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Query: UMLS:C0029713 (immaturity)
 4,335 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acquired immunodeficiency syndrome (AIDS) in infants has different clinical and immunological characteristics from adult AIDS because of immunological immaturity of the fetus and newborn when infection is produced. Differential diagnosis with primary immunodeficiency diseases, mainly with severe combined immunodeficiency and hypogammaglobulinemia is often difficult, but clinical, epidemiological and immunological data aid in establishing diagnosis. Repeated bacterial infections and abnormal antibody production are common in such children and gammaglobulin therapy is indicated to prevent them and avoid continuous immunological stimulation that viral replication and disease progression.
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PMID:[Diagnostic clinical and immunologic characteristics of infection by the human immunodeficiency virus in infants]. 335 37

Experimental host versus graft (HVG) disease is the fatal immunodeficiency syndrome which is induced in susceptible strains of inbred mice by the perinatal inoculation of related F1 hybrid spleen cells. The allogenic HVG reaction results in severe T-cell depletion, but hyperplasia of B cells, of which some are F1 donor in origin. To investigate the role of F1 donor B cells in the development of hyperglobulinemia in HVG mice which respond poorly to primary antigenic challenge, antibodies to horseradish peroxidase (HRP) of (T6 x RFM)F1 donor B-cell origin were used as markers for the engraftment of primed donor B cells in RFM hosts, and as sequential measures of the allogenic reaction on them. F1 donor B cells sensitized to HRP survived different stages of the HVG reaction after inoculation on Day 1 or Day 8 after birth. Tests for the anti-HRP antibody output of RFM host cells, and engrafted HRP-primed and unprimed (T6 x RFM)F1 donor cells suggested that the hyperglobulinemia seen in HVG mice was caused principally by antigen-primed, F1 donor B cells stimulated by the allogenic effect, with or without further exposure to the antigen(s) to which the donors had been sensitized prior to transplantation. The poor primary responses were attributed to the engraftment of the many donor B cells already committed, to the immunological immaturity of the host B cells, and to the lack of T-cell help for adult unprimed F1 donor B cells. Taken together with previous work, the data also suggest that antigen-primed donor B cells were engrafted in preference to equally histoincompatible donor T cells and unprimed donor B cells.
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PMID:Sensitized (T6 x RFM)F1 donor B cells contribute to hypergammaglobulinemia and to poor primary responses in RFM mice with allogenic host versus graft disease. 348 42

Development of cell-mediated immunity in young ruminants appears to be under the influence of the thymus. In sheep, prenatal removal of the thymus has little effect on postnatal growth of lambs. However, lambs are immunodeficient compared with normal controls, and they exhibit depressed delayed hypersensitive skin responses to antigens such as tuberculin purified protein derivative. Lymphopenia accompanying the immunodeficiency appears to be due to depletion of a particular population of T-cells (thymus derived) that have reduced response to mitogens and decreased numbers as the lamb matures. Young lambs are less responsive than adult sheep to vaccination with irradiated Trichostrongylus colubriformis larvae. The basis of this lowered responsiveness appears to be not only the immaturity of the cell-mediated immune response but also the segregation of the lambs into high and low responders. This immune responsiveness is possibly under the genetic control of the ovine major histocompatibility complex. It may be possible to select and breed sheep and cattle for responsiveness to vaccination against parasitic, viral, and bacterial diseases.
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PMID:Development of cell-mediated immunity in young ruminants. 388 81

There is a strong relationship between nutritional status and resistance to infection. This relationship must receive attention more especially as human being is young. Newborns and infants have some immunological immaturity in regard to systemic immunity as well as local (particularly intestinal), immune defense. Malnutrition is an aggravating factor vis a vis such an immunodeficiency. It modifies the regulating activities of the different lymphocyte populations, of the macrophages, of the complementary system. These disorders are bound to energy, proteins, vitamins and mineral deficiencies. But many metabolic phenomenons have still to be explored, as well as the effect of such a dysimmunity on immunization. Bowel epithelial cells, cross-roads between immunity and nutrition, seem to be the point we ought to select in order to dislocate the infection--malnutrition couple.
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PMID:[The nutritional immunodeficiency syndrome]. 392 2

Human T lymphocytes bear characteristic membrane antigens which allow for identification on these cells and their subpopulations with monoclonal antibody reagents directed against the specific cell-surface antigens. During a study of T lymphocyte subpopulations in a group of 41 infants from a high risk nursery, three of the seven black infants studied were found to be missing cells reactive with the monoclonal antibody OKT4 which identifies the helper-inducer subset of T cells. Immunological evaluation of these infants and study of their family members revealed that the OKT4 non-reactive lymphocytes reacted normally with another antibody, OKT4A, which also identifies the helper-inducer subset of T cells. The deficiency of the antigen recognized by the OKT4 antibody appeared not to reflect T cell immaturity and was not associated with obvious immunodeficiency. The OKT4 negative phenotype appeared to be transmitted in an autosomal recessive mode. Our studies suggest that heterozygosity for this phenotype is relatively common among the black population and that heterozygotes are not easily distinguishable from the random population on the basis of lymphocyte reactivity with the OKT4 monoclonal antibody.
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PMID:Ethnic heterogeneity in the distribution of the OKT4 antigen on lymphocytes: studies in three black families. 393 38

The neonatal period is a state of relative immunodeficiency during which newborns are particularly vulnerable to bacterial, protozoal, and viral infections. In addition, they localize infection poorly, mount a sluggish antibody response to injected antigens and are relatively anergic. Both in vivo and in vitro studies suggest that functional immaturity of neonatal macrophages may contribute to this immunologic hyporesponsiveness. Resistance to viral and bacterial infection and production of antibody can be enhanced in neonates by injection of adult macrophages. Specific functional defeats in newborns' monocytes have been demonstrated in their capacity to chemotax, to resist intracellular multiplication of virus and to effect antibody-dependent cell-mediated cytotoxicity towards virus-infected target cells. Monocytes from newborns also appear to present antigen poorly, and to co-operate with T-lymphocytes in the suppression of IgG-production by B cells.
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PMID:Mononuclear phagocytes in the newborn: their relation to the state of relative immunodeficiency. 635 60

Recipients of allogeneic bone marrow transplants are characterized by an immunodeficiency of varying intensity and duration. We have previously demonstrated the presence of in vivo activated suppressor T lymphocytes in immunodeficient patients with chronic graft-versus-host disease. To determine the basis of the immunodeficiency of transplant recipients early after transplantation, the lymphocytes of transplant recipients were analyzed phenotypically by E-rosette formation and staining with monoclonal antibodies (OKT-3, -6, and -8) and functionally by their blastogenic response to mitogens. Only 15% of transplant recipients' assays 0-3 months and 16% of assays 3-12 months following transplant were in the normal range. Transplant recipients during the first year after transplantation were characterized by an increased percentage (57%) of patients with a normal percentage of E-rosette-forming cells but reduced PHA responsiveness. In vitro coculture experiments demonstrated that their lack of PHA responsiveness was not due to the presence of in vivo activated suppressor cells or a decrease in mitogen-presenting cells. Staining with monoclonal antibodies revealed that the T lymphocytes from the majority of recipients at 0-3 months following transplantation contained a percentage of OKT8-positive cells greater than or equal to the percentage of OKT3-positive cells. This pattern (OKT8 greater than or equal to OKT3) was not found in the peripheral blood T lymphocytes of normal people but was found in 13 of 15 thymuses. Monoclonal staining with OKT6, a thymocyte-specific antibody, revealed positive staining of more than 10% of the peripheral blood leukocytes in the majority of recipients 0-3 months following transplantation, compared with only a few normals. We concluded that the circulating T lymphocytes of transplant recipients are phenotypically and functionally immature, and that their relative immaturity contributes to the transplant recipients' immunodeficiency.
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PMID:Immature T lymphocytes in the peripheral blood of bone marrow transplant recipients. 636 45

The immune system was studied in 30 cases of local infection (pneumonia) and 56 cases of generalized infection (sepsis). Predominantly children with immunologic deficiency of the humoral type (77% of the cases) characterized by unscheduled fatty transformation of the thymus, underdevelopment of B-zones of lymphoid organs, low level of IgM production and the lack of IgG and IgA production were found to die with pneumonia, whereas children with physiological immaturity of the immune system and in smaller numbers (41% of the cases) with deficiency of immunity of the cellular and phagocytic type as confirmed by immaturity of the thymic tissue or its dysplasia with hypoplasia of lymphoid organs died with sepsis. Immunological deficiency of the humoral type is accompanied by suppurative destructive lesions of the respiratory organs, immunodeficiency of the cellular and phagocytic type by necrotic changes in the septic focus and mucous membranes of the organs contacting the environment.
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PMID:[The immune system and its relation with infection process in children]. 660 38

Partial immaturity of the immunocompetent system is accounted for by the increased susceptibility to infections seen in human newborns. This immunodeficiency that includes specific and non-specific branches of immunity, affects both humoral and cellular components. Authors present a revision of the present knowledge, including their experience in this field.
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PMID:[Immunologic condition of the newborn (author's transl)]. 696 71

To study the efficacy of intravenous immunoglobulin in symptomatic infection with human immunodeficiency virus (HIV) we enrolled 35 patients with CD4 lymphocyte counts below 300/microliter in a randomized three-arm study. In addition to standard HIV treatment (e.g., zidovudine, aerosolized pentamidine), 13 patients were treated with 7.5 g and 11 with 40 g of a 7 S intravenous IgG preparation every 4 weeks over a period of 1 year. A control group of 11 patients remained on standard treatment. Clinical and laboratory parameters, including lymphocyte proliferation and in vitro immunoglobulin synthesis were evaluated prior to intravenous IgG administration. HIV-specific immunological abnormalities such as increased B-cell activation and B-cell immaturity were observed in all three study groups at the beginning of the study. Mitogen-induced lymphocyte proliferation was diminished. These disturbances were not influenced by intravenous IgG treatment. Further laboratory data and the course of the HIV infection (fever, antibiotic treatment, hospitalization, Candida and herpes simplex or cytomegalovirus infection) remained unchanged. Thus, our data with an observation period of 12 months do not support the use of intravenous IgG treatment in adult symptomatic HIV-infected patients with CD4 counts lower than 300/microliter.
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PMID:The use of intravenous immunoglobulins in symptomatic HIV infection. Results of a randomized study. 791 23


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