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PubMed2006

Innate and adaptive immune responses of the central nervous system.

The central nervous system (CNS) is an immunologically specialized organ. The blood-brain barrier regulates the passage of molecules and cells into the CNS. Robust immune responses occur in the CNS even though there is normally an absence of MHC molecules, lack of normal lymphatic drainage, and reduced immune surveillance. This review discusses the immunological elements of the healthy CNS and the pattern of responses that evolve during innate and adaptive immunity in this organ. We also discuss the contribution of astrocytes, cerebrovascular endothelial cells, microglia, macrophages, and dendritic cells to the integrity and pathology of the CNS during CD4+ T-cell autoimmune responses directed against neuroantigens.

Animals↗
PubMed1991

[Inflammatory demyelinating diseases if the peripheral nervous system: immunological concepts and experimental models].

Some inflammatory diseases of the peripheral nervous system, most prominently the Guillain-Barré syndrome, are currently regarded to be of autoimmune origin. Experimental models show clearly that the balance between cellular and humoral autoimmune reaction against peripheral myelin components significantly determines the appearance of the disease. Yet, important questions, such as target antigens of the antimyelin reaction are still unresolved.

Animals↗
PubMedDate not supplied

[Immunotherapy in allergy].

This report includes a partial interpretation of the possible mechanisms of action related with the efficacy of specific immunotherapy with allergens. This cannot be explained by only one mechanism which regulates the immune reaction, which is why there is the relief that there is a large field in immunology which has yet to be explore.

Allergens↗
PubMedDate not supplied

Gene therapy: models to study the immunological way.

Gene engineering to enhance tumour immunogenicity and elicit curative responses against established tumours and tumour recurrences has become an attractive prospect. Gene engineering enables new genes to be selectively inserted into the genome of a tumour cell, or the construction of new fusion plasmids coding tumour antigens and immunomodulatory molecules. The rationale behind current research is to enhance the immune recognition of tumour antigens through their association with the molecules on which immune recognition depends. The immunotherapy data obtained in many experimental tumour systems provide a realistic assessment of the potential and limits of this technological approach. Experimental vaccination of rodents has been shown to induce a significant immune memory, even against poorly immunogenic tumours, that can prevent tumour growth and cure initial metastases, but is poorly effective against established tumours. Its use in tumour prevention is a fresh dawning perspective.

Animals↗
PubMed1981

The activity of an anti-allergic compound, proxicromil, on models of immunity and inflammation.

A tricyclic chromone, proxicromil (sodium 6,7,8,9-tetrahydro-5-hydroxy-4-oxo-10-propyl-naphtho (2,3-b) pyran-2-carboxylate), has been tested for activity against certain immunological and inflammatory reactions. When given parenterally it suppressed the development of delayed hypersensitivity reactions in sensitized mice and guinea-pigs but did not affect the rejection of skin allografts in mice. The compound had no activity against certain in vitro correlates of delayed hypersensitivity reactions (lymphocyte transformation and lymphokine activity), but did have an inhibitory effect on lymphokine (MIF) productions at 10(-4) M but not at 10(-5) M. Proxicromil was also found to be active in non-immunologically mediated models of inflammation and in models having an immunological component which are known to be sensitive to non-steroidal anti-inflammatory drugs (adjuvant arthritis, reversed passive Arthus reaction). The activity of this compound was enhanced when administered in arachis oil when compared to its activity in saline. Proxicromil has not direct activity on the development of immune responsiveness but appear to suppress the expression of delayed hypersensitivity and immune complex mediated hypersensitivity reactions by virtue and its anti-inflammatory properties. This activity is not associated with inhibition of cyclo-oxygenase.

Animals↗
PubMed1993

Dynamic interaction between Leishmania infection in mice and Th1-type CD4+ T-cells: complexity in outcome without a requirement for Th2-type responses.

The interaction between Leishmania parasites and Th1 cells is investigated using a simple mathematical model of immunological responses and parasite population growth within the host. The model generates patterns of resistance and susceptibility to infection that mirror observed trends in experimental infections of mice and of humans exposed to infection in areas of endemic transmission. The heterogeneity in outcome predicted by the model can arise either through differences in the values of the parameters that characterize the genetic background of the host or as a consequence of differences in the size of the infecting inoculum of the parasite. Detailed analyses of equilibrium states and of the time course of infection within a host suggest that a limitation in the availability of precursor T-cells, as a consequence of high levels of recruitment into the activated pool, may play a significant role in the progression of infection in susceptible hosts. A brief discussion is presented of the implications of model prediction for therapeutic intervention.

Animals↗
PubMed1985

The X----Y----Z scheme after 23 years.

Mathematical modelling of the course of the immune response is undoubtedly one of the most progressive and most promising areas of modern immunology. Mathematical models (along with computer programs) can be taken as "the only means of thoroughly testing and examining a large and intricate theory" (Partridge et al. 1984). The first phase of construction of mathematical models is the formulation of assumptions based on the knowledge of the facts to be modelled (manifested usually in a scheme of the presumed course of the modelled process). The first mathematical models of immune response were based on the hypothesis of a two-stage differentiation of cells participating in the humoral response, published in Prague 23 years ago (Sercarz and Coons 1962; Sterzl 1962) and illustrated by the X----Y----Z scheme. Many contemporary mathematical models still stem from this scheme which undoubtedly fits the fundamental data concerning the immune system.

Animals↗
PubMed2005

Nonhuman primates are relevant models for research in hematology, immunology and virology.

Nonhuman primates have been used for biomedical research for several decades. They have proved to be models that are relevant to humans because of the high level of gene homology which underlies physiological and biochemical similarities. The similarity of monkeys to humans has been used to investigate pathophysiological mechanisms in hematology, immunology and virology. New therapeutic procedures can be assessed in primates by using materials, in particular pharmacological reagents, and methods designed for humans. The relevance of these models also relies on the use of species-specific pathogens and the availability of recombinant, homologous cytokines. The introduction of more and more sophisticated cell and gene therapy protocols in hematopoietic cell transplantation and immunotherapy requires the development of preclinical trials similar to clinical settings. For several decades now, baboons and cynomolgus/rhesus monkeys have been the most useful primate models in experimental hematology, and this has contributed to numerous therapeutic advances. Primate models of AIDS have been developed to study the pathogenesis, transmission and immune responses to infection, and to test vaccines and drugs. Primate research should be restricted in quantity, and mainly designed with the aim of removing uncertainty as to the safety and clinical benefit to the patient, of new biomedical protocols.

Allergy and Immunology↗
PubMed1996

Partial laminin alpha2 chain restoration in alpha2 chain-deficient dy/dy mouse by primary muscle cell culture transplantation.

Laminin-2 is a component of skeletal and cardiac basal lamina expressed in normal mouse and human. Laminin alpha2 chain (LAMA2), however, is absent from muscles of some congenital muscular dystrophy patients and the dystrophia muscularis (dy/dy) mouse model. LAMA2 restoration was investigated following cell transplantation in vivo in dy/dy mouse. Allogeneic primary muscle cell cultures expressing the beta-galactosidase transgene under control of a muscular promoter, or histocompatible primary muscle cell cultures, were transplanted into dy/dy mouse muscles. FK506 immunosuppression was used in noncompatible models. All transplanted animals expressed LAMA2 in these immunologically-controlled models, and the degrees of LAMA2 restoration were shown to depend on the age of the animal at transplantation, on muscle pretreatment, and on duration time after transplantation in some cases. LAMA2 did not always colocalize with new or hybrid muscle fibers formed by the fusion of donor myoblasts. LAMA2 deposition around muscle fibers was often segmental and seemed to radiate from the center to the periphery of the injection site. Allogeneic conditionally immortalized pure myogenic cells expressing the beta-galactosidase transgene were characterized in vitro and in vivo. When injected into FK506-immunosuppressed dy/dy mice, these cells formed new or hybrid muscle fibers but essentially did not express LAMA2 in vivo. These data show that partial LAMA2 restoration is achieved in LAMA2-deficient dy/dy mouse by primary muscle cell culture transplantation. However, not all myoblasts, or myoblasts alone, or the muscle fibers they form are capable of LAMA2 secretion and deposition in vivo.

Age Factors↗
PubMed1988

Maternal-fetal interactions and the maintenance of HLA polymorphism.

There is some empirical evidence that a fetus with an HLA antigen not present in its mother has a higher survival than a fetus sharing antigens with its mother. We have developed both single locus and two-locus theoretical models to examine this mode of selection. First, this immunologically based model appears to have the potential to maintain many alleles at a single locus and to result in an excess of heterozygotes when selection is strong. Second, substantial gametic disequilibrium is maintained between alleles at two loci for this selection mode when recombination is that observed between HLA loci A, B, and DR. Overall, it appears that this mode of selection has the potential to strongly affect genetic variation in the HLA region.

Alleles↗
PubMed1997

T-cell transfer and cytokine/TCR gene deletion models in the study of inflammatory bowel disease.

Until recently there existed no appropriate immunological animal models for human inflammatory bowel diseases (IBD). Today a number of models, mostly in the mouse and rat, have proved useful in the study of several aspects of IBD, including the histopathology and the disease-inductive and -protective cell types, subsets and cytokines, for example CD4+ T cells, IFN gamma, IL-12, IL-2, IL-10 and TGF beta. Furthermore, these recent IBD models make it possible to examine various chemo- and immunotherapeutic approaches. This review focuses on IBD development in adoptive T-cell transfer models and in gene-deleted mice.

Animals↗
PubMed1996

Computer simulation and data analysis of effector-target interactions: the extraction of binding parameters from effector and target conjugate frequencies data by using linear and nonlinear data-fitting transformations.

Binding isotherms for effector-target conjugation when effector conjugate frequencies are measured by holding constant the number of effector cells and by varying the number of target cells are characterized by two parameters, the maximum effector conjugate frequency, alpha max, and gamma, which is related to the dissociation constant of the conjugates formed, K d. The suitability of four linear transformations of these binding isotherms, as well as nonlinear data-fitting techniques, to provide estimates of alpha max and gamma is discussed. The strength and weakness of these procedures were investigated by calculating alpha max and gamma from different sets of 100 or 500 replicate "experiments," which were generated by using an algorithm that provides noise contributions to the conjugate frequencies with gaussian distributed errors. Both unweighted and weighted data points were used in these calculations. A similar analysis can also be performed for binding isotherms in which target conjugate frequencies are measured at different values of effector cells by holding constant the number of target cells. In this case, the binding isotherms are characterized by two parameters, the maximum target conjugate frequency, beta max, and delta, which is also related to K d. The results obtained demonstrate that if the experimental conditions are chosen properly, linear transformations and nonlinear fitting techniques provide reliable estimates for the binding parameters. Not all procedures, however, provide estimates with the same accuracy, and special emphasis to this fact must be given if the binding assays are performed at low values of the number of effector cells.

Algorithms↗
PubMed1997

Lymphocyte homeostasis.

B- and T-lymphocyte populations have an independent homeostatic regulation of resting (B and T) and activated (B) or memory (T) cell compartments. This organization may provide an efficient mechanism to ensure simultaneously a first natural barrier of protection against common pathogens, the maintenance of immunological T-cell memory and a reservoir of repertoire diversity capable of dealing with new antigenic challenges.

Animals↗
PubMed2005

Regenerative capacity and the developing immune system.

Many components of the vertebrate immune system have evolved with dual, interrelated functions of both protecting injured tissues from infection and providing for tissue maintenance and repair of injuries. The capacity for organ regeneration, prominent among invertebrates and certain phylogenically primitive vertebrates, is poorly developed in mammals. We have proposed that evolution of the mammalian immune system has produced inflammatory cellular interactions at sites of injury which have optimized tissue defense and facilitated tissue repair, but that these improvements included concomitant loss of regenerative capacity. This chapter briefly reviews work in two regenerating systems: scar-free repair of fetal mammalian skin and regeneration of amputated limbs in larval frogs. In both organs the potential to regenerate anatomically and functionally complete new structures is lost gradually during ontogeny and this loss coincides with development of an immune system producing an inflammatory response in injured tissues. Failure of organ regeneration has long been associated with scarring or fibrosis and this phenomenon is a direct result of inflammatory interactions of immune cells and fibroblasts at sites of injury. Several aspects of immunity related to repair are reviewed, including the importance of antigen-presenting cells and lymphocytes, relevant cytokines and growth factors released by these and other cells, immune functions of extracellular matrix components, and immunological functions of fibroblasts. Skin repair in various transgenic mouse models has been especially informative. Further study of immune mechanisms associated with the loss of regenerative capacity in the skin and amphibian limb will be useful for efforts to promote mammalian organ regeneration.

Animals↗