both innate and adaptive immunity. Our results suggest that immuno-gene therapy with Flt3L and CD40L may need adjuvant modalities to achieve strong immune response.

Animals↗

PubMed2007

Flying under the radar: the immunobiology of hepatitis C.

The hepatitis C virus (HCV) is a remarkably successful pathogen, establishing persistent infection in more than two-thirds of those who contract it. Its success is related to its abilities to blunt innate antiviral pathways and to evade adaptive immune responses. These two themes may be related. We propose that HCV takes advantage of the impaired innate response to delay the organization of an effective adaptive immune attack. The tolerogenic liver environment may provide cover, prolonging this delay. HCV's error-prone replication strategy permits rapid evolution under immune pressure. Persistent high levels of viral antigens may contribute to immune exhaustion. Finally, the virus may benefit from the efficient enlistment of memory T and B cells in the pursuit of a moving target.

Animals↗

PubMed2006

Sexual dimorphism in immune response genes as a function of puberty.

BACKGROUND: Autoimmune diseases are more prevalent in females than in males, whereas males have higher mortality associated with infectious diseases. To increase our understanding of this sexual dimorphism in the immune system, we sought to identify and characterize inherent differences in immune response programs in the spleens of male and female mice before, during and after puberty. RESULTS: After the onset of puberty, female mice showed a higher expression of adaptive immune response genes, while males had a higher expression of innate immune genes. This result suggested a requirement for sex hormones. Using in vivo and in vitro assays in normal and mutant mouse strains, we found that reverse signaling through FasL was directly influenced by estrogen, with downstream consequences of increased CD8+ T cell-derived B cell help (via cytokines) and enhanced immunoglobulin production. CONCLUSION: These results demonstrate that sexual dimorphism in innate and adaptive immune genes is dependent on puberty. This study also revealed that estrogen influences immunoglobulin levels in post-pubertal female mice via the Fas-FasL pathway.

Animals↗

PubMed2005

The role of Toll-like receptor signalling in the pathogenesis of arthritis.

Recent evidence highlighted the role of Toll-like receptors (TLRs) as key recognition structures of the innate immune system. The activation of TLRs initiates the production of inflammatory cytokines, chemokines, tissue destructive enzymes, and type I interferons. In addition, TLR signalling plays an important role in the activation and direction of the adaptive immune system by the upregulation of costimulatory molecules of antigen presenting cells. Considering the important role of TLR signalling as a critical link between innate and adaptive immunity it has been proposed that a dysregulation in TLR signalling might be associated with autoimmunity. In this review, recent studies on TLR signal transduction pathways activated by corresponding ligands are summarized and evidence for a possible role of TLR signalling in the pathogenesis of rheumatoid arthritis is discussed.

Animals↗

PubMed2004

New lessons from old pathogens: what parasitic infections have taught us about the role of nuclear factor-kappaB in the regulation of immunity.

The nuclear factor-kappaB (NF-kappaB) family of transcription factors is activated by many infectious and inflammatory stimuli. This family regulates the expression of multiple genes, whose products include cytokines, chemokines, adhesion molecules, and antiapoptotic factors that are important components of the innate and adaptive immune response. A prominent role of NF-kappaB transcription factors in resistance to a variety of infectious diseases was revealed by studies with mice that lack individual family members. However, little is known about the basis for these effects or about the role of individual family members during a coordinated immune response to infection. Diverse parasites such as Toxoplasma gondii, Leishmania major, and Trichuris muris provide a unique opportunity to understand the role of the NF-kappaB system in the development of innate and adaptive immunity to these infections. The basis for resistance and susceptibility to these parasites is well understood, and studies using these experimental systems have provided unique insights into the role of NF-kappaB in the regulation of T-helper 1 cell (Th1) and Th2 type responses. It has become clear that NF-kappaB family members have cell lineage-specific functions and that their relative importance varies with type of infection as well as route of pathogen entry. Thus, studies with models of parasitic infection have revealed that individual NF-kappaB family members perform distinct, nonoverlapping, and biologically significant functions in the regulation of immunity and inflammation.

Animals↗

PubMed2005

Innate immune responses to infection.

The human host survives many infectious challenges in the absence of preexisting specific (adaptive) immunity because of the existence of a separate set of protective mechanisms that do not depend on specific antigenic recognition. These antigen-independent mechanisms constitute innate immunity. Antimicrobial peptides are released at epithelial surfaces and disrupt the membranes of many microbial pathogens. Toll-like receptors on epithelial cells and leukocytes recognize a range of microbial molecular patterns and generate intracellular signals for activation of a range of host responses. Cytokines released from leukocytes and other cells exhibit a vast array of regulatory functions in both adaptive and innate immunity. Chemokines released from infected tissues recruit diverse populations of leukocytes that express distinct chemokine receptors. Natural killer cells recognize and bind virus-infected host cells and tumor cells and induce their apoptosis. Complement, through the alternative and mannose-binding lectin pathways, mediates antibody-independent opsonization, phagocyte recruitment, and microbial lysis. Phagocytes migrate from the microcirculation into infected tissue and ingest and kill invading microbes. These innate immune mechanisms and their interactions in defense against infection provide the host with the time needed to mobilize the more slowly developing mechanisms of adaptive immunity, which might protect against subsequent challenges.

Animals↗

PubMed2006

Microglia and inflammation: impact on developmental brain injuries.

Inflammation during the perinatal period has become a recognized risk factor for developmental brain injuries over the past decade or more. To fully understand the relationship between inflammation and brain development, a comprehensive knowledge about the immune system within the brain is essential. Microglia are resident immune cells within the central nervous system and play a critical role in the development of an inflammatory response within the brain. Microglia are critically involved with both the innate and adaptive immune system, regulating inflammation and cell damage within the brain via activation of Toll-like receptors, production of cytokines, and a myriad of other intracellular and intercellular processes. In this article, microglial physiology is reviewed along with the role of microglia in developmental brain injuries in humans and animal models. Last, microglial functions within the innate and adaptive immune system will be summarized. Understanding the processes of inflammation and microglial activation is critical for formulating effective preventative and therapeutic strategies for developmental brain injuries.

Biomarkers↗

PubMed2002

Activation of the immune system by bacterial CpG-DNA.

The past decade has seen a remarkable process of refocusing in immunology. Cells of the innate immune system, especially macrophages and dendritic cells, have been at the centre of this process. These cells had been regarded by some scientists as non-specific, sometimes perhaps even confined to the menial job of serving T cells by scavenging antigen and presenting it to the sophisticated adaptive immune system. Only over the last few years has it become unequivocally clear that cells of the innate immunity hold, by variation of context and mode of antigen presentation, the power of shaping an adaptive immune response. The innate immune response, in turn, is to a significant degree the result of stimulation by so-called pathogen-associated molecular patterns (PAMPs). One compound with high stimulatory potential for the innate immune system is bacterial DNA. Here we will review recent evidence that bacterial DNA should be ranked with other PAMPs such as lipopolysaccharide (LPS) and lipoteichoic acid. We will further review our present knowledge of DNA recognition and DNA-dependent signal transduction in cells of the immune system.

CpG Islands↗

PubMed2006

Mechanisms of airway obliteration after lung transplantation.

Post-transplant bronchiolitis obliterans, also called bronchiolitis obliterans syndrome, affects up to 50-60% of patients who survive 5 yr after surgery according to its clinical definition, which is based on the degree of obstructive airway disease. Alloimmune-independent and -dependent mechanisms produce injuries and inflammation of epithelial cells and subepithelial structures, leading to aberrant tissue repair. The triggering of innate immunity by various infections or chemical injuries after, for example, gastroesophageal reflux, may lead to the release of danger signals that are able to activate dendritic cells, a crucial link with adaptive immunity. Inflammation can also increase the expression and display of major histocompatibility alloantigens and thus favor the initiation of rejection episodes. These phenomena may be limited in time and location or may be protracted. Reducing the risk of alloimmune-independent factors may be as important as treating acute episodes of lung rejection. Excessive immunosuppression may be deleterious by increasing the risk of infection, thereby triggering innate and adaptive immunity. New potential therapeutic targets are emerging from the research performed on leukotriene receptors, chemokine receptors, and growth factors. Neutralizing these molecules reduces the initial mononuclear and polynuclear infiltrates or the subsequent fibroproliferative process and the neovascular changes, feeding this process.

Bronchiolitis Obliterans↗

PubMed2006

From plasmacytoid to dendritic cell: morphological and functional switches during plasmacytoid pre-dendritic cell differentiation.

Plasmacytoid dendritic cell precursors (pDC/IPC) are the major producers of type I interferon and have the unique ability to link innate and adaptive immunity. After producing large amounts of type I IFN in response to microbial stimulation, they can differentiate into DC capable of stimulating naive T cells and modulate the adaptive immune response. In this review, we focus on the transition between these two highly specialized cell types, which is accompanied by major morphological, structural and functional changes, many of which remain to be fully characterized. We propose that the plasmacytoid and dendritic morphologies correspond to distinct differentiation states and effector functions.

Animals↗

PubMed2004

Protection of Penaeus monodon against white spot syndrome virus using a WSSV subunit vaccine.

Although invertebrates lack a true adaptive immune response, the potential to vaccinate Penaeus monodon shrimp against white spot syndrome virus (WSSV) using the WSSV envelope proteins VP19 and VP28 was evaluated. Both structural WSSV proteins were N-terminally fused to the maltose binding protein (MBP) and purified after expression in bacteria. Shrimp were vaccinated by intramuscular injection of the purified WSSV proteins and challenged 2 and 25 days after vaccination to assess the onset and duration of protection. As controls, purified MBP- and mock-vaccinated shrimp were included. VP19-vaccinated shrimp showed a significantly better survival (p<0.05) as compared to the MBP-vaccinated control shrimp with a relative percent survival (RPS) of 33% and 57% at 2 and 25 days after vaccination, respectively. Also, the groups vaccinated with VP28 and a mixture of VP19 and VP28 showed a significantly better survival when challenged two days after vaccination (RPS of 44% and 33%, respectively), but not after 25 days. These results show that protection can be generated in shrimp against WSSV using its structural proteins as a subunit vaccine. This suggests that the shrimp immune system is able to specifically recognize and react to proteins. This study further shows that vaccination of shrimp may be possible despite the absence of a true adaptive immune system, opening the way to new strategies to control viral diseases in shrimp and other crustaceans.

Animals↗

PubMed1996

The role of hemolymph coagulation in innate immunity.

Invertebrate animals, which lack adaptive immune systems, have developed defense systems that respond to common antigens on the surface of potential pathogens. Hemolymph coagulation is one such defense system in innate immunity. The discovery of lipopolysaccharide-sensitive and (1-->3)-beta-D-glucan-sensitive serine protease zymogens in horseshoe crab (limulus) hemocytes, both of which trigger the coagulation cascade, has exemplified how the animals detect and respond to foreign materials.

Amino Acid Sequence↗

PubMed2005

Immunological processes in malaria pathogenesis.

Malaria is possibly the most serious infectious disease of humans, infecting 5-10% of the world's population, with 300-600 million clinical cases and more than 2 million deaths annually. Adaptive immune responses in the host limit the clinical impact of infection and provide partial, but incomplete, protection against pathogen replication; however, these complex immunological reactions can contribute to disease and fatalities. So, appropriate regulation of immune responses to malaria lies at the heart of the host-parasite balance and has consequences for global public health. This Review article addresses the innate and adaptive immune mechanisms elicited during malaria that either cause or prevent disease and fatalities, and it considers the implications for vaccine design.

Animals↗

PubMed1998

Immunisation and the maturation of infant immune responses.

Maturation of the adaptive immune system occurs early in development and by 14 weeks gestation the developing foetus has circulating differentiated T cells and B cells capable of responding to antigen. While the immune system is capable of responding appropriately at birth to protein antigens, its capacity to respond to carbohydrates is limited. A consequence of this is the success of bacteria with carbohydrate capsules in causing invasive paediatric infections. Vaccines containing purified carbohydrates alone are thus limited in their immunogenicity and fail to provide protection for those most at risk. Conjugate vaccine technology, where a carbohydrate antigen is chemically coupled to a protein carrier, has overcome the limitation of carbohydrates as vaccine antigens. The first such vaccine to enjoy widespread use, the Haemophilus influenzae type b conjugate vaccines, have met with enormous success and have almost eradicated invasive Hib disease in those countries where their use in infancy is routine. Conjugate technology is thus being applied to a number of other vaccines in development, including Neisseria meningitidis groups A and C and Streptococcus pneumoniae vaccines.

Bacterial Vaccines↗

PubMed2007

History and update on host defense against vaginal candidiasis.

Vulvovaginal candidiasis (VVC), caused by Candida albicans, remains a significant problem in women of childbearing age. While cell-mediated immunity is considered the predominant host defense mechanism against mucosal candidal infections, two decades of research from animal models and clinical studies have revealed a lack of a protective role for adaptive immunity against VVC caused by putative immunoregulatory mechanisms. Moreover, natural protective mechanisms and factors associated with susceptibility to infection have remained elusive. That is until recently, when through a live challenge model in humans, it was revealed that protection against vaginitis coincides with a non-inflammatory innate presence, whereas symptomatic infection correlates with a neutrophil infiltrate in the vaginal lumen and elevated fungal burden. Thus, instead of VVC being caused by a putative deficient adaptive immune response, it is now being considered that symptomatic vaginitis is caused by an aggressive innate response.

Animals↗