Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0029713 (immaturity)
 4,335 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Three-color automated flow cytometry was carried out on peripheral blood CD4+ and CD8+ T-lymphocytes of 42 HIV-positive patients using tri-color anti-CD4 or anti-CD8, phycoerythrin-anti-CD38, and fluorescein-anti-HLA-DR, mAbs to elucidate further the T-cell activation hypothesis recently proposed to explain CD4+ T-cell abnormalities observed during HIV infection. CD4+ CD38+ T-cells constituted the major part of circulating CD4+ T-cells in HIV-infected patients and their HLA-DR molecule positivity increased as their disease progressed. The level of CD38 and HLA-DR expression on CD4+ T-cells was positively correlated to that of CD8+ T-cells and to the level of beta 2-microglobulin. Next, to determine whether CD38 expression was associated with a selective expansion or deletion of V beta gene-defined subsets, we compared the V beta gene frequencies between CD38+ and CD38- T-cells from HIV-infected CDC stage II patients using 13 mAbs specific to V beta families. While selective expansion of certain V beta families was observed in CD4+ and CD8+ T-cells the T-cell receptor V beta subset distribution was similar among CD38+ and CD38-, CD4+ and CD8+ T-cells, suggesting that CD38+ expression was either independent of an HIV-encoded antigen-driven process or rather indicative of T-cell immaturity. It is proposed that the phenotype of circulating CD4+ and CD8+ T-cells of HIV-infected patients is a feature of two different mechanisms: (i) an in vitro activation state responsible for increased DR expression and selective expansion of V beta gene-defined subsets, and (ii) T-cell immaturity due to an increased turnover of these cells and accounting for increased CD38 expression.
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PMID:During HIV infection, CD4+ CD38+ T-cells are the predominant circulating CD4+ subset whose HLA-DR positivity increases with disease progression and whose V beta repertoire is similar to that of CD4+ CD38- T-cells. 755 81

Pre-eclampsia/toxemia (PET) is an idiopathic hypertensive disorder of pregnancy elicited in susceptible mothers by exposure to placental trophoblast. Three facts regarding the placenta in PET are known: an association with large placentas (excessive trophoblast), a tendency for superficial implantation, and inappropriate trophoblastic immaturity, as assessed by ultrastructural and biochemical criteria. A unitary hypothesis is that PET is related to a maturation defect leading to excessive accumulation of inappropriately immature intermediate trophoblast in the placental implantation site. We studied the implantation site of PET and control placentas from three gestational age groups (25 to 30, 30 to 35, and 36 to 40 weeks old [five per group]) by morphometry and immunohistochemistry using antibodies to three phenotypic markers (cytokeratin, human placental lactogen (HPL), and beta 2-microglobulin) and two markers of cell dynamics (proliferating cell nuclear antigen [PCNA] and bcl-2]). Implantation sites in the PET group had increased amounts of intermediate trophoblast (cell number and longitudinal extent) with an increased proliferative index (percentage of PCNA positive) and evidence of phenotypic immaturity (HPL negative). Intermediate trophoblast from both groups was uniformly bcl-2 negative and beta 2-microglobulin positive. Based on these data and the findings of other investigators, we propose that the diagnostic term "atypical implantation site" be added to acute atherosis, villous infarction, and increased syncytial knotting as a characteristic of placentas from pre-eclamptic pregnancies.
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PMID:Pre-eclampsia is associated with an excess of proliferative immature intermediate trophoblast. 777 87