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Results for “Immunologic Deficiency Syndromes”

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At least 199 records · Page 11Linked to original sources
PubMed1994

Age-sensitive T cell phenotypes covary in genetically heterogeneous mice and predict early death from lymphoma.

We have assessed several age-sensitive indicators of immune status in young (i.e., 6 to 11-month-old) mice of a genetically heterogeneous population to see if these varied in parallel and to determine if one or more of the status indices predicted life span or cancer incidence. We report that the number of memory (i.e., CD44hi) T cells within the CD8 subset is correlated with number of memory cells in the CD4 population, and inversely correlated with the number of naive (i.e., CD45RBhi) CD4 cells at both 6 and 11 months of age, suggesting that the conversion of naive to memory cells may occur at similar rates in both T cell subsets. Mice that ranked high in the proportion of memory T cells (within the CD4 and CD8 pools) at 6 months of age tended to retain their ranking at 11 months, suggesting that the pace or extent of memory cell formation may be a consistent trait that distinguishes mice at least within a genetically heterogeneous population. Mice that at 6 months of age exhibited high levels of CD4 or CD8 memory T cells, low levels of naive CD4 cells, or low levels of T cells able to proliferate in response to Con A and IL-2 were found to be significantly more likely than their littermates to die within the first 18 months of life. Cases of follicular cell lymphoma, lymphocytic and lymphoblastic lymphoma, and hepatic hemangiosarcoma were seen within the group of mice dying at early ages.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1983

Diffuse pulmonary gallium accumulation with a normal chest radiogram in a homosexual man with Pneumocystis carinii pneumonia. A case report.

A homosexual man with A.I.D.S. (acquired immunologic deficiency syndrome) and pneumocystis infestation was found to have diffuse Ga-67 uptake in the lungs with a coincident negative chest x-ray. While Ga-67 accumulates diffusely in the lungs in a variety of conditions, the present case is the first described in a patient with A.I.D.S. in which Ga-67 was positive before roentgenographic abnormalities were demonstrated. Thus, the use of Ga-67, when A.I.D.S. is suspected, could help establish a diagnosis more promptly.

Acquired Immunodeficiency Syndrome↗
PubMed1993

Mechanisms in immune recovery after bone marrow transplantation. Management of posttransplant immune deficiency.

PURPOSE: Bone marrow transplantation usually entails the ablation of the recipient's immune system. The recovery of immunity post-marrow transplantation is a complex process dependent on a number of pre- and posttransplant factors. This knowledge has led to the development of novel approaches to supportive care of the patient, as well as to methods of augmenting immunity. DESIGN: Hematopoietic growth factors are now used to speed neutrophil recovery. Certain lymphokines are being investigated for the enhancement of cell-mediated immunity, and gamma globulin preparations are used to support the deficiency in humoral immunity. CONCLUSIONS: This review summarizes the basic concepts of immune reconstitution posttransplant and discusses some of the therapeutic interventions that have been investigated. In addition, some general recommendations are offered regarding supportive care.

Anti-Infective Agents↗
PubMedDate not supplied

You can make a difference in the administration of intravenous immunoglobulin therapy.

Intravenous immunoglobulin is a preparation of immune globulins containing antibodies given intravenously to patients with both inherited and acquired immunodeficiency disorders, such as primary immune deficiency diseases, idiopathic thrombocytopenia purpura, chronic lymphocytic leukemia, and bone marrow transplantation. This article discusses immune globulin products, routes of administration, and the role of the infusion nurse in the administration of intravenous immunoglobulin to the patient.

Bone Marrow Transplantation↗
PubMed2004

Cytokines and immunodeficiency diseases: critical roles of the gamma(c)-dependent cytokines interleukins 2, 4, 7, 9, 15, and 21, and their signaling pathways.

In this review, we discuss the role of cytokines and their signaling pathways in immunodeficiency. We focus primarily on severe combined immunodeficiency (SCID) diseases as the most severe forms of primary immunodeficiencies, reviewing the different genetic causes of these diseases. We focus in particular on the range of forms of SCID that result from defects in cytokine-signaling pathways. The most common form of SCID, X-linked SCID, results from mutations in the common cytokine receptor gamma-chain, which is shared by the receptors for interleukin (IL)-2, IL-4, IL-7, IL-9, IL-15, and IL-21, underscoring that X-linked SCID is indeed a disease of defective cytokine signaling. We also review the signaling pathways used by these cytokines and the phenotypes in humans and mice with defects in the cytokines or signaling pathways. We also briefly discuss other cytokines, such as interferon-gamma and IL-12, where mutations in the ligand or receptor or signaling components also cause clinical disease in humans.

Animals↗
PubMed2006

Early indicators of immunodeficiency in adults and children: protocols for screening for primary immunological defects.

Early recognition of primary immunodeficiency is essential to reduce morbidity and mortality, and yet failure to recognize these conditions is still a major problem for clinicians around the world. The problem is that general practitioners, physicians and paediatricians lack familiarity with these rare disorders, and lack guidance regarding the appropriate use of immunological investigations. A working party from the European Society for Immunodeficiencies (ESID) has published screening protocols for these rare disorders, which aim to help select which tests should be done in which patients. The success of these proposals will depend on all immunologists disseminating this information in a format that is suitable for the busy generalist, who may not be familiar with these immunological tests and concepts. Laboratories should expect increasing requests for these screening investigations, and should make themselves familiar with these protocols so that appropriate second-line investigations can be arranged in a timely fashion. Speedy and effective communication between the laboratory and clinician is essential, and clinically interpreted reports are mandatory. Although these protocols are part of a screening process, their effectiveness in practice remains to be established, and further refinement will be required over time. The early involvement of the clinical immunologist in cases of suspected immunodeficiency is key.

Adult↗
PubMed2006

Patient-centred screening for primary immunodeficiency: a multi-stage diagnostic protocol designed for non-immunologists.

Efficient early identification of primary immunodeficiency disease (PID) is important for prognosis, but is not an easy task for non-immunologists. The Clinical Working Party of the European Society for Immunodeficiencies (ESID) has composed a multi-stage diagnostic protocol that is based on expert opinion, in order to increase the awareness of PID among doctors working in different fields. The protocol starts from the clinical presentation of the patient; immunological skills are not needed for its use. The multi-stage design allows cost-effective screening for PID within the large pool of potential cases in all hospitals in the early phases, while more expensive tests are reserved for definitive classification in collaboration with an immunologist at a later stage. Although many PIDs present in childhood, others may present at any age. The protocols presented here are therefore aimed at both adult physicians and paediatricians. While designed for use throughout Europe, there will be national differences which may make modification of this generic algorithm necessary.

Adult↗
PubMed1989

Present status of tumor immunology in clinical gynecology.

The function of the immune system is to protect the body from damage caused by invading microorganisms, that is, bacteria, viruses, fungi, and parasites. The humoral mechanism functions through plasma cells producing antibodies that control bacterial infections. Viruses, fungi and parasites are controlled through the thymus dependent T lymphocytes. It is now clear that cancers also invoke immunologic reactions in their hosts. Cancer cells, like bacteria and viruses have their own characteristic antigens. An antigen is defined as a substance, usually a protein or polysaccharide, that the body recognizes as foreign, and to whose presence it reacts by forming antibodies. Antigenic differences represent the first known qualitative distinction between cancer cells and their normal counterparts. These qualitative differences between normal and cancer cells had escaped other methods of investigation, but were revealed by immunological techniques that take advantage of the extraordinary power of discrimination of the immune defense mechanism itself. This mechanism is capable of distinguishing even minute differences between protein molecules, probably one different amino acid in a chain of several thousand. Burnet's clonal selection theory has become the central dogma of immunology. It can be summarized by saying that lymphocytes have been destined from time immemorial to identify a specific antigen. When the lymphocyte encounters that antigen it becomes a sensitized lymphocyte, and on contact with similar antigens again produces an immune response including the production of very potent pharmacologic agents called lymphokines. Immunodeficiency diseases are identified by increased frequency of infections in patients. The impaired immunity decreases the patient's protection against developing a malignancy. Autoimmunity is the reaction of the immune system against the body's own tissue.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2006

DNA damage and tumor surveillance: one trigger for two pathways.

Biological evolution ensures that several backup mechanisms always exist to prevent the failure of cellular processes of critical importance for life. This notion applies to processes aimed at preventing cancer development. Recent research suggests that the DNA damage response, activated in one of the earliest cellular responses to transformation, may elicit two independent tumor surveillance mechanisms. The first, and most well known, is activation of the proapoptotic molecule p53 and subsequent cellular suicide. The second, reported in a recent study, is induction of the expression of ligands for the activating immune receptor NKG2D. That DNA damage induces two independent tumor surveillance responses demonstrates how one tumor surveillance mechanism may be assisted by another to secure efficient protection against early tumorigenesis. The results also support the immunosurveillance theory of cancer and suggest that it may operate at very early stages of tumorigenesis.

Animals↗
PubMed1990

Characterization of the immunodeficiency of RIIIS/J mice: immune response to polysaccharide antigens.

RIIIS/J mice lack an autosomal dominant gene(s) that influences the magnitude of the antibody response to several polysaccharide antigens of bacterial origin. Low responsiveness is demonstrable whether polysaccharide is administered as a T-helper-cell-independent or -dependent antigen conjugated to an immunogenic carrier; however, RIIIS/J mice make good anti-hapten antibody responses to haptenated polysaccharides. The low antibody responses of RIIIS/J mice to type III pneumococcal polysaccharide do not appear to be the results of an imbalance in the activity of regulatory T lymphocytes. Compared with other strains of mice, RIIIS/J mice elicit low antibody responses to lipopolysaccharide (LPS). They do not develop a cyclic primary or secondary antibody response to Escherichia coli O113 LPS; the latter is not due to a lack of mitogenic response to E. coli O113 LPS. They also produce auto-anti-idiotypic antibody after being immunized with trinitrophenyl-Ficoll.

Animals↗
PubMed1987

Immunological surveillance against DNA-virus-transformed cells: correlations between natural killer cell cytolytic competence and tumor susceptibility of athymic rodents.

Adenovirus type 2 (Ad2)-transformed hamster and rat cells are susceptible to lysis by natural killer (NK) cells from the host of origin and are nontumorigenic in immunocompetent hamsters and rats, respectively. These NK-cell-susceptible, virus-transformed cells are, however, highly tumorigenic in athymic (nude) mice--animals with intact NK-cell responses. In vitro lysis of these xenogeneic, Ad2-transformed cells by nude-mouse NK cells was found to be defective. In contrast, Ad2-transformed hamster and rat cells were highly susceptible to lysis by nude-rat NK cells. Furthermore, xenogeneic, Ad2-transformed hamster cells were nontumorigenic in nude rats unless the NK-cell responses of the challenged animals were compromised. The results of the nude-rat studies show that thymus-dependent, cytotoxic T-lymphocyte-mediated, host cellular immune responses are not essential for rejection of xenogeneic cells transformed by nononcogenic Ad2. The data suggest instead that immunologically nonspecific host cellular immune responses, such as those mediated by NK cells, are sufficient for rejection of Ad2-transformed cells. These results indicate that biologically important differences exist in the NK-cell-mediated defenses mounted by nude mice and nude rats against transformed cells that may account for the different patterns of tumor induction by various neoplastic cell types in these athymic animals.

Adenoviridae↗
PubMed1988

Adoptive immunotherapy of murine cytomegalovirus adrenalitis in the immunocompromised host: CD4-helper-independent antiviral function of CD8-positive memory T lymphocytes derived from latently infected donors.

The ability of memory T lymphocytes derived from latently infected mice to control murine cytomegalovirus disease in the immunocompromised host was studied by adoptive transfer experiments. At a stage of pathogenesis when virus had already colonized target tissues, a therapeutic antiviral function could be ascribed to the CD8+ subset. This in vivo function was not restricted to sites in which intravenously infused lymphocytes usually are trapped or home in, such as the lungs or the spleen, respectively, but was also evident in the adrenal glands, a site to which antiviral effector cells have to specifically migrate. Specific infiltration of adrenal gland cortical tissue by donor-derived CD8+ memory T lymphocytes was demonstrated. CD4+ memory T lymphocytes had no antiviral effect by themselves and also were not required for the function of the CD8+ effector cells in this short-term immunotherapy model. These findings should help settle the debate about which subset of T lymphocytes comprises the effector cells that can directly control cytomegalovirus infection in the murine model system.

Adrenal Gland Diseases↗