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At least 415 records · Page 23Linked to original sources
PubMed2006

From rabies to transmissible spongiform encephalopathies: an immune-mediated microbial trigger involving molecular mimicry could be the answer.

The concept of experimental allergic encephalomyelitis (EAE) being linked to both rabies post-vaccination encephalomyelitis and multiple sclerosis (MS) has raised the intriguing question whether animal studies carried out for the induction and transmission of transmissible spongiform encephalopathies (TSEs) using brain antigens including prions do have a similar immunopathogenetic mechanism. Although an essential link between autoimmunity and MS has been well established, its role in the pathogenesis of TSEs is generally lacking. However, auto-antibodies to myelin proteins and/or other neuronal antigens such as neurofilaments and prion proteins have been reported in animals with bovine spongiform encephalopathy (BSE) and scrapie as well as in patients with Creutzfeld-Jakob disease (CJD) and kuru. Acinetobacter has been suggested as a possible triggering microbial factor in the initiation of the autoimmune responses in these diseases because bacterial molecular sequences resemble brain antigens, especially in animals affected with BSE and patients with MS and CJD. These possibilities need to be evaluated further with longitudinal prospective studies carried out on larger numbers of animals or humans with such diseases. The transplantation of saline suspensions of brain homogenates will evoke immunological responses and therefore, the results in the study of MS and other neurological diseases have to be interpreted with caution.

Actinobacteria↗
PubMed2005

[Rituximab: a original biotherapy in auto-immune disorders].

SUBJECT: After several decades of hegemony of the T lymphocyte, recent work has suggested the importance of the B lymphocyte in auto-immune diseases. As a consequence, there has emerged over the last few years the idea of using anti-B lymphocyte therapy, in particular rituximab (a chimeric anti-CD20 monoclonal antibody). CURRENT TOPICS AND IMPORTANT RESULTS: This review addresses various current topics: a) the role of B lymphocytes in auto-immune diseases, notably their capacity to be antigen presenting cells and to be activated by original systems like Blys/Baff; b) the mechanism of action of rituximab (apoptosis, complement-dependent cytotoxicity and antibody-dependent cell cytotoxicity) and the phenomena explaining failures and cases escaping treatment, in particular among lymphoproliferations; c) The results include efficacy and tolerance data for the principal auto-immune affections. Among these, the most promising indications would seem to be for rheumatoid polyarthritis and systemic lupus erythematosis, although some preliminary open studies point to an effect in Goujerot-Sjögren's syndrome, neuropathies, auto-immune cytopenia, idiopathic thrombocytopenic purpura, cryoagglutinins, blistering cutaneous affections... PERSPECTIVES AND PROJECTS: Controlled studies will be required to determine the true efficacy and tolerance of this molecule, as it is imperative to validate these new immunotherapeutic strategies, above all when they concern innovative and expensive therapy. Nevertheless, these different observations arouse great hopes and at the same time exciting questions, notably as to the role of B lymphocytes in auto-immune diseases.

Antibodies, Monoclonal↗
PubMed2001

Regulation of antibacterial and antifungal innate immunity in fruitflies and humans.

Insects have been very successful in adapting to their environment, and the ability of the insect immune system to detect and elicit the appropriate response against various invading pathogens has helped in this success. Unlike the vertebrate immune system, which consists of both innate and adaptive components, insect immunity probably consists entirely of an innate immune response, as no evidence of an adaptive response has been found. The innate immune response is described as either a reaction against "lack of self," or the interaction between host germline-encoded receptors and molecules unique to a particular class of invading organisms. Once the invading organism is recognized, the host immune response can be activated via signaling pathways that lead to the appropriate reaction. This review endeavors to put forth how through genetic, molecular, and biochemical studies of the fruit fly Drosophila melanogaster, as well as other insects, it is now understood that aspects of the insect and vertebrate innate immune system are very similar.

Animals↗
PubMed2000

Immune system protects integrity of tissues.

The immune system neither discriminates between "Self" and "Nonself", nor it acts when confronting "Danger", rather, it reacts to disruption of tissue integrity allowing its renewal. The "integrity" hypothesis proposes three groups of signals that coordinate actions of dendritic cells and immunocytes during the initiation of the specific immune response, and suggests explanations for tolerance, memory formation, and repertoire selection, including differences with other theories.

Biological Evolution↗
PubMed1997

Do holes in the T-cell repertoire have a center-surround regulatory structure? A rationale for the bifurcation of the Th1 and Th2 pathways of differentiation.

Regulatory strategies controlling the balance of Th1 versus Th2 T-helper cell responses have been a long-standing mystery with important consequences for immunological disease. A novel model is presented to explain the comparative differentiation of Th1 and Th2 T cells as part of a mechanism to ensure self-tolerance. This model is based on the assumption that thymic interactions of T cell antigen receptors with self major histocompatibility complex ligands may vary in efficacy. By this model, fully agonistic major histocompatibility complex ligands elicit apoptosis during thymic selection to generate 'holes' in the repertoire. Conversely, major histocompatibility complex ligands having some degree of partial efficacy (i.e. a mixed agonist/antagonist) may promote Th2 differentiation whereas fully antagonistic major histocompatibility complex ligands elicit Th0 differentiation. Differentiation of Th2 T cells may continue in the extrathymic tissues upon continued interactions with self major histocompatibility complex ligands having mixed agonist/ antagonist properties. By this mechanism, each 'hole' in the repertoire will develop an inhibitory surround comprised to Th2 T cell clones having partial reactivities to a particular self major histocompatibility complex ligand. During immune responses to self-mimicking foreign antigens, the more numerous Th2 T cells of the inhibitory surround would prevent clonal expansion and Th1 differentiation of any fully autoreactive T cell.

Animals↗
PubMed2003

Migration and T-lymphocyte effector function.

The development of immunity depends upon the capacity of responding T cells to become mobilized from lymphoid tissues where they are primed to sites of antigen exposure, wherever they occur in the body. Activation-induced alterations in the ability of T cells to migrate signify a fundamental change in biological function. Considerable attention is now focused on identifying mechanisms that regulate the migration and persistence of T cells that disseminate to non-lymphoid compartments as effector cells, and those that are retained in the lymphoid compartment. There are many unanswered questions about the developmental relationships and roles in protective immunity of antigen-experienced T cells that partition in different tissues.

Cell Movement↗
PubMed1997

AIDS: decline and fall of immune surveillance?

Recent observations cast doubt on the view that cytotoxic T cells play a key role in keeping HIV-1 infection in check, and that it is the decline in this mechanism of immune surveillance that permits progression to AIDS.

Acquired Immunodeficiency Syndrome↗
PubMed1995

Environmental antigens and atopic disease: underlying mechanisms and prospects for therapy and prophylaxis.

Natural exposure to non-pathogenic antigens, the so-called 'environmental antigens', experimentally elicits a characteristic pattern of T-cell immunity, involving selective suppression of the T-cell-dependent IgE responses that trigger allergic reactions. This 'immune deviation' results in the generation of long-lived T-cell memory, which confers active protection against allergic sensitization. Corresponding primary immune responses to environmental antigens in humans occur most frequently during infancy, and the development of allergic sensitization can be viewed as a failure of this natural immune-deviation process. In this article, potential strategies for primary prevention of allergic disease in infants involving, in particular, the exploitation of oral and mucosal tolerance to stimulate protective CD8+ T-cell-mediated immune deviation, are discussed.

Allergens↗
PubMed2002

Beyond self and nonself: fuzzy recognition of the immune system.

Self-nonself discrimination of the immune system is a widely accepted principle of immunology; however, abundant existing and physiologic functions of harmless autoimmunity as well as degeneracy of antigen recognition expose the over-simplification of the two-valued doctrine. Here, based on infinite-value fuzzy logic, we propose that the immune repertoire, as a consequence of central tolerance, is able to recognize both self and nonself antigens to a certain degree, compensating for the inadequacy of the two-valued self-nonself doctrine. Subthreshold recognition of self antigens is necessary for the generation of regulatory T cells, survival of both naive and memory T cells and other physiologic functions. The kind and magnitude of the immune response depend on the affinity between the antigen (self and foreign) and the T-cell receptor, and microenvironmental and cellular threshold. The outcome of self-nonself discrimination is influenced fundamentally by central tolerance and further dynamic regulation of threshold molecules both in time and space. Understanding the fuzzy feature of the immune system may shed light on mechanisms of autoimmune diseases, cancers and other chronic diseases, and lead to the design of novel vaccines or immunotherapies.

Abatacept↗
PubMed2006

Autoantibodies to intracellular autoantigens and their B-cell epitopes: molecular probes to study the autoimmune response.

A common laboratory finding in systemic autoimmune diseases is the presence of autoantibodies against intracellular autoantigens. Although their pathogenesis is not fully understood, autoantibodies are important tools for establishing diagnosis, classification, and prognosis of autoimmune diseases. Autoantibodies mainly target multicomponent complexes containing both protein antigens and (ribo)-nucleic acid(s), such as the spliceosome or Ro/La RNPs. In this review, we address the main characteristics and the clinical value of the main autoantibody types with respect to their disease association, and we describe the corresponding autoantigens, their biologic function, and their B-cell antigenic determinants (epitopes). The structural characteristics and clinical associations of these epitopes, and their utility as tools to investigate the autoimmune response, are discussed in detail. New insights into the pathogenetic role of epitopes in systemic autoimmunity are also examined. In this regard, using the defined structures of the B-cell antigenic epitopes, complementary epitopes can be designed according to the "molecular recognition" theory. These complementary epitopes can be used as probes to study pathogenetic and immunoregulatory aspects of the anti-idiotypic response. The origin of humoral autoimmunity and the spreading of the epitopes in systemic lupus erythematosus are also discussed. Finally, the ability of post-translational modifications to induce autoreactive immune attack via the generation of neo-epitopes is summarized.

Autoantibodies↗
PubMed2002

The dynamics of germinal centre selection as measured by graph-theoretical analysis of mutational lineage trees.

We have developed a rigorous graph-theoretical algorithm for quantifying the shape properties of mutational lineage trees. We show that information about the dynamics of hypermutation and antigen-driven clonal selection during the humoral immune response is contained in the shape of mutational lineage trees deduced from the responding clones. Age and tissue related differences in the selection process can be studied using this method. Thus, tree shape analysis can be used as a means of elucidating humoral immune response dynamics in various situations.

Algorithms↗