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PubMedDate not supplied

If the "adaptive" immune system can recognize a significant portion of the pathogenic universe to which the "innate" immune system is blind, then...

The "adaptive" immune repertoire functionally recognizes pathogens (and their toxic products) that the "innate" defense system misses. This requires that the self-nonself discrimination and the regulation of effector output be dependent primarily on somatic learning mechanisms (i.e. on the somatically generated, large, random "adaptive" immune paratopes repertoire).

Humans↗
PubMed2000

Natural interferon alpha/beta-producing cells link innate and adaptive immunity.

Innate immune responses to pathogens critically impact the development of adaptive immune responses. However, it is not completely understood how innate immunity controls the initiation of adaptive immunities or how it determines which type of adaptive immunity will be induced to eliminate a given pathogen. Here we show that viral stimulation not only triggers natural interferon (IFN)-alpha/beta-producing cells (IPCs) to produce vast amounts of antiviral IFN-alpha/beta but also induces these cells to differentiate into dendritic cells (DCs). IFN-alpha/beta and tumor necrosis factor alpha produced by virus-activated IPCs act as autocrine survival and DC differentiation factors, respectively. The virus-induced DCs stimulate naive CD4(+) T cells to produce IFN-gamma and interleukin (IL)-10, in contrast to IL-3-induced DCs, which stimulate naive CD4(+) T cells to produce T helper type 2 cytokines IL-4, IL-5, and IL-10. Thus, IPCs may play two master roles in antiviral immune responses: directly inhibiting viral replication by producing large amounts of IFN-alpha/beta, and subsequently triggering adaptive T cell-mediated immunity by differentiating into DCs. IPCs constitute a critical link between innate and adaptive immunity.

Cell Differentiation↗
PubMed2007

Lamellar pro-inflammatory cytokine expression patterns in laminitis at the developmental stage and at the onset of lameness: innate vs. adaptive immune response.

REASONS FOR PERFORMING STUDY: Recent research has indicated that inflammation plays a role in the early stages of laminitis and that, similar to organ failure in human sepsis, early inflammatory mechanisms may lead to downstream events resulting in lamellar failure. Characterisation of the type of immune response (i.e. innate vs. adaptive) is essential in order to develop therapeutic strategies to counteract these deleterious events. OBJECTIVES: To quantitate gene expression of pro-inflammatory cytokines known to be important in the innate and adaptive immune response during the early stages of laminitis, using both the black walnut extract (BWE) and oligofructose (OF) models of laminitis. METHODS: Real-time qPCR was used to assess lamellar mRNA expression of interleukins-1beta, 2, 4, 6, 8, 10, 12 and 18, and tumour necrosis factor alpha and interferon gamma at the developmental stage and at the onset of lameness. RESULTS: Significantly increased lamellar mRNA expression of cytokines important in the innate immune response were present at the developmental stage of the BWE model, and at the onset of acute lameness in both the BWE model and OF model. Of the cytokines characteristic of the Th1 and Th2 arms of the adaptive immune response, a mixed response was noted at the onset of acute lameness in the BWE model, whereas the response was skewed towards a Th1 response at the onset of lameness in the OF model. CONCLUSIONS: Lamellar inflammation is characterised by strong innate immune response in the developmental stages of laminitis; and a mixture of innate and adaptive immune responses at the onset of lameness. POTENTIAL RELEVANCE: These results indicate that anti-inflammatory treatment of early stage laminitis (and the horse at risk of laminitis) should include not only therapeutic drugs that address prostanoid activity, but should also address the marked increases in lamellar cytokine expression.

Animals↗
PubMed1997

Dependence of the adaptive immune response on innate immunity: some questions answered but new paradoxes emerge.

Recently a new model of vertebrate immunity has been gaining popularity. In this new model it is hypothesized that activation of innate immunity is a prerequisite for an adaptive immune response to an antigen. Following activation the innate system induces key costimulator molecules on APC, which are essential for antigen-driven clonal expansion of T and B cells. The model largely explains the need for adjuvants in the induction of adaptive immunity, provides a possible mechanism for the immune system to perceive the biological nature of a pathogen and thereby produce the most effective immune response, and transfers much of the onus of self-non-self discrimination from the adaptive to the innate immune system. In the present article we highlight two paradoxes raised by the new model. First, by linking adaptive immunity to innate recognition the immune system is unable to take full advantage of the genetic diversity of T and B cell antigen receptors. Thus, the ability of the immune system to combat a pathogen is totally dependent on the efficiency of recognition by the innate system and, therefore, the germ-line mutation rate of the genes involved in the innate response. Second, if signals from the innate system induce costimulatory molecules on APC, then one would expect the accidental clonal expansion of many autoreactive T and B cells. We suggest that one means of resolving the first paradox is to propose that the major reason for the evolution of adaptive immunity was to provide, via immunological memory, resistance to reinfection, rather than simply to combat the primary infection by the pathogen. In the case of autoreactivity we suggest that autodestruction is prevented by immune responses being tightly regulated at the effector T cell level. Finally, we argue that the two paradoxes, rather than undermining the new model of immunity, highlight our lack of understanding of key elements of the vertebrate immune system.

Adaptation, Physiological↗
PubMed2006

Alternative adaptive immunity in invertebrates.

Vertebrate adaptive immunity is characterized by challenge-specific long-term protection. This specific memory is achieved through the vast diversity of somatically rearranged immunological receptors such as antibodies. Whether or not invertebrates are capable of a comparable phenotypic plasticity and memory has long been a matter of debate. A recent study on Anopheles gambiae mosquitoes now establishes Down syndrome cell adhesion molecule (Dscam) as a key immune surveillance factor with characteristics analogous to antibodies.

Adaptation, Biological↗
PubMed2006

Vaccine with beta-defensin 2-transduced leukemic cells activates innate and adaptive immunity to elicit potent antileukemia responses.

Murine beta-defensin 2 (MBD2) is a small antimicrobial peptide of the innate immune system. Recent study showed that MBD2 could not only recruit immature dendritic cells but also activate them by Toll-like receptor 4 and thus may provide a critical link between the innate immune system and the adaptive immune response. In this report, we examined the antileukemia activity of MBD2 in a murine model of acute lymphoid leukemia (ALL) L1210. L1210 cells were engineered to secrete biologically functional MBD2. MBD2-modified L1210 (L1210-MBD2) showed significantly reduced leukemogenecity, resulting in a 80% rate of complete leukemia rejection. Inoculation of mice with L1210-MBD2 induced enhanced CTL and natural killer (NK) activity and augmented interleukin-12 and IFN-gamma production. All the recovered mice from the inoculation showed a protective immunity to the following challenge with parental L1210 cells and generate leukemia-specific memory CTL. Vaccines with irradiated L1210-MBD2 cells could cure 50% leukemia-bearing mice. Depletion of CD8+ T cells but not CD4+ T cells completely abrogated the antileukemia activity of MBD2. Interestingly, NK cells were also required for the MBD2-mediated antileukemia response, although ALL generally display a high degree of resistance to NK-mediated lysis. Our results suggest that MBD2 can activate both innate and adaptive immunity to generate potent antileukemia response, and MBD2 immunotherapy warrants further evaluation as a potential treatment for ALL.

Acute Disease↗
PubMed2003

Differences in participation of innate and adaptive immunity to respiratory syncytial virus in adults and neonates.

Innate and adaptive immune responses to respiratory syncytial virus (RSV) in neonates were assessed by cord blood mononuclear cell (MC) cytokine expression and proliferation and these responses were compared with those from adult peripheral blood MCs. In adult cells, inactivated and live virus invoked cytokines reflecting both innate and adaptive immunity (interleukin [IL]-6, interferon [IFN]-gamma, IL-2, tumor necrosis factor [TNF]-alpha, and IL-10). Low levels of IL-4 were detected, although only with inactivated virus. In contrast, in neonatal cells, inactivated virus invoked large levels of the innate immune cytokines IL-6, TNF-alpha, and IL-10 and reduced levels of IFN-gamma and IL-12 but no adaptive cytokines. Live virus induced fewer innate (IL-6, IL-10, and IFN-gamma) and no adaptive immune cytokines. RSV-induced proliferation was absent in neonatal MCs, although positive in adult MCs. Thus, exposure to RSV does not appear to occur before birth, and adaptive immune insufficiency or greater innate responses may account for early life RSV-induced illnesses.

Adult↗
PubMed2003

Prostanoids and MPO-halide system products as a link between innate and adaptive immunity.

and The crosstalk between innate adaptive immunity is regulated by cytokines and complex interactions between cells of the immune system. A variety of endogenous agents are involved in the regulation of the cytokine network. Especially, eicosanoids and ROIs have a great impact on the regulation of cytokine production. Eicosanoids (prostanoids, leukotrienes and lipoxins) are produced mainly by inflammatory cells while their receptors are distributed on the cells of both arms of the immune system. Depending on the predominant prostanoid produced and the profile of prostanoid receptors expression on immune cells, eicosanoids can selectively regulate the production of Th1 and Th2 driven cytokines. Inflammatory cells (neutrophils, macrophages), are also a rich source of large amounts of ROIs. In this paper we have focused on the role of taurine chloramine (TauCl), the physiological product of neutrophil MPO-halide system, in the regulation of immune system. It is well documented that TauCl has pleiotropic effects on the inductive phase of the immune response. TauCl's immunoregulatory properties result from its ability to modulate the production of cytokines and eicosanoids. Finally, we conclude that eicosanoids and ROIs provide an important link between the afferent branches and the innate and adaptive immune response.

Animals↗
PubMed1994

Primitive vertebrate immunity: what is the evolutionary derivative of molecules that define the adaptive immune system?

The adaptive immune system is capable of responding to an infinite number of antigens with the antigen-specific receptors immunoglobulin (Ig) and the T cell receptor (TCR). Ig binds soluble antigens while TCR recognizes antigen bound in clefts of polymorphic self-encoded major histocompatibility complex (MHC) class I and class II molecules. All of these molecules are wholly or partially composed of Ig superfamily domains. TCR and Ig use V-set Ig superfamily domains, always in heterodimeric forms, in antigen recognition. Although the ways in which TCR and Ig bind antigen are fundamentally different, the structure of the heterodimeric V domains is probably identical. The antigen-binding cleft of MHC proteins has a structure unlike Ig superfamily domains, although several investigators have proposed that this cleft is evolutionarily derived from Ig domains. We believe the MHC cleft is a primitive structure, perhaps related to the peptide-binding domains of intracellular chaperone proteins. A model is proposed whereby chaperone proteins were the primordial MHC molecules, presenting peptides derived from invariant proteins residing inside cells for recognition by lymphocytes with minimally diverse receptors. Such a system may be reflected today by the epithelial immune system, apparently governed by monomorphic MHC molecules and lymphocytes with unconventional antigen-specific receptors.

Adaptation, Physiological↗
PubMed2004

The interface between innate and adaptive immunity.

This focus analyzes some of the ways the innate immune system influences adaptive immune responses. Here the main principles and themes that govern this intricate relationship are discussed.

Adaptation, Physiological↗
PubMed1987

The ancestor of the adaptive immune system was the CAM system for organogenesis.

The adaptive immune system as we understand it is uniquely possessed by vertebrate species and by none other. Nevertheless, it is generally thought that this system represents the ultimate sophistication of much older cell-cell interaction mechanisms. In this paper, I have suggested that plasma membrane cell adhesion proteins that were involved in ontogenic organogenesis since time immemorial were the ultimate ancestor of the adaptive immune system. N-CAM of the chicken for neuronal organogenesis already possesses four beta 2-microglobulin-like domains and it is this domain from which the adaptive immune system sprang. The germ for this beta 2-microglobulin-like domain is already found in the cell adhesion protein of the slime mold straddling the border between unicellular and multicellular eukaryotes. A slightly different version of the above view has recently been expressed by my colleagues.

Amino Acid Sequence↗
PubMed2007

Translational mini-review series on Toll-like receptors: networks regulated by Toll-like receptors mediate innate and adaptive immunity.

The Toll-like receptor (TLR) family provide key components of mammalian immunity and are part of the earliest surveillance mechanisms responding to infection. Their activation triggers the innate immune response, and is crucial to the successful induction of Th1/Th2-phenotyped adaptive immunity. Innate immunity was long considered to be non-specific and somewhat simple compared to adaptive immunity, mediated via the engulfment and lysis of microbial pathogens by phagocytic cells such as macrophages and neutrophils, and involving no complex protein-protein interactions. The emergence of the TLR field has contributed to a revision of our understanding, and innate immunity is now viewed as a highly complex process, in line with adaptive immunity. This review will give a brief overview of our current knowledge of TLR biology, and will focus on TLRs as key components in complex networks that activate, integrate and select the appropriate innate and adaptive immune responses in the face of immunological danger.

Animals↗
PubMed2000

Heat shock proteins generate beta-chemokines which function as innate adjuvants enhancing adaptive immunity.

Heat shock proteins (HSP) are widely distributed and highly immunogenic molecules. A novel property reported here is that stimulation with HSP70 of CD8-enriched T cells derived from naive non-human primates caused a dose-dependent increase in concentrations of the beta-chemokines RANTES, macrophage inflammatory protein (MIP)-1alpha or MIP-1beta. However, the concentrations of these beta-chemokines were greatly increased when the CD8 T cells derived from HSP70-immunized non-human primates were stimulated with HSP70. HSP linked to peptides or proteins combined generation of beta-chemokines with an adjuvant function by enhancing specific T cell proliferative responses and IgG and IgA antibodies. The beta-chemokine and adjuvant functions were also elicited by topical mucosal administration of HSP linked to an antigen. We postulate that microbial HSP can stimulate beta-chemokine production which may be responsible for innate adjuvanticity, as was found in cells eluted from normal rectal mucosal tissue, and constitutes a significant component of the mucosal-associated lymphoid system. Furthermore, stimulation of innate immunity may drive adaptive immunity and account for the protective effects of HSP against tumors and viruses.

Adjuvants, Immunologic↗
PubMed1999

Thymic independence of adaptive immunity to the intracellular pathogen Shigella flexneri serotype 2a.

Shigella flexneri is a facultative intracellular pathogen. While immunity to several intracellular pathogens is mediated by T lymphocytes, it is unknown whether cellular immune responses are important to adaptive immunity to S. flexneri. We show that vaccination with S. flexneri serotype 2a confers protection to mice that lack T lymphocytes or gamma interferon (IFN-gamma), specific depletion of T lymphocytes does not alter the protection, and adoptive transfer of splenocytes from vaccinated mice does not confer protection to naive mice. In contrast, vaccination conferred no protection to mice that lack B lymphocytes and adoptive transfer of immune sera conferred partial protection to naive mice. These data demonstrate that in the mouse bronchopulmonary model, adaptive immunity to S. flexneri 2a is an antibody-mediated, B-lymphocyte-dependent process and can be generated in the absence of T lymphocytes or IFN-gamma.

Adaptation, Physiological↗
PubMed2004

Innate immunity in early chordates and the appearance of adaptive immunity.

In the urochordate Ciona intestinalis some membrane Immunoglobulin superfamily members with ancestral features of antigen receptors are homologs of vertebrate adhesion molecules acting as virus receptors. They include the following: the junction adhesion molecule (reovirus receptor) (JAM), the Cortical thymocyte marker of Xenopus (CTX family) (Coxsackie's virus receptor) and the poliovirus receptor (PVR). In humans these genes belong to the same linkage group, of which 4 paralogous groups exist. This situation is consistent with the notion that the Ciona set of genes would correspond to a preduplication state. In addition, the human region 3q13 and its paralogs, harbour genes remotely related to the nectin family that can be detected in Protostomes (human CRTAM and CD80-86 related to Drosophila Beat). In addition, this linkage group contains several CDs important for the immune system CD166, CD47 and many members of the tetraspanin family. The VC1-like core of the nectin is homologous to the VCI core of the MHC-linked tapasin and to the VC1 segments of, for example, specific antigen receptors of vertebrates, and could be related to a primitive antigen receptor gene. It is suggested that the virus binding property of the members of this family was exploited, and that they were recruited in the vertebrate immune system following the introduction of the somatic rearrangement machinery. In this way the adaptive immune system could have developed from a set of receptors involved in a primitive local innate immunity involving NF-kappaB-mediated apoptosis.

Amino Acid Sequence↗
PubMed2006

Porcine innate and adaptative immune responses to influenza and coronavirus infections.

Both innate and adaptative immune responses contribute to the control of infectious diseases, including by limiting the spreading of zoonotic diseases from animal reservoirs to humans. Pigs represent an important animal reservoir for influenza virus infection of human populations and are also naturally infected by coronaviruses, an important group of viruses, which includes the recently emerged severe acute respiratory syndrome (SARS) virus. Studies on both innate and adaptative immune responses of pigs to influenza virus and coronaviruses contribute, therefore, to a better control of these infections in their natural hosts and will be briefly reviewed in this article. Pro-inflammatory cytokines, including type I interferon (IFN), tumor necrosis factor-alpha (TNF-alpha), and interleukin-6 (IL-6), were found in lung secretions of influenza virus infected pigs, and correlated with the intensity of clinical signs, whereas prior vaccination against influenza strongly reduced the production of infectious virus and cytokines in the lungs upon challenge, which was associated with clinical protection. An early type I IFN production was also found in coronavirus infected pigs, including at mucosal sites. IFN induction by coronavirus is shown to involve interaction between a viral glycoprotein and a leukocyte subset, likely equivalent to plasmacytoid dendritic cells, present in the mucosae and associated lymphoid tissues. Given the IFN mediated antiviral and immunomodulatory effects, the use of IFN or IFN inducers may prove an efficient strategy for a better control of influenza virus and coronavirus infections in pigs. Because influenza and coronaviruses target mucosal surfaces, adaptative immune responses have to be characterized at mucosal sites. Thus, nasal and pulmonary antibody responses were analyzed in influenza virus infected or vaccinated pigs showing short-lived, but potentially protective local IgA and IgG antibody (Ab) responses. Interestingly, primary influenza virus infection induced long-lived increase of lung CD8(+) T cells and local lymphoproliferative responses. Pigs infected by a respiratory coronavirus (PRCV) showed virus-specific IgG Ab-secreting cells in the bronchial lymph nodes, whereas the transmissible gastroenteritis coronavirus (TGEV) induced more IgA Ab-secreting cells in gut tissues, which illustrates the importance of the route of antigen administration for inducing local immune effector mechanisms. Porcine viral infections provide, therefore, valuable models for evaluating the immune parameters that are important for controlling transmission of important viral zoonotic infections.

Animals↗
PubMedDate not supplied

Immunological biomarkers of ageing in man: changes in both innate and adaptive immunity are associated with health and longevity.

Scientific and clinical advances in the last century have led to increased numbers of individuals living to older ages. Thus a major concern is how to live these years with a high quality of life. The ageing immune system is less well able to cope with infectious diseases than the youthful immune system probably as a consequence of altered immune response to pathogens. Thus, both innate and adaptive immune responses show age-related changes that could be decisive for healthy ageing and survival. Longitudinal studies in healthy elderly have allowed the definition of the ''immune risk phenotype" (IRP) a predictor of mortality in elderly individuals that is based on several parameters of the adaptive immune response. Here, we hypothesize that failures in innate immunity observed in frail elderly are related to those alterations described in adaptive immunity defined as the IRP. It will be important to include assays of NK cell markers and functions in future longitudinal studies in order to investigate this point in detail as well as to consider the trace element zinc as an essential co-factor for optimal NK cell activity.

Aged, 80 and over↗