SEARCH · PubMed Health

Results for “Receptors, Pattern Recognition”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 631 records · Page 35Linked to original sources

PubMed2006

Deletion of TLR3 alters the pulmonary immune environment and mucus production during respiratory syncytial virus infection.

The detection of a viral infection by pattern recognition receptors (PAMPs) is an integral part of antiviral immunity. In these studies we have investigated the role of TLR3, which recognizes dsRNA, in Respiratory Syncytial virus (RSV) infection using B6 background mice with a TLR3 deletion. Although we observed no changes in viral growth, we did find that TLR3-/- mice demonstrated significant increases in mucus production in the airways of RSV-infected mice. The qualitative assessment was observed by examining differentially stained lungs, followed by immunohistochemical staining for gob5, a mucus-associated protein. The histopathologic observations were verified using quantitative gene expression analyses examining gob5 gene expression. Changes in pulmonary mucus production were accompanied by an increase in pulmonary IL-13 as well as IL-5 expression and eosinophils in the airways of TLR3-/- mice. Examining leukocytes in the airway indicated an accumulation of eosinophils in TLR3-/- mice, but not wild-type mice, after RSV infection. Isolated lung draining lymph node cells from TLR3-/- mice produced significant increases in Th2-type cytokines, IL-5, and IL-13, compared with wild-type TLR3+/+ mice only after RSV infection. To demonstrate a causative link, we depleted TLR3-/- mice of IL-13 during RSV infection and found that mucus and gob5 expression in the lungs was attenuated. Together, these studies highlight that although TLR3 may not be required for viral clearance, it is necessary to maintain the proper immune environment in the lung to avoid developing pathologic symptoms of disease.

Animals↗

PubMed2006

Lipoteichoic acid increases TLR and functional chemokine expression while reducing dentin formation in in vitro differentiated human odontoblasts.

Gram-positive bacteria entering the dentinal tissue during the carious process are suspected to influence the immune response in human dental pulp. Odontoblasts situated at the pulp/dentin interface are the first cells encountered by these bacteria and therefore could play a crucial role in this response. In the present study, we found that in vitro-differentiated odontoblasts constitutively expressed the pattern recognition receptor TLR1-6 and 9 genes but not TLR7, 8, and 10. Furthermore, lipoteichoic acid (LTA), a wall component of Gram-positive bacteria, triggered the activation of the odontoblasts. LTA up-regulated the expression of its own receptor TLR2, as well as the production of several chemokines. In particular, an increased amount of CCL2 and CXCL10 was detected in supernatants from LTA-stimulated odontoblasts, and those supernatants augmented the migration of immature dendritic cells in vitro compared with controls. Clinical relevance of these observations came from immunohistochemical analysis showing that CCL2 was expressed in vivo by odontoblasts and blood vessels present under active carious lesions but not in healthy dental pulps. In contrast with this inflammatory response, gene expression of major dentin matrix components (type I collagen, dentin sialophosphoprotein) and TGF-beta1 was sharply down-regulated in odontoblasts by LTA. Taken together, these data suggest that odontoblasts activated through TLR2 by Gram-positive bacteria LTA are able to initiate an innate immune response by secreting chemokines that recruit immature dendritic cells while down-regulating their specialized functions of dentin matrix synthesis and mineralization.

Cell Differentiation↗

PubMed2006

NAK-associated protein 1 participates in both the TLR3 and the cytoplasmic pathways in type I IFN induction.

TLR3 and the cytoplasmic helicase family proteins (retinoic acid-inducible gene I (RIG-I) and melanoma differentiation-associated gene 5 (MDA5)) serve as dsRNA pattern-recognition receptors. In response to poly(I:C), a representative of dsRNA, and viral infection, they have been shown to activate the transcription factor IFN regulatory factor (IRF)-3, which in turn induces activation of the IFN-beta promoter. RIG-I/MDA5 recognizes dsRNA in the cytoplasm, whereas TLR3 resides in the cell surface membrane or endosomes to engage in extracytoplasmic recognition of dsRNA. Recent reports suggest that TLR3 induces cellular responses in epithelial cells in response to respiratory syncytial virus (RSV). The modus for TLR3 activation by RSV, however, remains unresolved. By small interference RNA gene-silencing technology and human cell transfectants, we have revealed that knockdown of NAK-associated protein 1 (NAP1) leads to the down-regulation of IFN-beta promoter activation >24 h after poly(I:C) or virus (RSV and vesicular stomatitis virus) treatment. NAP1 is located downstream of the adapter Toll-IL-1R homology domain-containing adapter molecule (TICAM)-1 (Toll/IL-1R domain-containing adapter-inducing IFN-beta) in the TLR3 pathway, but TICAM-1 and TLR3 did not participate in the IRF-3 and IFN-beta promoter activation by RSV infection. Virus-mediated activation of the IFN-beta promoter was largely abrogated by the gene silencing of IFN-beta promoter stimulator-1 (mitochondria antiviral signaling (MAVS), VISA, Cardif), the adapter of the RIG-I/MDA5 dsRNA-recognition proteins. In both the TLR and virus-mediated IFN-inducing pathways, IkappaB kinase-related kinase epsilon and TANK-binding kinase 1 participated in IFN-beta induction. Thus, RSV as well as other viruses induces replication-mediated activation of the IFN-beta promoter, which is intracellularly initiated by the RIG-I/MDA5 but not the TLR3 pathway. Both the cytoplasmic and TLR3-mediated dsRNA recognition pathways converge upon NAP1 for the activation of the IRF-3 and IFN-beta promoter.

Cytoplasm↗

PubMed2006

Distinct responses of lung and spleen dendritic cells to the TLR9 agonist CpG oligodeoxynucleotide.

Dendritic cells (DCs) sense various components of invading pathogens via pattern recognition receptors such as TLRs. CpG oligodeoxynucleotides (ODNs), which mimic bacterial DNA, inhibit allergic airways disease and promote responses in the spleen to bacterial components. Because many TLR agonists are currently being tested for potential therapeutic effects, it is important to characterize the expression and function of TLRs in different tissues. We show that both myeloid and plasmacytoid DCs in the spleen express TLR9, the receptor for CpG ODNs, but lung DCs show no detectable expression in either subset. TLR4 expression in contrast was detected on both lung and spleen DCs. LPS was superior to CpG ODN in increasing the allostimulatory potential of lung DCs and their expression of CD40. However, both agonists efficiently stimulated spleen DCs. CpG ODNs administered to mice efficiently inhibited Th2 cytokine production both in the lung draining lymph node and in the spleen. Surprisingly, inhibition of Th2 cytokine production was evident despite high levels of expression of GATA-3 and additional transcription factors that regulate Th2 responses. Although in the spleen CpG ODNs induced IL-6, a key cytokine induced via TLR9-MyD88 signaling, no IL-6 was detectable in lung LN cells. These studies show for the first time that lung DCs lack TLR9 expression, but, despite this deficiency, CpG ODNs induce potent inhibitory effects on Th2 cytokine production in the lung without inducing expression of the proinflammatory cytokine, IL-6, which has been linked to chronic diseases in the lung and the gut.

Adjuvants, Immunologic↗

PubMed2006

Galectin-3 induces death of Candida species expressing specific beta-1,2-linked mannans.

Lectins play a critical role in host protection against infection. The galectin family of lectins recognizes saccharide ligands on a variety of microbial pathogens, including viruses, bacteria, and parasites. Galectin-3, a galectin expressed by macrophages, dendritic cells, and epithelial cells, binds bacterial and parasitic pathogens including Leishmania major, Trypanosoma cruzi, and Neisseria gonorrhoeae. However, there have been no reports of galectins having direct effects on microbial viability. We found that galectin-3 bound only to Candida albicans species that bear beta-1,2-linked oligomannans on the cell surface, but did not bind Saccharomyces cerevisiae that lacks beta-1,2-linked oligomannans. Surprisingly, binding directly induced death of Candida species containing specific beta-1,2-linked oligomannosides. Thus, galectin-3 can act as a pattern recognition receptor that recognizes a unique pathogen-specific oligosaccharide sequence. This is the first description of antimicrobial activity for a member of the galectin family of mammalian lectins; unlike other lectins of the innate immune system that promote opsonization and phagocytosis, galectin-3 has direct fungicidal activity against opportunistic fungal pathogens.

Candida↗

PubMed2006

Engagement of CD14 mediates the inflammatory potential of monosodium urate crystals.

Phagocyte ingestion of monosodium urate (MSU) crystals can induce proinflammatory responses and trigger acute gouty inflammation. Alternatively, the uptake of MSU crystals by mature macrophages can be noninflammatory and promote resolution of gouty inflammation. Macrophage activation by extracellular MSU crystals involves apparent recognition and ingestion mediated by TLR2 and TLR4, with subsequent intracellular recognition linked to caspase-1 activation and IL-1beta processing driven by the NACHT-LRR-PYD-containing protein-3 inflammasome. In this study, we examined the potential role in gouty inflammation of CD14, a phagocyte-expressed pattern recognition receptor that functionally interacts with both TLR2 and TLR4. MSU crystals, but not latex beads, directly bound recombinant soluble (s) CD14 in vitro. CD14(-/-) bone marrow-derived macrophages (BMDMs) demonstrated unimpaired phagocytosis of MSU crystals but reduced p38 phosphorylation and approximately 90% less IL-1beta and CXCL1 release. Attenuated MSU crystal-induced IL-1beta release in CD14(-/-) BMDMs was mediated by decreased pro-IL-1beta protein expression and additionally by decreased caspase-1 activation and IL-1beta processing consistent with diminished NACHT-LRR-PYD-containing protein-3 inflammasome activation. Coating of MSU crystals with sCD14, but not sTLR2 or sTLR4, restored IL-1beta and CXCL1 production in CD14(-/-) BMDMs in vitro. Gain of function of CD14 directly enhanced TLR4-mediated signaling in response to MSU crystals in transfected Chinese hamster ovary cells in vitro. Last, MSU crystal-induced leukocyte influx at 6 h was reduced by approximately 75%, and local induction of IL-1beta decreased by >80% in CD14(-/-) mouse s.c. air pouches in vivo. We conclude that engagement of CD14 is a central determinant of the inflammatory potential of MSU crystals.

Animals↗

PubMed2026

A highly prevalent lupus risk haplotype increases IRF7-dependent induction of IFN-α, enhancing antiviral defense and exacerbating autoimmunity.

UNLABELLED: Genome-wide association studies have identified genetic polymorphisms at 11p15 associated with Systemic Lupus Erythematosus (lupus). Statistical fine mapping prioritizes a highly prevalent coding haplotype within the IRF7 gene. Analysis of ancient DNA confirms that this haplotype has persisted at high frequencies in the global population for millennia. The IRF7 risk haplotype is sufficient to increase nuclear localization of IRF7 and transcriptional activity downstream of pattern recognition receptor pathways. This risk haplotype increases IRF7 DNA binding strength and alters IRF7 DNA sequence specificity, resulting in genotype-dependent increases in IFN-α production in numerous biological systems, including monocytes and airway epithelial cells. CRISPR engineering of a homologous risk variant in mouse Irf7 results in both enhanced innate control of virus infection and increased autoantibody titers in a model of autoimmunity. Altogether, we establish a persistent and prominent genetic IRF7 haplotype that amplifies IRF7 activity in a manner that has immunological risks and benefits. HIGHLIGHTS: Genetic analysis using modern and evolutionary datasets identifies a persistent and highly prevalent lupus-associated coding haplotype in IRF7 at 11p15 The IRF7 lupus risk haplotype increases IFN-α production by monocytes and airway epithelial cells The IRF7 lupus risk haplotype increases IRF7 DNA binding strength and alters DNA sequence specificity A homologous lupus risk variant in mouse Irf7 enhances control of vesicular stomatitis virus and exacerbates autoantibody production.

Journal Article↗

PubMed2001

The search for novel adjuvants for early life vaccinations: can "danger" motifs show us the way?

Potent but safe adjuvants are required to circumvent the many limitations of the newborn immune system to induce rapidly effective and long lasting immunity to subunit vaccines. By the use of pattern recognition receptors, antigen-presenting cells (APC) can very efficiently be activated by "danger" motifs expressed by various pathogens. APC activated by "danger" motifs, such as immunostimulatory sequences of bacterial DNA, can not only transmit the activation signal from the innate immunity to the adaptive compartment, but also shape the antigen-specific immune responses. Molecules or compounds expressing "danger" motifs could, therefore, be considered for use as adjuvants for subunit vaccines. In this review, the authors discuss the promises and potential drawbacks that such novel adjuvants could hold for their use in experimental and clinical early life vaccinations.

Adjuvants, Immunologic↗

PubMed2001

CD14: a bridge between innate immunity and adaptive IgE responses.

Total IgE levels are known to be under genetic control. Linkage studies have indicated that one or more loci on chromosome 5q may control total IgE, as well as asthma and bronchial hyperresponsiveness to non-specific stimuli. Our group has undertaken a systematic analysis of chromosome 5q, and has recently characterized five single nucleotide polymorphisms at position -1619, -1359, -1145, -809, and -159 in the promoter of the gene encoding CD14, the myeloid pattern recognition receptor that is critical for efficient innate immune responses to lipopolysaccharide and bacterial ligands. Individuals homozygous for the three major CD14 haplotypes found in the Children Respiratory Study population (n = 390) were analyzed for serum levels of total IgE and soluble CD14. A strong inverse correlation was found between these two parameters, i.e. carriers of the -1359T/-1145A/-159C haplotype had the highest levels of IgE, and the lowest levels of sCD14. Conversely, carriers of the -1359G/-1145G/-159T haplotype had the highest levels of sCD14 and the lowest IgE values. Our results suggest that genetic variation in CD14, a key gene of innate immunity, may modulate the effects that exposure to bacterial ligands has on the development of Th2 responses.

Child↗

PubMed2001

Parameters influencing membrane CD14 expression and soluble CD14 levels in sepsis.

INTRODUCTION: Membrane (mCD14) and soluble (sCD14) CD14 are pattern recognition receptors for bacterial cell wall fragments. They play an important role in the generation of the innate immune response against bacterial pathogens. Differential expression of these receptors may be relevant for the clinical course of patients with sepsis. PATIENTS AND METHODS: 32 patients with an early onset of sepsis (duration of symptoms < 24h) were examined repeatedly by flow cytometry for expression of mCD14, and by ELISA for levels of sCD14, leukocyte elastase and C-reactive Protein (CRP). RESULTS: At study entry, mCD14 expression was reduced in all patients with sepsis, but returned to normal levels during the course of the disease in survivors only. mCD14 was found to be inversely correlated with severity of disease, leukocyte elastase, and C-reactive protein. Among patients with severe disease and Apache II scores >or= 20, sCD14 levels at study entry were significantly higher in those who survived by day 28, as compared to non-survivors (p = 0.02). CONCLUSION: The data presented are compatible with a recently published hypothesis derived from in vitro experiments suggesting that leukocyte elastase may be responsible for cleavage of mCD14 from the monocyte surface. The data also suggest that higher sCD14 levels may be beneficial in sepsis. Persistently reduced mCD14 expression seems to be a marker for severity of disease in patients with sepsis.

APACHE↗

PubMed2001

IC14, a CD14 specific monoclonal antibody, is a potential treatment for patients with severe sepsis.

CD14 is a pattern recognition receptor for the bacterial cell wall components from Gram-positive and Gram-negative bacteria as well as mycobacteria. Binding of lipopolysaccharide (LPS) or other cell wall constituents to CD14 initiates signal transduction through the Toll-like receptors resulting in the release of pro-inflammatory cytokines and the initiation of the systemic inflammatory response. In rabbits and non-human primates, CD14 specific antibodies were shown to attenuate responses to LPS or Escherichia coli challenge including pro-inflammatory cytokine release, acute lung injury, hypotension and changes in lung, liver, spleen and adrenal gland morphology. In healthy human subjects, single doses of a chimeric CD14 antibody (IC14) have been shown to be well tolerated and result in a dose-related degree of saturation of CD14 receptors on monocytes and granulocytes. Pretreatment of healthy subjects with IC14 2 h prior to LPS resulted in an attenuation of the LPS-induced fever, clinical symptoms, and leukocyte activation and degranulation. IC14 inhibited the release of TNF-alpha, IL-6, and IL-10 and delayed the release of sTNFR(I) and IL-1ra. Further studies are in progress to characterize the safety and clinical pharmacology of IC14 in patients with severe sepsis.

Animals↗

PubMed2003

Recent advances in the development of immunostimulatory oligonucleotides.

Some immune cells recognize distinct molecular structures present in pathogens through specific pattern recognition receptors that are able to distinguish prokaryotic DNA from vertebrate DNA. The detection of invading microbial DNA is based on the recognition of unmethylated deoxycytidyl-deoxyguanosin dinucleotide (CpG) motifs. Synthetic oligonucleotides (ODNs) containing these CpG motifs are able to activate both innate and acquired immune responses through a signaling pathway involving Toll-like receptor 9 (TLR9). Depending on the sequence, length, as well as number and positions of CpG motifs in an ODN, distinct immunostimulatory profiles can be observed. These immunostimulatory profiles can be further modified and fine-tuned by appropriate chemical modifications, leading to preclinical and clinical development of CpG ODNs in cancer, allergy, asthma and infectious diseases.

Adjuvants, Immunologic↗

PubMed2004

[The role of myeloid differential protein-2 in innate immunity].

As typical PRRs (pattern-recognition receptors), TLRs (Toll-like receptors) play an important role during innate immunity recognition. MD-2 (myeloid differential protein-2) may contain distinct functional domains that can separately and simultaneously bind TLRs (TLR4 or TLR2) and TLR ligands, such as lipopolysaccharide (LPS). The special structure of MD-2 may result in its three main functions: (1) An association with TLR4 that amplifies TLR4 responsiveness to ligands, especially LPS. (2) Enabling TLR2-mediated responses to LPS and enhancing TLR2-mediated responses to bacteria and their cell wall components. (3) Increasing the expression of TLR2 and TLR4 and possibly influencing the correct intracellular distribution of TLR4. Importantly, while MD-2 regulation of TLR expression and distribution is well established, determining whether the interaction is direct or not will require further study. Thus, MD-2 is not only an assistant molecule of TLR4 but is also a key regulatory molecule in innate immunity, and may play important roles during infection, inflammation, immune responses and many other pathologic and physiologic processes.

Animals↗

PubMed2005

Side effects of anticytokine strategies.

Anticytokine strategies probably represent the most important breakthrough in the treatment of inflammatory diseases in the last decade. However, blocking the bioactivity of proinflammatory cytokines, crucial activators of host defence, has proved to be accompanied by an increased susceptibility to infections, especially with Mycobacteria, Salmonellae and fungal pathogens. Multiple mechanisms for these side effects have been proposed, such as inhibition of gamma-interferon production, decreased expression of pattern-recognition receptors, and leucocyte apoptosis. Caution is therefore warranted when these treatments are given to patients with an increased risk for infections. A range of side effects other than infection have been reported.

Adalimumab↗

PubMed2005

Immune functions in crustaceans: lessons from flies.

In recent years insects, notably Drosophila, have emerged as a popular model for studying immune responses to bacterial and fungal pathogens. Due to the availability of the complete genome sequence, genome-wide scans of immune responses have been performed using microarray analyses. These analyses have revealed the presence of two major pathways: Toll and Imd. Each pathway consists of four steps: (i) recognition through pattern recognition receptors; (ii) modulation by serine proteases; (iii) signal transduction leading to translocation of transcription factors and (iv) humoral and cellular responses. We have compared the information from insects with those currently available in crustaceans, and have identified commonalities and differences. Remarkably, in both insects and crustaceans, little is known about their anti-viral responses. Future research will have to focus on these anti-viral immune responses ultimately to control viral diseases, which are at present a major threat to culturing penaeid shrimp.

Animals↗

PubMed2005

[The synergistic effects of lipopolysaccharide, bacterial lipoprotein and bacterial DNA on mouse alveolar macrophage activation].

OBJECTIVE: To investigate the synergistic effects of lipopolysaccharide (LPS), bacterial lipoprotein (BLP), and bacterial DNA on the expression of pattern recognition receptors (PRRs) on the cell surface of mouse alveolar macrophages and cellular activation at the level of receptor and its possible mechanism. METHODS: Mouse alveolar macrophages were isolated, cultivated and randomly divided into 7 groups: control group, LPS group, CpG oligonucleoetide (CpG-ODN) group, BLP group, LPS + BLP group, LPS + CpG-ODN group, and LPS + BLP + CpG-ODN group. Six hours later the supernatants were collected to detect the level of tumor growth factor alpha (TNFalpha) by ELISA. RT-PCR was used to detect the expression of the main PRRs: CD14, SR, TLR2, TLR4, and TLR9. RESULTS: The TNFalpha levels in the supernatant were 234 pg/ml +/- 30 pg/ml in the LPS group, 274 pg/ml +/- 30 pg/ml in the BLP group, and 308 pg/ml +/- 28 pg/ml in the CpG-ODN group, all significantly higher than that in the control group (92 pg/ml +/- 27 pg/ml, P < 0.01 or P < 0.01). The TNFalpha levels in the supernatant were 483 pg/ml +/- 31 pg/ml in the LPS + BLP group, and 511 pg/ml +/- 46 pg/ml in the LPS + CpG-ODN group, both significantly higher than those of the groups of the 3 factor alone (all P < 0.05). And the TNFalpha levels in the supernatant was 665 pg/ml +/- 24 pg/ml in the LPS + BLP + CpG-ODN group, significantly higher than those of the LPS + ODN group and LPS + BLP group (both P < 0.05). LPS, BL, and CpG-ODN alone, combinations of any 2 of them, and the combination of the three all up-regulated the expression of CD14 mRNA more and more strongly in sequence. LPS, BLP, and CpG-ODN alone all up-regulated the expression of SR mRNA (all P < 0.01), however, the combinations of any 2 factors or of the 3 factors failed to further up-regulate the expression of SR. LPS and BLP up-regulated the expression of TLR2 mRNA (both P < 0.05), LPS combined with BLP showed a stronger up-regulation of TLR2 mRNA (P < 0.05) than those by LPS and BLP alone. CPG-ODN alone failed to up-regulate the expression of TLR2 mRNA (P > 0.05) but significantly increased the up-regulation by LPS (P < 0.05). In comparison with the combinations of any 2 factors, LPS and BLP with CPG-ODN together up-regulated the expression of TLR2 mRNA more strongly (all P < 0.05). LPS, BLP, and CpG-ODN alone did not significantly up-regulate the expression of TLR4 mRNA (P > 0.05), LPS + BLP significantly regulated the expression of TLR4 mRNA than the groups of any factor alone (all P < 0.05). LPS + BLP + CpG-ODN further up-regulated the expression of TLR4 mRNA. LPS and CpG-ODN, especially LPS + CpG-ODN significantly up-regulated the expression of TLR9 mRNA (all P < 0.05). BLP failed to up-regulate the expression of TLR9 mRNA (P > 0.05) and did not coordinate the upregulation by LPS, however, in comparison with any combinations of the 3 factors, the combination of LPS, BLP, and ODN up-regulated the expression of TLR9 mRNA the most strongly (all P < 0.05). CONCLUSION: Bacterial LPS, BLP and bacterial DNA not only up-regulate the expression of PRRs of each other, but also synergistically increase the each other's effects on the cell surface of mouse alveolar macrophages.

Animals↗

PubMed2005

NOD2/CARD15 gene polymorphisms in idiopathic pulmonary fibrosis.

BACKGROUND: Micro-organisms, behaving in a non-infectious fashion, may be among the exogenous factor(s) believed to trigger idiopathic pulmonary fibrosis (IPF). One possible strategy to identify an individual's susceptibility to such microbial triggers, which are likely to be ubiquitous, is to investigate the molecular processes involved in their recognition. NOD2/CARD15 is a specific pattern recognition receptor protein, whose genetic variants have been previously associated with susceptibility to Crohn's disease. AIM: The aim of this work was to determine the frequencies of the three major NOD2/CARD 15 gene mutations (R702W, G908R and 1007fsinC) in a series of 76 subjects affected by IPF, and to compare them with those found in three groups of controls: a group with sarcoidosis (a disorder in which an involvement of the NOD2/CARD15 gene has already been investigated and rejected in different ethnic groups; 67 subjects) and two groups of healthy subjects (218 and 208 subjects, respectively), matched for gender, age, and ethnicity. RESULTS: We found no differences in frequencies of NOD2/CARD15 gene polymorphisms among the four groups investigated. CONCLUSION: We conclude that the NOD2/CARD15 gene is not likely to be involved in susceptibility to IPF in Italians.

Aged↗

PubMed2006

[The cow, the boy and the lymph node--immunological principles for vaccines].

Vaccines stimulate the immune system by activating professional antigenpresenting cells, such as dendritic cells. Dendritic cells express a number of pattern recognition receptors (PRR) on their surface, receptors that recognize structures on viruses and bacteria. These receptors stimulate maturation of dendritic cells that thereafter migrate to regional lymph nodes where they present vaccine antigens to T-cells. PRR- ligands of the vaccine are decisive for the efficacy of the immune response. This article discusses cellular principles and mechanisms for vaccine responses; including antigen processing and presentation, T-cell circulation, Th1-, Th2- and CTL T-cell responses and T-B cell cooperation, as well as primary and secondary T and B cell responses and lymphocyte recirculation and homing.

Animals↗