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Results for “adaptive immunity”

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At least 19 recordsLinked to original sources
PubMed2005

Natural killer cells in hepatitis C virus infection: from innate immunity to adaptive immunity.

Natural killer (NK) cells are specialized lymphocytes that provide a first line of defense through their ability to kill pathogen-infected cells and transformed cells. The function of NK cells is regulated by a fine balance of inhibitory and activating signals, which are mediated by a diverse array of cell-surface receptors. We recently found that expression of the inhibitory receptor CD94/NKG2A is up-regulated on NK cells in patients with chronic hepatitis C. HLA-E, a ligand for NKG2A, was expressed in all human hepatoma cell lines tested as well as in nontransformed hepatocytes, but not in K562 cells, a classic NK-sensitive target. NK cells isolated from patients with chronic hepatitis C (HCV-NK) were less capable of killing hepatoma cells and of producing interferon-gamma in response to hepatoma cells than those from healthy donors, whereas there was no significant difference in NK responsiveness toward K562 cells. Of note is the finding that maturation and activation of monocyte-derived dendritic cells were negatively modulated in the presence of HCV-NK and hepatoma cells, which were restored by the addition of anti-NKG2A antibody during the coculture of HCV-NK and hepatoma cells. Research revealed that dendritic cells recognize danger signals from microorganisms by monitoring pathogen-associated molecular patterns via Toll-like receptors. Our findings have shed light on NK receptors as an important interface that transmits danger signals from abnormal cells to immune systems. Aberrant expression of CD94/NKG2A should have negative impact on innate resistance and subsequent adaptive immunity toward HCV-infected or transformed cells in chronic hepatitis C.

Cell Communication↗
PubMed2004

Genetic analysis of innate immunity: TIR adapter proteins in innate and adaptive immune responses.

The innate immune system senses pathogens largely through signals initiated by a collection of phylogenetically related proteins known as "Toll-like receptors" (TLRs), of which 10 representatives are encoded in the human genome. Our understanding of the sensing role played by the TLRs began with the positional cloning of a spontaneous mutation (Lps(d)) in the gene encoding the mammalian lipopolysaccharide (LPS) receptor. Other key innate immunity proteins have been disclosed by germline mutagenesis, and are discussed in the present review.

Animals↗
PubMed2003

Platelet-mediated modulation of adaptive immunity. A communication link between innate and adaptive immune compartments.

Platelets are highly reactive components of the circulatory system with well-documented hemostatic function. Recent studies extend platelet function to modulation of local inflammatory events through the release of chemokines, cytokines, and a number of immunomodulatory ligands, including CD154. We hypothesized that platelet-derived CD154 modulates adaptive immunity. The data reported herein demonstrate that platelets, via CD154, induce dendritic cell maturation, B cell isotype switching, and augment CD8(+) T cell responses both in vitro and in vivo. Platelet transfusion studies demonstrate that platelet-derived CD154 alone is sufficient to induce isotype switching and augment T lymphocyte function during viral infection, leading to enhanced protection against viral rechallenge. Additionally, depletion of platelets in normal mice results in decreased antigen-specific antibody production.

Adaptation, Physiological↗
PubMed2006

Aging of the immune system: how much can the adaptive immune system adapt?

The competency of the adaptive immune function decreases with age, primarily because of the decline in production of naive lymphocytes in the bone marrow and thymus as well as the expansion of incompetent memory lymphocytes. Here I discuss the recent progress on age-associated changes in lymphocytes and their effect on the adaptive immune system.

Aged↗
PubMed2004

Innate immunity contributes to cochlear adaptive immune responses.

Inner ear immune responses mediated by antigen-specific processes are thought to contribute to hearing loss in humans. Systemic activation of innate immunity contributes to immune responses in the central nervous system. We hypothesized that activation of innate immunity can prime the inner ear for adaptive immune responses and exacerbate disease. Mice were systemically immunized with antigen. Three weeks after initial antigen exposure, the antigen was injected intrathecally coincident with systemic injection of lipopolysaccharide (LPS), an activator of innate immunity. Responses were measured by quantifying the leukocyte infiltrate and cochlear IL-1beta expression. LPS stimulation markedly amplified the adaptive immune response to exogenous antigen in the inner ear. These data indicate that the cochlea is activated by systemic events that stimulate innate immunity and when antigen is present in the inner ear, a robust cochlear adaptive response is generated. If true in humans, this implies that priming may be an important component in the development of immune-mediated hearing loss.

Adjuvants, Immunologic↗
PubMed2004

A mouse model of human adaptive immune functions: HLA-A2.1-/HLA-DR1-transgenic H-2 class I-/class II-knockout mice.

HLA-A2.1-/HLA-DR1-transgenic H-2 class I-/class II-knockout mice were created and their immunological potential evaluated in response to hepatitis B DNA vaccine. Every single immunized mouse developed hepatitis B virus-specific antibodies, HLA-DR1-restricted helper, and HLA-A2.1-restricted cytolytic T cell responses directed at the same immunodominant epitopes as those identified in naturally infected or vaccinated humans. These mice were specifically protected against a hepatitis B-recombinant vaccinia virus infection with a 10,000-fold or more reduction of the virus load at day 4 post-challenge. These mice represent a unique in vivo experimental model for human immune function studies without any interference with mouse MHC response which dwarfed the prediction of human responses. Furthermore, they enable the complete monitoring of immune adaptative responses for preclinical screening of candidate vaccines.

Amino Acid Sequence↗
PubMed2002

RICK/Rip2/CARDIAK mediates signalling for receptors of the innate and adaptive immune systems.

The immune system consists of two evolutionarily different but closely related responses, innate immunity and adaptive immunity. Each of these responses has characteristic receptors-Toll-like receptors (TLRs) for innate immunity and antigen-specific receptors for adaptive immunity. Here we show that the caspase recruitment domain (CARD)-containing serine/threonine kinase Rip2 (also known as RICK, CARDIAK, CCK and Ripk2) transduces signals from receptors of both immune responses. Rip2 was recruited to TLR2 signalling complexes after ligand stimulation. Moreover, cytokine production in Rip2-deficient cells was reduced on stimulation of TLRs with lipopolysaccharide, peptidoglycan and double-stranded RNA, but not with bacterial DNA, indicating that Rip2 is downstream of TLR2/3/4 but not TLR9. Rip2-deficient cells were also hyporesponsive to signalling through interleukin (IL)-1 and IL-18 receptors, and deficient for signalling through Nod proteins-molecules also implicated in the innate immune response. Furthermore, Rip2-deficient T cells showed severely reduced NF-kappaB activation, IL-2 production and proliferation on T-cell-receptor (TCR) engagement, and impaired differentiation to T-helper subtype 1 (TH1) cells, indicating that Rip2 is required for optimal TCR signalling and T-cell differentiation. Rip2 is therefore a signal transducer and integrator of signals for both the innate and adaptive immune systems.

Adaptor Proteins, Signal Transducing↗
PubMed2004

Forward genetic dissection of afferent immunity: the role of TIR adapter proteins in innate and adaptive immune responses.

The innate immune system senses pathogens largely through signals initiated by proteins known as 'Toll-like receptors' (TLRs), of which ten representatives are known to be encoded in the human genome. The understanding of the biochemical circuitry that maintains the innate capacity for immune recognition and response has loomed as a major hurdle in immunology. A total of five adapter proteins with cytoplasmic domain homology to the TLRs are known to exist in mammals. These proteins show preferential association with individual TLR family members, giving a particular character to the signals that distinct microorganisms initiate, and also initiate the adaptive immune response. The adaptive immune response is dependent upon upregulation of costimulatory molecules (UCM) such as CD80 and CD86. Forward genetic analysis has revealed that this upregulation depends upon an adapter encoded by a locus known as Lps2, and upon type I interferon receptor signaling.

Animals↗
PubMed1975

[Study of the immunodepressive effect of passive immunization on a model of adaptive immunity].

The effect of various doses of specific serum administered in passive immunization on the formation of primary and secondary adaptive immunity in mice of the CBA strain was studied. Primary and secondary response was more sensitive to passive immunization on a model of adaptive immunity than in vivo. Most sensitive to the immunodepressive action of specific antibodies IgM and IgG were plaque-forming cells, and most resistant -- rosette-forming cells and cells. This led to a supposition that antibodies administered in passive immunization depressed the development of the immunological response acting at the level of T- and B cells.

Animals↗
PubMed1997

Innate immunity: impact on the adaptive immune response.

For many years, innate immunity has been considered as a separate entity from the adaptive immune response and has been regarded to be of secondary importance in the hierarchy of immune functions. For the past few years, however, interest in innate immunity has grown enormously, so that now it is studied intensively in many laboratories that seek to integrate these two distinct types of immune function. Our intent in this review is to point out the similarities and differences in these two types of host response to infection, and to indicate our present level of understanding of how these can be integrated into a more complete description of the immune response.

Immunity, Innate↗
PubMed2006

DNA damage: a trigger of innate immunity but a requirement for adaptive immune homeostasis.

Chromosome breakage is frequently associated with viral infection and cellular transformation, but it is also required for two processes that are crucial for the development and function of adaptive immunity: V(D)J recombination and class-switch recombination. The cellular responses that result from this type of DNA damage, which are mostly activated by the protein kinase ataxia-telangiectasia mutated (ATM), lead to cell-cycle arrest at several checkpoints and efficient DNA repair. This Review focuses on the important roles of these DNA-damage responses in the activation of innate immunity and the targeting of the innate immune response to infected or transformed cells, as well as in the development and function of adaptive immunity.

Animals↗
PubMed2005

Tamm-Horsfall glycoprotein links innate immune cell activation with adaptive immunity via a Toll-like receptor-4-dependent mechanism.

Tamm-Horsfall glycoprotein (THP) is expressed exclusively in the kidney and constitutes the most abundant protein in mammalian urine. A critical role for THP in antibacterial host defense and inflammatory disorders of the urogenital tract has been suggested. We demonstrate that THP activates myeloid DCs via Toll-like receptor-4 (TLR4) to acquire a fully mature DC phenotype. THP triggers typical TLR signaling, culminating in activation of NF-kappaB. Bone marrow-derived macrophages from TLR4- and MyD88-deficient mice were nonresponsive to THP in contrast to those from TLR2- and TLR9-deficient mice. In vivo THP-driven TNF-alpha production was evident in WT but not in Tlr4-/- mice. Importantly, generation of THP-specific Abs consistently detectable in urinary tract inflammation was completely blunted in Tlr4-/- mice. These data show that THP is a regulatory factor of innate and adaptive immunity and therefore could have significant impact on host immunity in the urinary tract.

Animals↗
PubMed2003

Innate immune responses support adaptive immunity: NKT cells induce B cell activation.

Invariant NKT cells are a peculiar subset of T lymphocytes whose features, highly conserved both in the mouse and the human system, strongly recall those of other "innate lymphocytes". Following recognition of CD1d-presented glycosphingolipid antigens invariant NKT promptly release high amount of diverse cytokines concurring to the activation of the actors of both innate and acquired immune responses. For this reason, in recent years NKT cells have been the object of intensive study, aimed to understand their role in diverse patho-physiological conditions and to exploit the possibility to take advantage of their "adjuvant-like" activity in the formulation of new vaccines. As antibodies are an essential part of many immune responses, we focused our attention on invariant NKT-B cell interactions analyzing their influences on B cell activation and effector functions. The results of this study demonstrate that human invariant NKT cells can provide direct help for B cell proliferation and antibody production through CD1d-restricted mechanisms. Remarkably, help to B lymphocytes by invariant NKT cells is delivered also in the absence of exogenous antigen, suggesting the existence of an endogenous ligand presented by CD1d on B cells.

Antigens, CD1↗