Gulf Coast Regional Blood Center

About: Gulf Coast Regional Blood Center is a based out in . It is known for research contribution in the topics: Population & Allele. The organization has 6297 authors who have published 6917 publications receiving 198369 citations.

A case of infantile acute monocytic leukemia caused by vertical transmission of the mother's leukemic cells

Abstract: A case of infantile acute monocytic leukemia (AMoL), which was probably transmitted from a pregnant woman with leukemia to her unborn infant, is presented. A woman had AMoL when her third infant was born. This infant, who was a boy, also suffered from AMoL when he was 20 months of age. The infant's leukemic cells had the same cytochemical and immunophenotypic patterns as the mother's leukemic cells. By cytogenetic analysis, the majority of the infant's leukemic marrow cells had the 46,XX karyotype and showed no Y body by quinacrine staining. Moreover, the phenotype for human major histocompatibility system, HLA-A, HLA-B, and HLA-DR of the infant's leukemic cells was consistent with that of the mother's lymphocytes. Thus, the infant's leukemic clone was found to be identical to the mother's leukemic clone. His lymphocytes could not react with the mother's leukemic cells or his own leukemic cells in mixed lymphocyte culture, suggesting that the HLA homozygosity of the mother may have played a role in inducing immunologic tolerance to the immigrated leukemic cells in the infant. This is the first report of an infantile leukemia transmitted from a mother with leukemia, supposedly through the placenta.

Assessing basophil activation by using flow cytometry and mass cytometry in blood stored 24 hours before analysis

Abstract: Background Basophil activation tests (BATs) have promise for research and for clinical monitoring of patients with allergies. However, BAT protocols vary in blood anticoagulant used and temperature and time of storage before testing, complicating comparisons of results from various studies. Objective We attempted to establish a BAT protocol that would permit analysis of blood within 24 hours of obtaining the sample. Methods Blood from 46 healthy donors and 120 patients with peanut allergy was collected into EDTA or heparin tubes, and samples were stored at 4°C or room temperature for 4 or 24 hours before performing BATs. Results Stimulation with anti-IgE or IL-3 resulted in strong upregulation of basophil CD203c in samples collected in EDTA or heparin, stored at 4°C, and analyzed 24 hours after sample collection. However, a CD63 hi population of basophils was not observed in any conditions in EDTA-treated samples unless exogenous calcium/magnesium was added at the time of anti-IgE stimulation. By contrast, blood samples collected in heparin tubes were adequate for quantification of upregulation of basophil CD203c and identification of a population of CD63 hi basophils, irrespective of whether the specimens were analyzed by means of conventional flow cytometry or cytometry by time-of-flight mass spectrometry, and such tests could be performed after blood was stored for 24 hours at 4°C. Conclusion BATs to measure upregulation of basophil CD203c and induction of a CD63 hi basophil population can be conducted with blood obtained in heparin tubes and stored at 4°C for 24 hours.

Phospholipase Cγ2 Is Essential for Specific Functions of FcεR and FcγR

Abstract: Phospholipase Cgamma2 (PLCgamma2) plays a critical role in the functions of the B cell receptor in B cells and of the FcRgamma chain-containing collagen receptor in platelets. Here we report that PLCgamma2 is also expressed in mast cells and monocytes/macrophages and is activated by cross-linking of Fc(epsilon)R and Fc(gamma)R. Although PLCgamma2-deficient mice have normal development and numbers of mast cells and monocytes/macrophages, we demonstrate that PLCgamma2 is essential for specific functions of Fc(epsilon)R and Fc(gamma)R. While PLCgamma2-deficient mast cells have normal mitogen-activated protein kinase activation and cytokine production at mRNA levels, the mutant cells have impaired Fc(epsilon)R-mediated Ca(2+) flux and inositol 1,4,5-trisphosphate production, degranulation, and cytokine secretion. As a physiological consequence of the effect of PLCgamma2 deficiency, the mutant mice are resistant to IgE-mediated cutaneous inflammatory skin reaction. Macrophages from PLCgamma2-deficient mice have no detectable Fc(gamma)R-mediated Ca(2+) flux; however, the mutant cells have normal Fc(gamma)R-mediated phagocytosis. Moreover, PLCgamma2 plays a nonredundant role in Fc(gamma)R-mediated inflammatory skin reaction.