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Biomedical subjects

Mauro Krampera

Publications and source records attributed to Mauro Krampera.

26 records · Page 2Linked to original sources
PubMed2003

Thymic epithelial cells promote survival of human T-cell acute lymphoblastic leukemia blasts: the role of interleukin-7.

BACKGROUND AND OBJECTIVES: T-cell lymphoblastic leukemia (T-ALL) cells originate within the thymus from the clonal expansion of T cell precursors. Among thymic stromal elements, epithelial cells (TEC) are known to exert a dominant inductive role in survival and maturation of normal, immature T-cells. In this study we explored the possible effect of TEC on T-ALL cell survival and analyzed the role of interleukin-7 (IL-7) within the microenvironment generated by T-ALL-TEC interactions. DESIGN AND METHODS: T-ALL blasts derived from 10 adult patients were cultured with TEC obtained from human normal thymuses. The level of blast apoptosis was measured by annexin V-propidium iodide co-staining and flow cytometry. The proliferative response of leukemic cells to interaction with TEC was evaluated by thymidine incorporation at various time intervals of culture. To assess the role of IL-7, lympho-epithelial co-cultures were carried out in the presence of anti-IL-7 or anti IL-7R blocking antibodies and the level of apoptosis of T-ALL blasts was analyzed. RESULTS: When T-ALL cells were cultured in the presence of TEC monolayers, the percentage of viable cells increased significantly and this survival was sustained with time in culture. In addition, the interaction with TEC induced a considerable proliferative response in T-ALL cells (15-fold greater than that of the control cells after 7 days of culture). The presence of IL-7 or IL-7R blocking antibodies in lympho-epithelial co-cultures consistently reduced the TEC-mediated apoptosis inhibition in T-ALL blasts (70% decrease). INTERPRETATION AND CONCLUSIONS: These results point to the role of thymic epithelium in the regulation of T blast survival. In addition, they show that interaction between IL-7 and its receptor has the major role in modulating T-ALL survival within the microenvironment generated by the T-ALL/TEC interaction.

Adolescent↗
PubMed2002

Bone marrow mesenchymal stem cells inhibit the response of naive and memory antigen-specific T cells to their cognate peptide.

Mesenchymal stem cells (MSCs) have been recently shown to inhibit T-cell proliferation to polyclonal stimuli. We characterized the effect of MSCs of bone marrow origin on the T-cell response of naive and memory T cells to their cognate antigenic epitopes. The immune response to murine male transplantation antigens, HY, was selected because the peptide identity and major histocompatibility complex (MHC) restriction of the immunodominant epitopes are known. C57BL/6 female mice immunized with male cells were the source of memory T cells, whereas C6 mice transgenic for HY-specific T-cell receptor provided naive T cells. Responder cells were stimulated in vitro with male spleen cells or HY peptides in the presence or absence of MSCs. MSCs inhibited HY-specific naive and memory T cells in a dose-dependent fashion and affected cell proliferation, cytotoxicity, and the number of interferon gamma (IFN-gamma)-producing HY peptide-specific T cells. However, the MSC inhibitory effect did not selectively target antigen-reactive T cells. When MSCs were added to the T-cell cultures in a Transwell system or MSCs were replaced by MSC culture supernatant, the inhibitory activity was abrogated. T-cell reactivity was also restored if MSCs were removed from the cultures. The expression of MHC molecules and the presence in culture of antigen-presenting cells (APCs) or of CD4(+)/CD25(+) regulatory T cells were not required for MSCs to inhibit. We conclude that MSCs inhibit naive and memory T-cell responses to their cognate antigens. Overall our data suggest that MSCs physically hinder T cells from the contact with APCs in a noncognate fashion.

Amino Acid Sequence↗
PubMed2002

Efficacy of Helicobacter pylori eradication in raising platelet count in adult patients with idiopathic thrombocytopenic purpura.

BACKGROUND AND OBJECTIVES: There are data consistent with an association between idiopathic thrombocytopenic purpura (ITP) and Helicobacter pylori (HP) infection. In addition, a significant increase of platelet count following HP eradication has been reported in a proportion of ITP patients. We describe here our experience on the efficacy of anti-HP treatment in ITP patients. DESIGN AND METHODS: Between December 1998 and May 2001 sixteen adult patients with ITP and documented HP infection were treated with standard antibiotic therapy for HP eradication (amoxicillin and clarithromycin plus pantoprazole combination). Of these patients, 7 had untreated ITP with mild/moderate thrombocytopenia (median platelet count 70x10(9)/L, range 41-91), 5 had relapsed following a previous steroid treatment (median platelet count 39x10(9)/L, range 30-90) and 4 were refractory to steroids (median platelet count 18.5x10(9)/L, range 9-30). RESULTS: An improvement of platelet count was observed in 11/15 patients (73.3%) who achieved HP eradication. The difference between the mean platelet count SD before and after HP eradication was statistically significant (51.6 28.2x10(9)/L vs. 143.3 131.1x10(9)/L; p=0.01). Complete or partial responses were obtained in 11/16 treated patients (68.7%). This result still persisted after a median follow-up of 11.7 months. INTERPRETATION AND CONCLUSIONS: Our data confirm the efficacy of Helicobacter pylori eradication in increasing platelet count in adult ITP patients.

Adult↗