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PubMed2004

Divergent roles for C-type lectins expressed by cells of the innate immune system.

In recent years there has been increasing interest in the diversity and function of carbohydrates present on a range of endogenous mammalian glycoproteins and pathogen surfaces. It is clear that carbohydrate structures are not merely structural components of the molecules which bear them but are, in many instances, a source of information to be decoded by biological systems including the immune system. Macrophages and other antigen presenting cells express a variety of pattern recognition molecules which allow discrimination between self and non-self ligands and are well known for their ability to recognise and internalise foreign antigens. The role of carbohydrates as molecular determinants of self/non-self has been recognised for many years and a family of proteins known as the C-type lectins are implicated as the main players in carbohydrate recognition within the immune system. More recently, C-type lectin receptors which bind ligands other than carbohydrates have been identified, and there are additional receptors which bind both carbohydrate and non-carbohydrate ligands. In this review article we seek to shed light on the varied roles of this family of receptors, particularly those receptors expressed by antigen presenting cells and those with known ligands. We also review more recent data on several members of this family.

Animals↗
PubMed2005

Type I interferons and the innate immune response--more than just antiviral cytokines.

The role of type I interferon (referred to as IFN in this review) in early antiviral immunity is well known. More recently IFN has been shown to be a potent regulator of adaptive immunity. It is now becoming clear that a broad range of viruses, bacteria and even parasites express ligands capable of stimulating a growing number of signalling pathways that results in, often subtype specific, induction of IFN. Of particular interest are the signalling pathways associated with the Toll-like receptors. This family of receptors, each able to induce signals in response to a variety of ligands, initiates the pro-inflammatory response. They also contain members that have the capacity to induce IFN, making use of, and perhaps promoting the evolution of its pleiotropic responses. Greater knowledge of the events that result in induction of IFN is necessary in understanding the specificity of expression of an increasingly complex and important aspect of our immune system. This may reveal to us further therapeutic opportunities, either in the use of IFN or in the manipulation of their expression. This review details the established knowledge and recent advances made in understanding how and under what circumstances the IFNs are expressed, starting with brief overviews of IFN and Toll-like receptors before following the molecular processes from induction of IFN, activation of the JAK-STAT pathway and finally the expression of interferon stimulated genes and their functions.

Animals↗
PubMed2005

Innate immune defence in the human gastrointestinal tract.

The mucosal surface of the gastrointestinal tract represents a major entry point and ecological niche for many microbes. It forms an important immune barrier, absorbing nutrients, whilst preventing invasion by organisms. Of the extra-ordinarily diverse species that comprise the microbial world, relatively few organisms are able to succeed in breaching this barrier in an otherwise healthy host. The production and secretion of antimicrobial peptides (AMPs) from surface epithelia and circulating immune cells are likely to play a key role in host protection and homeostasis. A number of these peptides are constitutively produced providing resident protection, whereas others are induced during infection and inflammation. In addition to directly eradicating microorganisms, it is becoming increasingly apparent that AMPs are multi-functional with diverse immuno-modulatory properties. This review focuses on three families of AMPs, defensins, cathelicidins, and lysozyme, and discusses their role in mucosal defence.

Antimicrobial Cationic Peptides↗
PubMed2005

Dap12 and Trem2, molecules involved in innate immunity and neurodegeneration, are co-expressed in the CNS.

Polycystic lipomembranous osteodysplasia with sclerosing leukoencephalopathy (PLOSL) is a recessively inherited disease characterized by early onset dementia associated with bone cysts. Our group has recently established the molecular background of PLOSL by identifying mutations in DAP12 and TREM2 genes. To understand how loss of function of the immune cell activating DAP12/TREM2 signaling complex leads to dementia and loss of myelin, we have analyzed here Dap12 and Trem2 expression in the mouse CNS. We show that Dap12 and Trem2 are expressed from embryonic stage to adulthood, and demonstrate a highly similar expression pattern. In addition, we identify microglial cells and oligodendrocytes as the major Dap12/Trem2-producing cells in the CNS and, consequently, as the predominant cell types involved in PLOSL pathogenesis. These findings provide a good starting point for the study of the molecular mechanisms of this inherited dementia and new evidence for the involvement of the immune system in neuronal degeneration.

Adaptor Proteins, Signal Transducing↗
PubMed2004

Cysteine proteases in phytopathogenic bacteria: identification of plant targets and activation of innate immunity.

Phytopathogenic bacteria use the type-III secretion system (TTSS) to inject effector proteins into plant cells, presumably to colonize their hosts. The function of these proteins inside plant cells has remained a mystery for years. The recent discovery that the effectors XopD, AvrXv4, AvrPphB, and AvrRpt2 have cysteine protease functions reveals that the proteolysis of host substrates is an important strategy employed by pathogens to alter plant physiology. Moreover, the characterization of these proteases and their targets provides new insight to mechanisms of bacterial virulence and the activation of plant immunity.

Bacteria↗
PubMed2005

Plasmacytoid dendritic cells--virus experts of innate immunity.

Plasmacytoid dendritic cells (pDC) have emerged as a principal subset of dendritic cells in both human and mouse. PDC morphology, surface markers, their migration in vivo and the ability to rapidly produce large amounts of type I interferons (IFN-alpha/beta) in response to toll like receptor (TLR) triggering sets them apart from other dendritic cell subsets. This review highlights the features that make pDC uniquely able to sense and respond to viral infection.

Animals↗
PubMed2003

'Complementing' viral infection: mechanisms for evading innate immunity.

Through co-evolution with their hosts, viruses have developed a variety of immune escape and control mechanisms. In addition to strategies used to avoid the cellular and humoral immune responses, many viral families encode proteins capable of neutralizing the host's first line of defense, complement. The diversity of these complement avoidance mechanisms and proposed mechanisms by which viruses not only avoid, but also use the immune system to their advantage are discussed.

Animals↗
PubMed2003

Innate immunity: involvement of new neuropeptides.

Secretory granules of chromaffin cells from the adrenal medulla store catecholamines and a variety of peptides that are secreted in the extracellular medium during exocytosis. Among these fragments, several natural peptides displaying antimicrobial activities at the micromolar range have been isolated and characterized. We have shown that these peptides, derived from the natural processing of chromogranins (CGs), proenkephalin-A (PEA) and free ubiquitin (Ub), are released into the circulation and display antibacterial and antifungal activities. In this review we focus on three naturally secreted antimicrobial peptides corresponding to CGA1-76 (vasostatin-I), the bisphosphorylated form of PEA209-237 (enkelytin) and Ub. In addition, the antimicrobial properties of the synthetic active domains of vasostatin-I (CGA47-66 or chromofungin) and Ub (Ub65-76 or ubifungin) are reported.

Amino Acid Sequence↗
PubMed2005

Innate immunity and hypersensitivity syndrome.

Viral infections are frequently followed by an increased risk of allergic disorders. We have recently demonstrated an intimate relationship between human herpesvirus 6 (HHV-6) reactivation and drug-induced hypersensitivity syndrome (DIHS). Kano et al. have demonstrated that a dramatic decrease in circulating B and NK cells as well as serum immunoglobulin levels was observed in DIHS at the onset but not in controls. Although these alterations returned to normal on full recovery, NK cells in patients with DIHS displayed a defective ability to express CD122 (IL-2/15R beta) even long after recovery. To test the effect of NK cells, we next investigated NK-depletion experiments. A significant increase in HHV-6 DNA was only detected in NK-depleted cultures of PBMC from DIHS patients in the presence of the causative drug. Because gamma delta-T cells play an important role in viral infections, we investigated whether gamma delta-T cells are also important for preventing HHV-6 reactivation. Expansion of gamma delta-T cells was only observed in undepleted cultures of PBMC, not in NK-depleted cultures, from patients in the presence of the causative drug. Thus, cross-talk between NK cells and gamma delta-T cells or B cells would represent a first line of defense against latent virus, such as HHV-6.

Animals↗
PubMed2006

Measles virus-dendritic cell interaction via SLAM inhibits innate immunity: selective signaling through TLR4 but not other TLRs mediates suppression of IL-12 synthesis.

Two hallmarks of measles virus (MV) infection are the ability of the virus to cause immunosuppression and the resultant enhanced susceptibility of the infected host to microbial insults. We investigated the effect of MV infection on the ability of dendritic cells (DCs) to induce IL-12 via toll-like receptor (TLR) signaling. When infected with MV, transgenic mice which expressed human SLAM receptor on their DCs were defective in the selective synthesis of IL-12 in DCs in response to stimulation of TLR4 signaling, but not to engagements of TLR2, 3, 7 or 9. MV suppressed TLR4-mediated IL-12 induction in DCs even in the presence of co-stimulation with another ligand for TLR2, 3, 7, or 9. While MV V and C proteins were not responsible for IL-12 inhibition, interaction of MV hemagglutinin with human SLAM facilitated the suppression. These results suggest that MV, by altering DC function, renders them unresponsive to secondary pathogens via TLR4.

Animals↗
PubMed2000

Original involvement of antimicrobial peptides in mussel innate immunity.

Recently, the existence and extended diversity of antimicrobial peptides has been revealed in two mussel species. These molecules are classified into four groups according to common features of their primary structure: defensins, mytilins, myticins and mytimycin. In Mytilus galloprovincialis, gene structure reveals synthesis as precursors in circulating hemocytes. Synthesised even in absence of challenge, the precursors mature and the peptides are stored in granules as active forms. The different peptides are engaged in the destruction of bacteria inside phagocytes, before being released into hemolymph to participate in systemic responses. Such involvement in anti-infectious responses is unique, and apparently more related to those of mammalian phagocytes than to those of insects.

Animals↗
PubMed2003

Protection from lethal infection is determined by innate immune responses in a mouse model of Ebola virus infection.

A mouse-adapted strain of Ebola Zaire virus produces a fatal infection when BALB/cj mice are infected intraperitoneally (ip) but subcutaneous (sc) infection with the same virus fails to produce illness and confers long-term protection from lethal ip rechallenge. To identify immune correlates of protection in this model, we compared viral replication and cytokine/chemokine responses to Ebola virus in mice infected ip (10 PFU/mouse), or sc (100 PFU/mouse) and sc "immune" mice rechallenged ip (10(6) PFU/mouse) at several time points postinfection (pi). Ebola viral antigens were detected in the serum, liver, spleen, and kidneys of ip-infected mice by day 2 pi, increasing up to day 6. Sc-infected mice and immune mice rechallenged ip had no detectable viral antigens until day 6 pi, when low levels of viral antigens were detected in the livers of sc-infected mice only. TNF-alpha and MCP-1 were detected earlier and at significantly higher levels in the serum and tissues of ip-infected mice than in sc-infected or immune mice challenged ip. In contrast, high levels of IFN-alpha and IFN-gamma were found in tissues within 2 days after challenge in sc-infected and immune mice but not in ip-infected mice. Mice became resistant to ip challenge within 48 h of sc infection, coinciding with the rise in tissue IFN-alpha levels. In this model of Ebola virus infection, the nonlethal sc route of infection is associated with an attenuated inflammatory response and early production of antiviral cytokines, particularly IFN-alpha, as compared with lethal ip infection.

Animals↗
PubMed2006

Innate immune recognition and suppression of tumors.

In this chapter, we first summarized the strong evidence that now supports the existence of an effective cancer immune surveillance process that prevents cancer development in both mice and humans. We then focused the remainder of the chapter on methods of tumor recognition that contribute to natural host immune suppression of tumors. In particular, NKG2D is a type II transmembrane-anchored glycoprotein expressed as a disulfide-linked homodimer on the surface of all mouse and human natural killer cells (NK cells). Stimulation of NK cell through NKG2D triggers cell-mediated cytotoxicity and in some cases induces production of cytokines. NKG2D binds to family of ligands with structural homology to major histocompatibility complex (MHC) class I, however, NKG2D ligands often display upregulated surface expression on stressed cells and are frequently overexpressed by tumors unlike conventional MHC class I molecules. Evidence clearly implicate that NKG2D recognition plays an important role in tumor immune surveillance.

Animals↗