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Results for “Immunologic Deficiency Syndromes”
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[Diseases of the lung and respiratory tract in disorders of immunodeficiency in childhood and adolescence].
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[B cell function and its evaluation].
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Human cytomegalovirus-associated immunosuppression is mediated through interferon-alpha.
Human cytomegalovirus (HCMV) infections are commonly associated with a generalized immunologic hyporesponsiveness. The present study was designed to evaluate the potential mechanisms of HCMV-associated immunosuppression. In our initial experiments, monocytes in peripheral blood mononuclear cells (PBMCs) exposed to cell-free HCMV appeared morphologically less differentiated than monocytes in PBMCs exposed to a mock preparation. These morphologic changes were closely correlated with a decrease in monocyte oxidative activity and occurred under noncytopathic conditions. HCMV-associated suppression of monocyte differentiation did not require virus replication, occurred in PBMCs from either HCMV seropositive or seronegative donors, and required HCMV interaction with the nonadherent cells. An HCMV-induced soluble factor was found to not only reproduce the identical changes in purified monocytes but to inhibit the phagocytic activity of these cells. Additionally, the HCMV-induced factor accounted for a generalized defect in the ability of PBMCs to proliferate in response to mitogens and recall antigens. In subsequent experiments, interferon-alpha (IFN-alpha) was identified as the soluble factor involved in these immunosuppressive effects. Thus, PBMCs, when exposed to HCMV, produce a soluble factor, identified as IFN-alpha, that appears to be an important mediator of immunosuppression associated with HCMV infection.
[The importance of the immunogram for the prognosis of the course of odontogenic inflammatory diseases and of the performance of immunotherapy].
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B-cell-deficient mice develop experimental allergic encephalomyelitis with demyelination after myelin oligodendrocyte glycoprotein sensitization.
Myelin oligodendrocyte glycoprotein (MOG) induced experimental allergic encephalomyelitis (EAE) is an animal model for the central nervous system disease multiple sclerosis (MS). The roles of individual components of the immune system have not been completely defined in the mouse model, and to determine the role of B cells and Abs in the induction of EAE and demyelination, B cell-deficient muMT (H-2b) mice were immunized with MOG peptide 35-55. The muMT mice were susceptible to MOG-induced EAE and developed a chronic sustained disease, with inflammatory lesions and primary demyelination in the spinal cord, brain, and optic nerves, similar to that seen in wild-type C57BL/6 mice. The inflammatory cells in the central nervous system of muMT mice included both activated and memory T cells and macrophages. The data suggest that B cells and Abs are not necessary for primary demyelination in MOG-induced EAE in mice.
CD40 ligand is pivotal to efficient control of virus replication in mice infected with lymphocytic choriomeningitis virus.
CD40 ligand (CD40L) is an important molecule that is known to be involved in T-B collaboration and certain aspects of cell-mediated immunity. However, its role in antiviral immunity has not been clearly defined as of yet. Therefore, mice with a targeted defect in the gene encoding this molecule were infected with one of two strains of lymphocytic choriomeningitis virus differing markedly in their capacity to spread in the host. Infection with lymphocytic choriomeningitis virus is initially controlled primarily by CD8+ effector cells, whereas long-term immune surveillance also depends upon CD4+ cells and B cells. Our results reveal that the primary activation, clonal expansion, and differentiation of CD8+ T cells does not require expression of CD40L. However, lack of expression results in rapid impairment of CTL responsiveness and failure to permanently control virus replication. This happens not only in mice infected with the rapidly spreading virus strain but also at a late stage in mice infected with the strain of more limited potential for spreading. In the latter mice, virus replication is initially controlled very efficiently, but high levels of virus can be detected in the blood and internal organs approximately 6 mo after virus inoculation. Since the impairment of immune function seems to be more pronounced in CD40L-deficient mice than in mice lacking either CD4+ cells or B cells, these results indicate that CD40L is pivotal to sustain efficient antiviral immune surveillance, including CD8+ T cells, and suggest that CD40L is critically involved in cellular interactions in addition to T-B cooperation.
Combination chemotherapy and IL-15 administration induce permanent tumor regression in a mouse lung tumor model: NK and T cell-mediated effects antagonized by B cells.
Previous studies have demonstrated that IL-15 administration after cyclophosphamide (CY) injection of C57BL/6J mice bearing the i.m. 76-9 rhabdomyosarcoma resulted in a significant prolongation of life. In the present study, we investigated the immune response against the 76-9 experimental lung metastases after CY + IL-15 therapy. Administration of CY + IL-15, but not IL-15 alone, induced prolongation of life and cures in 32% of mice bearing established experimental pulmonary metastases of 76-9 tumor. The CY + IL-15 therapy resulted in increased levels of NK1.1+/LGL-1+ cells, and CD8+/CD44+ T cells in PBL. In vitro cytotoxic assay of PBL indicated the induction of lymphokine-activated killer cell activity, but no evident tumor-specific class I-restricted lytic activity. Survival studies showed that the presence of NK and T lymphocytes is necessary for successful CY + IL-15 therapy. Experiments using knockout mice implied that either alphabeta or gammadelta T cells were required for an antitumor effect induced by CY + IL-15 therapy. However, mice lacking in both alphabeta and gammadelta T cells failed to respond to combination therapy. Cured B6 and alphabeta or gammadelta T cell-deficient mice were immune to rechallenge with 76-9, but not B16LM tumor. B cell-deficient mice showed a significant improvement in the survival rate both after CY and combination CY + IL-15 therapy compared with normal B6 mice. Overall, the data suggest that the interaction of NK cells with tumor-specific alphabeta or gammadelta T lymphocytes is necessary for successful therapy, while B cells appear to suppress the antitumor effects of CY + IL-15 therapy.
Lung in acquired immune deficiency syndrome: infectious and immunological status assessed by bronchoalveolar lavage.
Bronchoalveolar lavage (BAL) has been performed in 63 patients with acquired immune deficiency syndrome (AIDS) and 20 patients with chronic generalized lymphadenopathy (CGL) for the diagnosis of lung opportunistic infections and analysis of immune effector cells of the lower respiratory tract. In patients with AIDS, Pneumocystis carinii was found in 63%. Cytomegalovirus (CMV) pneumonia was assessed by viral cultures of BAL fluid and microscopic examination: CMV was found in 62% and 39% respectively. Mycobacteria were encountered in 22% of cases. Altogether BAL yielded at least one opportunistic agent in 94% of patients who presented with clinical and/or radiographic pulmonary involvement, and in 80% of patients who presented with fever only. Conversely BAL was negative in all patients with CGL, except one positive CMV culture. Analysis of BAL cells revealed an increased cellularity in AIDS and CGL patients with normal numbers of alveolar macrophages. Alveolar lymphocytes were surprisingly increased in most patients with AIDS (mean 26.1 +/- 21.9%; range 1-76%) and CGL (mean 26.6 +/- 22.6%; range 3-76%) with criteria of activation contrasting with the blood lymphopenia. Evaluation of lung lymphocyte phenotypes revealed a marked decrease in T4 cell percentages, specially in AIDS, whereas the large majority of alveolar lymphocytes expressed the T8 phenotype. We conclude that BAL is a very reliable means for diagnosis of opportunistic lung infections and give interesting prospects to study local immunity in patients with AIDS and CGL.
The radiology corner: the small bowel in immunoglobulin deficiency syndromes.
Recent advances in immunology have permitted recognition of a group of patients who have gastrointestinal manifestations as part of an immunoglobulin deficency syndrome. Such immunoglobulin deficiency may be primary or may be secondary to a variety of diseases. We have classified and described the small bowel roentgen features associated with the various immunoglobulin deficiency syndromes as follows: 1. the sprue pattern, as seen in hypogammaglobulinemic sprue and in Ig-A deficient sprue; 2. multiple nodular defects; 3. inflammatory changes secondary to giardiasis, associated with immune deficiency diseases; 4. thickening of the small intestinal folds, as seen in the plasma cell dyscrasias, lymphoma, intestinal lymphangiectasia and amyloidosis.
[On the immunology of the antibody deficiency syndrome].
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[Secondary antibody deficiency syndrome].
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[CONTRIBUTIONS ON THE CLINICAL ASPECTS AND IMMUNOLOGY OF THE ANTIBODY DEFICIENCY SYNDROME].
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Hyper immunoglobulin M syndrome due to CD40 deficiency: clinical, molecular, and immunological features.
CD40 is a member of the tumor necrosis factor receptor family, which is expressed by a variety of cells including B cells, macrophages, dendritic cells, and other nonimmune cell types. CD40 activation is critical for B-cell proliferation, immunoglobulin (Ig)-isotype switching, and germinal center formation. In physiological conditions, the activation of CD40 occurs by binding to its natural ligand, CD154, which is expressed on activated T cells. The in vivo critical role of CD40-CD154 interaction on B-cell differentiation and isotype switching is provided by the discovery that mutations in either CD40 or CD154 gene cause the hyper IgM syndrome, termed HIGM3 or HIGM1, respectively, characterized by very low levels of serum IgG, IgA, and IgE, with normal or elevated IgM, associated with a defective germinal center formation. Originally considered humoral primary immunodeficiencies, the clinical features and the defect of T-cell priming, resulting from a defective T-B cell or dendritic cell interaction, is now considered as combined immunodeficiencies. In this article, we present a comprehensive overview of the clinical, genetic, and immunological features of patients with hyper IgM syndrome due to CD40 mutations.
Acquired immune deficiency syndrome (AIDS): speculations about its etiology and comparative immunology.
Acquired immune deficiency syndrome (AIDS) in many aspects resembles formerly recognized immune deficiencies, but in its complexity and presumed viral etiology, it is a unique entity. Examples of overlapping features of AIDS and immune defects, infectious complications, and neoplasms are discussed. It is not known what are the exact underlying mechanisms that permit or prohibit infectious and neoplastic complications among the immunodeficiency syndromes compared, but both overlapping and differing features of these entities are significant enough to hold a clue for future understanding. AIDS resembles feline leukemia as this latter syndrome was described 10 years ago. The retrovirus causing feline leukemia is highly immunosuppressive; preleukemic and viremic cats often succumb to opportunistic infections. If patients with early AIDS harbor retroviruses related to the human T cell leukemia virus in their organs (lymph nodes, bone marrow), serotherapy with monoclonal antibodies directed to this virus may stop and reverse the severe immunosuppression, thus preventing the development of opportunistic infections.
[Asplenism and hyposplenism as an immune deficiency syndrome].
The spleen has vital immunological functions (including the clearance of pathogenic microorganisms, the synthesis of antibodies and the provision of opsonins), which cannot be completely taken over by other organs in the case of hypo- or asplenism. Deficiency or absence of splenic activity, as it occurs for instance in sickle cell anemia, in congenital asplenia or after splenectomy, consequently entails complex immunological defects, which in their turn result in an increased susceptibility to severe bacteremia. Preventive measures, such as antibiotic prophylaxis, pneumococcal vaccination and detailed instruction of the patients and their families, are recommended in order to reduce the incidence of these life-threatening infections fatal to at least 1.4% of all splenectomized children.
[Histopathology of the antibody deficiency syndrome].
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[The antibody deficiency syndrome (ADS)].
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