0000000000775060

AUTHOR

H P Steffens

showing 2 related works from this author

Evidence against a key role for transforming growth factor-beta1 in cytomegalovirus-induced bone marrow aplasia.

1998

During immunodeficiency after sublethal haematoablative treatment, cytomegalovirus (CMV) infection interferes with haematopoietic reconstitution and can cause lethal bone marrow (BM) aplasia. The in vivo model of murine CMV infection has identified the BM stroma as the principal target site of CMV in the haematopoietic cord. The infected cell type is the reticular stromal cell which forms the stromal network and produces essential haemopoietins, such as stem-cell factor (SCF). The expression of SCF was found to be reduced in the infected stroma, but the stromal network was not disrupted and the number of infected stromal cells was too low to explain the functional deficiency. These facts ca…

Stromal cellmedicine.medical_treatmentCytomegalovirusGene ExpressionBone Marrow CellsBone Marrow AplasiaCD8-Positive T-LymphocytesKidneyVirus ReplicationMiceTransforming Growth Factor betaVirologymedicineAnimalsCytotoxic T cellBone Marrow DiseasesBone Marrow TransplantationMice Inbred BALB CbiologyTransforming growth factor betaVirologyHematopoiesisHaematopoiesisCytokinemedicine.anatomical_structureLiverCytomegalovirus Infectionsbiology.proteinFemaleImmunotherapyBone marrowStromal CellsTransforming growth factorJournal of General Virology
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Reconstitution of CD8 T cells is essential for the prevention of multiple-organ cytomegalovirus histopathology after bone marrow transplantation.

1998

Cytomegalovirus (CMV) infection in the period of temporary immunodeficiency after haematoablative treatment and bone marrow transplantation (BMT) is associated with a risk of graft failure and multiple-organ CMV disease. The efficacy of immune system reconstitution is decisive for the prevention of CMV pathogenesis after BMT. Previous data in murine model systems have documented a redundancy in the immune effector mechanisms controlling CMV. CD8 T cells proved to be relevant but not irreplaceable as antiviral effectors. Specifically, in a state of long-term in vivo depletion of the CD8 T-cell subset, CD4 T cells were educed to become deputy effectors controlling CMV by a mechanism involving…

CD4-Positive T-LymphocytesCongenital cytomegalovirus infectionCytomegalovirusGraft vs Host DiseaseCD8-Positive T-LymphocytesBiologyVirus ReplicationLymphocyte DepletionPathogenesisMiceImmune systemRisk FactorsIn vivoVirologymedicineAnimalsHumansCytotoxic T cellImmunodeficiencyBone Marrow TransplantationMice Inbred BALB CEffectorvirus diseasesmedicine.diseaseVirologyDisease Models AnimalTransplantation IsogeneicCytomegalovirus InfectionsImmunologyCD8Journal of General Virology
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