UMLS:C0029713 - FACTA Search

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

We examined 48 placentas of human immunodeficiency virus (HIV)-exposed pregnancies morphologically for HIV-specific changes and immunohistologically for the presence of HIV antigen and RNA. Findings were correlated to infectious states of the children and maternal risk factors. Few HIV antigen-positive Hofbauer cells and HIV RNA positive syncytiotrophoblast and Hofbauer cells were detected. HIV-positive cells in the placenta did not correlate with intrauterine infection and maternal immunologic parameters. Light microscopically, we found two changes: immaturity of the terminal villi and allantois vasculopathy. These changes, however, are not HIV specific. Our results show that vertical HIV transmission cannot be diagnosed by morphological examination of the placenta.
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PMID:Vertical human immunodeficiency virus transmission: a study of placental pathology in relation to maternal risk factors. 799 9

CD34 is expressed by essentially all human hematopoietic progenitors including cells of the megakaryocyte (MK) lineage. We have previously reported CD4 expression by some human MK (Blood 81:2,664, 1993). To study the role of maturation on CD4 expression by MK, we examined CD34+ bone marrow cells for their expression of CD41 (GPIIb-GPIIIa) and CD4 with specific monoclonal antibody (MoAb)-fluorochrome conjugates and for DNA polyploidization with propidium iodide or 7-aminoactinomycin D (7-AAD). Surprisingly, MK were at least 20-fold more common in the CD34+ progenitor pool (approximately 10%) than in the more mature CD34+ population (approximately 0.5%) of low density bone marrow cells. CD4 expression correlated with markers of immaturity in that CD4 was enriched among CD34+ cells, and the proportion of CD4+ MK declined with increasing ploidy. Almost all CD34+ polyploid ( > or = 8N) cells were CD4+. Despite these correlations with immaturity, CD34+CD4+ MK precursors were unable to produce MK colony-forming units (CFU-MK) when cultured under conditions that supported the growth of CFU-MK from CD34+CD4- MK lineage cells. MK became polyploid before the loss of either CD34 or CD4 expression. The presence of CD4 on these cells correlates with the onset of endomitotic reduplication and is associated with the loss of the ability of these cells to undergo normal mitotic division. The role of CD4 on immature MK as a differentiation antigen and/or receptor for the human immunodeficiency virus (HIV)-1 virus remains to be determined.
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PMID:Development of human megakaryocytes: I. Hematopoietic progenitors (CD34+ bone marrow cells) are enriched with megakaryocytes expressing CD4. 860 24

Job' syndrome and IgA immunodeficiency are a rare dysfunction of the immune system. In this work, we reported a case of a young woman who had recurrent episodes of bacterial infections in the urinary tract and genital, generalized erythematous eczematous patches and stomatitis of oral mucosa and fever. During the hospitalization, laboratory data showed high immunoglobulin IgE and low IgA levels. The T-lymphocyte presented a reduction of CD8+ cells. Tests of granulocyte function have showed a global deficit in the in vitro and in vivo chemotaxis. The correlation between these two clinic conditions is not completely clarified but it is possible to hypothesize that CD8+ lymphocytes produce an inhibition factor of chemotaxis. Job' syndrome is characterized by a selective reduction of CD8+ cells subpopulation which have an immunoregulatory function on the production of IgE by plasmacells. In the ipoIgA, an intrinsic inability of B-IgA cells to proliferate and to differentiate produce a defect in the IgA production. In these two clinic disorders there is an effective dysfunction of immune system. It is possible to hypothesize that an effective defect of CD8+ cells and an immaturity of B-cells may coexist in our patient. That justifies an abnormal production of Ig and a defect in granulocyte chemotaxis.
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PMID:[Job syndrome (hyper-IgE) and hypo-IgA. A rare association of immunodeficiencies]. 872 83

Severe viral infection in newborns has been attributed to immaturity of the immune system including a defect in natural killer cytotoxicity (NKC) and decreased production of cytokines that are important for natural killer (NK) function. We investigated the induction of interferon (IFN)-gamma and activation of NK activity in adult and cord blood mononuclear cells (BMC) after IL-12 treatment. The levels of mRNA in these BMC were measured by Northern blot and reverse transcription-polymerase chain reactions using primers specific for IFN-gamma. The levels of IFN-gamma protein were measured by ELISA. In the absence of IL-12, only adult BMC spontaneously produced low levels of IFN-gamma. After IL-12 treatment, induction of IFN-gamma expression was detected as early as 4 h in both cord and adult BMC. Both cord and adult cells showed similar levels of IFN-gamma mRNA and protein expression in response to IL-12 at a concentration as low as 10 U/mL. In contrast, upon phorbol ester and ionomycin treatment, adult BMC produced more IFN-gamma mRNA than cord BMC. In a 51Cr release assay with human immunodeficiency-infected H9 cells as indicators, both cord and adult cells responded to IL-12 induction of NKC. Our findings demonstrate that cord BMC are capable of responding to IL-12 stimulation, competent in synthesizing IFN-gamma, and able to mount NKC. Thus, it appears that the deficiency in IFN-gamma production or NKC in cord cells is not due to an inherent defect in IL-12 response of the cord cells.
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PMID:Interleukin-12 induces interferon-gamma expression and natural killer cytotoxicity in cord blood mononuclear cells. 882 1

Neurological dysfunction has been shown to be associated with human immunodeficiency virus (HIV) infection. The incidence of these abnormalities is greater in HIV-infected children when compared with adults, and the patterns of neurological disease are also known to differ from those observed in the adult population. The reasons for these differences are unclear but are most likely related to the immaturity of the host's immune and central nervous systems at the time of infection. This is thought to be particularly true for infants infected with HIV prenatally. To examine these questions, the brains of fetal rhesus macaques that were infected with SIVmac251 at various time points in utero were examined. Direct fetal inoculations were performed on gestational day (GD) 65 (n = 8; early second trimester), GD 110 (n = 4; early third trimester) and GD 130 (n = 2; mid third trimester), with harvest of fetal tissues on GD 80, 100, 130, or 145. Eleven sham controls were included with harvest at correlative time points. Specimens were examined by routine histology, immunohistochemistry, and in situ hybridization to localize viral antigens and SIV nucleic acid. Histologically, scattered glial nodules, spongiosis, and mineralization were found in the basal ganglia and deep white matter in 4 of the 14 fetuses (3 inoculated on GD 65 and one on GD 110). These fetuses and those without histological lesions had viral nucleic acid and SIV antigen in the stroma of the choroid plexus, meninges, and external granular layer of the cerebellum and in columns of cells in the cortical plate. In contrast to juvenile and adult macaques, very few SIV-positive perivascular mononuclear cells were present. These findings suggest that SIV has a different distribution in the brain of fetal macaques after direct infection when compared with adult or juvenile animals. Furthermore, the results of these studies suggest that differences in neurological disease between pediatric and adult patients with acquired immune deficiency syndrome are most likely related to the time of infection.
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PMID:Localization of simian immunodeficiency virus nucleic acid and antigen in brains of fetal macaques inoculated in utero. 886 58

Since 1976, we have performed more than 240 fetal tissue transplants (FLTs) to treat 63 patients with severe immunodeficiency disease (IDD), with inborn errors of metabolism (IEM), or with severe aplastic anemia. In both IDD and IEM, FLT into postnatal recipients has demonstrated beneficial effects (67%) of the patients were either cured or improved significantly). In 1988, we developed in utero FLT into human fetuses, taking advantage of the immunological tolerance of young fetuses. The transplants have involved fetuses suffering from various diseases at 12-28 weeks postfertilization with 2 of the 6 cases eventually resulting in abortion. With the 4 other fetuses, a favorable outcome was observed: 3 children are now more than 4 years old, and are alive and well with evidence of engraftment, reconstitution of immunity, and partial correction of beta zero thalassemia. In the fourth case, the fetus is alive and well and birth is expected soon. In utero transplantation of stem cells is a therapy with remarkable advantages: (a) tolerance induction due to the immune immaturity of the host, (b) lack of graft-versus-host disease due to the immaturity of the donor, (c) ideal isolation of the fetus in the maternal uterus, and (d) an optimal environment for donor fetal cell development in the vicinity of host fetal cells and growth factors.
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PMID:Treatment of human fetuses and induction of immunological tolerance in humans by in utero transplantation of stem cells into fetal recipients. 887 6

Although not 'ideal', xenograft models of human hematopoiesis have proved to be extremely useful experimental systems for the study of the in vivo engraftment/proliferation potential of human hematopoietic stem/progenitor cells (HSC). Among these, the human/sheep xenograft model is unique in several respects. This model takes advantage of fetal immunologic immaturity and developing 'homing' spaces in the fetal bone marrow to obtain donor HSC engraftment in normal recipients without marrow conditioning. This avoids both the possible stromal abnormalities associated with irradiation- and/or chemotherapy-induced immunodeficiency which may limit human HSC engraftment or long-term maintenance of human hematopoiesis, and the use of genetically deficient hosts which may result in restricted donor cell expression. In the human/sheep xenograft model, human HSC (1) colonizes the bone marrow, (2) persists for many years, (3) is capable of multilineage differentiation, (4) retains its ability to respond to human cytokines, and (5) retains its ability to engraft/differentiate in secondary recipients. Another unique aspect of the sheep model is its large size; this permits repeated evaluation of human cell activity in the same chimeric sheep over long periods. The model appears to discriminate between the different populations of human HSC and exhibits a degree of sensitivity that suggests this in utero approach may serve as a biologically relevant model for the identification, characterization, and study of the in vivo potential of human HSC from available sources.
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PMID:The human/sheep xenograft model: a large animal model of human hematopoiesis. 893 32

Various authors have reported a high rate of human papillomavirus (HPV) infection and HPV-related neoplasias in human immunodeficiency virus (HIV)-seropositive women. On the other hand, young women are most susceptible to cervical infection because of immaturity of the cervix, as it appears that HPV has more access to the basal cells of the differentiating epithelium. The purpose of the present work was to study cervical smears of 82 adolescent HIV-seropositive women (13-21 years of age) to search for cytological evidence of cervical intraepithelial neoplasias. Twenty-one cases showed characteristic features of HPV infection and squamous intraepithelial lesions (SIL; 25.6%). Sixteen cases aged from 17 to 21 years (mean age 19.5 years) had low-grade SIL (LSIL; 19.5%) and five cases aged from 18 to 21 years (mean age 20.2 years) had high-grade SIL (HSIL; 6.1%). There was no significant difference between the mean age of patients with LSIL and HSIL. Two cases had atypical squamous cells of undetermined significance (ASCUS). In the present work it was found that HIV-seropositive adolescents have a high risk for preneoplastic lesions of the cervix (25.6%) as well as a high incidence of more aggressive lesions (6.1% of HSIL) when compared to the general population of adolescents. As it can be assumed that, if the age of acquisition of the infection in both groups (in the general population and HIV-seropositive women) is the same, it is probable that HIV infection in adolescents not only increases the frequency of HPV infections but also facilitates the evolution to more aggressive preneoplastic lesions of the cervix due to HPV.
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PMID:Squamous intraepithelial lesions in cervical smears of human immunodeficiency virus-seropositive adolescents. 948 35

Newborn human infants, particularly those born prematurely, are susceptible to infection with a variety of microorganisms. We questioned whether limitations in the T cell repertoire contribute to the neonatal immunocompromised state. To describe developmental changes of the T cell repertoire, cDNA segments corresponding to third complementarity regions (CDR3) of human umbilical cord blood T cell receptors (TCR) from 24-41-wk gestational age were amplified with TCR family-specific probes. The resulting amplified CDRs were visualized by fingerprinting and single strand conformation polymorphism (SSCP) analysis. At 24-wk gestation there were no limitations in TCRBV family usage, and the degree of CDR3 size heterogeneity was not different from the adult. However, earlier in gestation, CDR3s were shorter for all families and gradually increased in size until term. The extent of oligoclonal expansion observed in cord blood was greater than in adult peripheral blood (p = 0.03). T cell oligoclonal expansion was greatest at 29-33-wk gestation and declined toward term. Expansions were detectable in both CD4+ and CD8+ subpopulations. Our findings indicate that the genetic mechanisms of repertoire diversification appear intact as early as 24 wk of gestation, but repertoire diversity is limited as a result of smaller CDR3 sizes. In addition, there was a developmentally regulated progression of oligoclonally expanded T cells. These differences in the TCRBV repertoire add to the body of evidence demonstrating immaturity of the neonatal immune system. However, the role that these subtle differences are likely to play in the relative immunodeficiency of the neonate remains to be determined.
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PMID:T cell receptor repertoire diversity and clonal expansion in human neonates. 950 80

Neonates face a high risk of infection because of the immaturity of their immune systems. Although the transplacental transfer of maternal antibodies to the fetus may convey improved postnatal immunity, this transfer occurs late in gestation and may fail to prevent in utero infection. Both fetal immunization and in utero exposure to antigen can result in a state of immunologic tolerance in the neonate. Tolerance induction of fetal and premature infant lymphocytes has become a paradigm for neonatal responsiveness. However, fetal IgM responses have been demonstrated to maternal immunization with tetanus toxoid and to congenital infections such as rubella, toxoplasma, cytomegalovirus and human immunodeficiency virus. Moreover, 1-week-old infants can respond to standard pediatric vaccination, and neonates immunized with polysaccharide antigens do not develop immunologic tolerance. Here, direct immunization of the baboon fetus with recombinant hepatitis B surface antigen produced a specific fetal IgG antibody response. No specific maternal antibody response was detected, eliminating the possibility of vertical antibody transmission to the fetus. Some infants also responded to later vaccinations with hepatitis B surface antigen, indicating that no immunological tolerance was induced by prior fetal immunization. These results characterize the ability of the fetal immune system to respond to in utero vaccination. We demonstrate that active fetal immunization can serve as a safe and efficient vaccination strategy for the fetus and neonate.
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PMID:Fetal immunization of baboons induces a fetal-specific antibody response. 1020 33

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