The in vivo effect of rabbit anti-AKR mouse brain-associated serum (RAMB) was determined on theta bearing lymphocytes present in the spleens and thymuses of mature C3H mice and AKR mice staged into preleukemic, leukaemic and overtly leukaemic states. Following seven daily injections of RAMB serum, the splenic plaque-forming cell (PFC) response to sheep erythrocytes (SRBC) and the percentage of theta-bearing lymphocytes in the spleen were significantly decreased in the C3H and the preleukaemic AKR mice. Decreases in thymic weight and thymocyte numbers were also apparent. Determinations of theta antigen density using in vitro cytoxicity tests indicated that splenic and thymic T lymphocytes (thymus-derived) remaining in the RAMB-treated C3H and preleukemic AKR mice consisted primarily of cells bearing less of the theta surface antigen. Histopathological studies of tissues from these two treated groups revealed cortical lymphocyte depletion in the thymus, and marginal and periarteriolar depletion in the spleen. Leukaemic AKR mice, administered seven injections of RAMB serum, demonstrated less dramatic changes in thymus weight, histopathology and theta-bearing cell percentages when compared with the data from the preleukaemic AKR or matureC3H mice. The results from testing overtly luekaemic AKR mice administered RAMB serum for the 7 or 9 days did not demonstrate differences from findings from groupsof overtly leukaemic control mice. These data indicate that the in vivo activity of RAMB serum in C3H mice and preleukaemic AKR mice is directed primarily toward the less mature T-lymphocyte population. This influence of RAMB serum is lesspronounced in leukaemic and the more overtly leukaemic mice, suggesting that a decreasedpopulation of RAMB-susceptible lymphocytes are present in these animals.
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NPJ Vaccines
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Grupo Integrado de Pesquisa em Biomarcadores, Instituto René Rachou-Fundação Oswaldo Cruz, Belo Horizonte, Minas Gerais, Brasil.
Streptococcus pneumoniae and influenza A virus (IAV) are significant agents of pneumonia cases and severe respiratory infections globally. Secondary bacterial infections, particularly by Streptococcus pneumoniae, are common in IAV-infected individuals, leading to critical outcomes. Despite reducing mortality, pneumococcal vaccines have high production costs and are serotype specific.
View Article and Find Full Text PDFBiochem Genet
December 2024
Department of Critical Care Medicine, Department of Hematology, The First Affiliated Hospital of Harbin Medical University, Harbin, 150001, Heilongjiang, China.
Cancer Cell
December 2024
Department of Surgery, University of Michigan Medical School, Ann Arbor, MI, USA; Center of Excellence for Cancer Immunology and Immunotherapy, University of Michigan Rogel Cancer Center, Ann Arbor, MI, USA; Department of Pathology, University of Michigan Medical School, Ann Arbor, MI, USA; Graduate Program in Cancer Biology, University of Michigan, Ann Arbor, MI, USA. Electronic address:
J Thromb Haemost
January 2025
Cardeza Foundation for Hematologic Research, Department of Medicine, Division of Hematology, Sidney Kimmel Medical College, Thomas Jefferson University, Philadelphia, Pennsylvania, USA. Electronic address:
Background: Phosphatidylserine (PS) is a procoagulant phospholipid enriched on surfaces of activated vascular cells including platelets, endothelium, monocytes, and microvesicles. As a molecular driver of thrombosis accessible to drug blockade, PS is an attractive pharmacologic target for modulating thrombogenesis, with potentially reduced bleeding risk compared to anticoagulant and antiplatelet therapies.
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Science
October 2024
Department of Chemical and Systems Biology, Stanford University, Stanford, CA 94305, USA.
Kinases are critical regulators of cellular function that are commonly implicated in the mechanisms underlying disease. Most drugs that target kinases are molecules that inhibit their catalytic activity, but here we used chemically induced proximity to convert kinase inhibitors into activators of therapeutic genes. We synthesized bivalent molecules that link ligands of the transcription factor B cell lymphoma 6 (BCL6) to inhibitors of cyclin-dependent kinases (CDKs).
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