15 results on '"Ferrarini, M"'
Search Results
2. Late Epstein-Barr virus infection of a hepatosplenic gamma delta T-cell lymphoma arising in a kidney transplant recipient
- Author
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Roncella, S., Giovanna Cutrona, Truini, M., Airoldi, I., Pezzolo, A., Valetto, A., Di Martino, D., Dadati, P., Rossi, A., Ulivi, M., Fontana, I., Nocera, A., Valente, U., Ferrarini, M., and Pistoia, V.
- Subjects
Adult ,Male ,T Cell Lymphoma ,Epstein-Barr Virus Infections ,Leukosialin ,CD3 Complex ,Sialoglycoproteins ,Splenic Neoplasms ,Gene Rearrangement, delta-Chain T-Cell Antigen Receptor ,Liver Neoplasms ,Receptors, Antigen, T-Cell, gamma-delta ,Epstein Barr Virus ,Lymphoma, T-Cell ,Kidney Transplantation ,Antigens, CD ,DNA, Viral ,Humans ,Leukocyte Common Antigens ,Cell Lineage - Abstract
gd T-cell lymphomas are only exceptionally observed in transplanted patients. Aim of this study was the detailed characterization of one such case.The patient developed spontaneous splenic rupture six years after kidney transplantation. The splenic red pulp was infiltrated by medium-sized and large lymphoid cells with two or more nucleoli. At autopsy, similar lymphoid cells infiltrated the hepatic sinusoids. Histologic, immunologic and molecular studies were carried out.By immunohistochemistry, the atypical lymphoid cells were found to express CD3, CD45 and CD43, indicating their T-lineage origin. Approximately 99% of spleen mononuclear cells (MNC) were CD3(+), gammadelta TcR+, CD4-, CD8-, alphabeta TcR-. A clonal gammadelta TcR rearrangement (Vgamma1-Jgamma1.3/2.3-Cgamma2; Vdelta1-Ddelta2-Jdelta1) was detected. The final diagnosis was peripheral T-cell lymphoma, hepato-splenic gammadelta-type. EBV infection of spleen MNC was documented by molecular studies. However, in situ hybridization for EBER-1 (EBV-RNA) showed that only a minority of malignant lymphoid cells (5-7%) were EBV-infected.It is concluded that EBV infection was as a late event involving an already transformed gd T-cell clone.
- Published
- 2000
3. Predictive value of 2-microglobulin ( 2-m) levels in chronic lymphocytic leukemia since Binet A stages
- Author
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Gentile, M., primary, Cutrona, G., additional, Neri, A., additional, Molica, S., additional, Ferrarini, M., additional, and Morabito, F., additional
- Published
- 2009
- Full Text
- View/download PDF
4. Clonal heterogeneity in chronic lymphocytic leukemia cells: superior response to surface IgM cross-linking in CD38, ZAP-70-positive cells
- Author
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Cutrona, G., primary, Colombo, M., additional, Matis, S., additional, Fabbi, M., additional, Spriano, M., additional, Callea, V., additional, Vigna, E., additional, Gentile, M., additional, Zupo, S., additional, Chiorazzi, N., additional, Morabito, F., additional, and Ferrarini, M., additional
- Published
- 2008
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- View/download PDF
5. Chronic lymphocytic leukemia nurse-like cells express hepatocyte growth factor receptor (c-MET) and indoleamine 2,3-dioxygenase and display features of immunosuppressive type 2 skewed macrophages
- Author
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Paolo Giannoni, Giorgia Travaini, Alessandra Pattarozzi, Ivana Pierri, Giovanna Cutrona, Genti Shyti, Laura Ottaggio, Manlio Ferrarini, Marco Calvaruso, Claudio Tripodo, Rodolfo Quarto, Daniela de Totero, Enrico Balleari, Roberto Benelli, Maria Cristina Mingari, Simona Zupo, Gabriella Pietra, Giannoni, P, Pietra, G, Travaini, G, Quarto, R, Shyti, G, Benelli, R, Ottaggio, L, Mingari, MC, Zupo, S, Cutrona, G, Pierri, I, Balleari, E, Pattarozzi, A, Calvaruso, M, Tripodo, C, Ferrarini, M, and de Totero, D.
- Subjects
STAT3 Transcription Factor ,C-Met ,Stromal cell ,medicine.medical_treatment ,Gene Expression ,Biology ,Monocytes ,chemistry.chemical_compound ,T-Lymphocyte Subsets ,medicine ,Humans ,Indoleamine-Pyrrole 2,3,-Dioxygenase ,Growth factor receptor inhibitor ,Phosphorylation ,Indoleamine 2,3-dioxygenase ,Cells, Cultured ,Follicular dendritic cells ,Macrophages ,Growth factor ,Articles ,Hematology ,Proto-Oncogene Proteins c-met ,Leukemia, Lymphocytic, Chronic, B-Cell ,Coculture Techniques ,Interleukin-10 ,C-MET ,INDOLEAMINE 2,3-DIOXYGENASE ,chronic lymphocytic leukemia, hepatocyte growth factor, c-MET, nurse-like cells ,hepatocyte growth factor ,nurse-like cells ,chemistry ,Hepatocyte Growth Factor Receptor ,Cancer research ,chronic lymphocytic leukemia ,Hepatocyte growth factor ,medicine.drug - Abstract
Hepatocyte growth factor, produced by stromal and follicular dendritic cells, and present at high concentrations in the sera of patients with chronic lymphocytic leukemia, prolongs the survival of leukemic B cells by interacting with their receptor, c-MET. It is, however, unknown whether hepatocyte growth factor influences microenvironmental cells, such as nurse-like cells, which deliver survival signals to the leukemic clone. We evaluated the expression of c-MET on nurse-like cells and monocytes from patients with chronic lymphocytic leukemia and searched for phenotypic/functional features supposed to be influenced by the hepatocyte growth factor/c-MET interaction. c-MET is expressed at high levels on nurse-like cells and at significantly higher levels than normal on monocytes from patients. Moreover, the hepatocyte growth factor/c-MET interaction activates STAT3(TYR705) phosphorylation in nurse-like cells. Indoleamine 2,3-dioxygenase, an enzyme modulating T-cell proliferation and induced on normal monocytes after hepatocyte growth factor treatment, was detected together with interleukin-10 on nurse-like cells, and on freshly-prepared patients' monocytes. Immunohistochemical/immunostaining analyses demonstrated the presence of c-MET(+) and indoleamine 2,3-dioxygenase(+) cells in lymph node biopsies, co-expressed with CD68 and vimentin. Furthermore nurse-like cells and chronic lymphocytic monocytes significantly inhibited T-cell proliferation, prevented by anti-transforming growth factor beta and interleukin-10 antibodies and indoleamine 2,3-dioxygenase inhibitors, and supported CD4(+)CD25(high+)/FOXP3(+) T regulatory cell expansion. We suggest that nurse-like cells display features of immunosuppressive type 2 macrophages: higher hepatocyte growth factor levels, produced by leukemic or other microenvironmental surrounding cells, may cooperate to induce M2 polarization. Hepatocyte growth factor may thus have a dual pathophysiological role: directly through enhancement of survival of the leukemic clone and indirectly by favoring T-cell immunosuppression.
- Published
- 2014
6. Chronic lymphocytic leukemia cells impair osteoblastogenesis and promote osteoclastogenesis: role of TNFα, IL-6 and IL-11 cytokines.
- Author
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Giannoni P, Marini C, Cutrona G, Matis S, Capra MC, Puglisi F, Luzzi P, Pigozzi S, Gaggero G, Neri A, Todoerti K, Morabito F, Ibatici A, Miglino M, Bergamaschi M, Bruno S, Sambuceti GM, Ravetti JL, Ferrarini M, Fais F, and de Totero D
- Subjects
- Cell Differentiation, Cells, Cultured, Cytokines, Humans, Osteoblasts, Osteoclasts, Interleukin-11 genetics, Interleukin-6 genetics, Leukemia, Lymphocytic, Chronic, B-Cell, Osteogenesis, Tumor Necrosis Factor-alpha genetics
- Abstract
Bone skeletal alterations are no longer considered a rare event in chronic lymphocytic leukemia (CLL), especially at more advanced stages of the disease. This study is aimed at elucidating the mechanisms underlying this phenomenon. Bone marrow stromal cells, induced to differentiate toward osteoblasts in osteogenic medium, appeared unable to complete their maturation upon co-culture with CLL cells, CLL-cell-derived conditioned media (CLL-cm) or CLL-sera (CLL-sr). Inhibition of osteoblast differentiation was documented by decreased levels of RUNX2 and osteocalcin mRNA expression, by increased osteopontin and DKK-1 mRNA levels, and by a marked reduction of mineralized matrix deposition. The addition of neutralizing TNFα, IL-11 or anti-IL-6R monoclonal antibodies to these cocultures resulted in restoration of bone mineralization, indicating the involvement of these cytokines. These findings were further supported by silencing TNFα, IL-11 and IL-6 in leukemic cells. We also demonstrated that the addition of CLL-cm to monocytes, previously stimulated with MCSF and RANKL, significantly amplified the formation of large, mature osteoclasts as well as their bone resorption activity. Moreover, enhanced osteoclastogenesis, induced by CLL-cm, was significantly reduced by treating cultures with the anti-TNFα monoclonal antibody infliximab. An analogous effect was observed with the use of the BTK inhibitor, ibrutinib. Interestingly, CLL cells co-cultured with mature osteoclasts were protected from apoptosis and upregulated Ki-67. These experimental results parallel the direct correlation between amounts of TNFα in CLL-sr and the degree of compact bone erosion that we previously described, further strengthening the indication of a reciprocal influence between leukemic cell expansion and bone structure derangement.
- Published
- 2021
- Full Text
- View/download PDF
7. ATR addiction in multiple myeloma: synthetic lethal approaches exploiting established therapies.
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Botrugno OA, Bianchessi S, Zambroni D, Frenquelli M, Belloni D, Bongiovanni L, Girlanda S, Di Terlizzi S, Ferrarini M, Ferrero E, Ponzoni M, Marcatti M, and Tonon G
- Subjects
- Animals, Apoptosis, Ataxia Telangiectasia Mutated Proteins genetics, Ataxia Telangiectasia Mutated Proteins metabolism, Cell Line, Tumor, Cell Survival, DNA Damage, DNA Repair, Humans, Melphalan pharmacology, Multiple Myeloma drug therapy, Multiple Myeloma genetics
- Abstract
Therapeutic strategies designed to tinker with cancer cell DNA damage response have led to the widespread use of PARP inhibitors for BRCA1/2-mutated cancers. In the haematological cancer multiple myeloma, we sought to identify analogous synthetic lethality mechanisms that could be leveraged upon established cancer treatments. The combination of ATR inhibition using the compound VX-970 with a drug eliciting interstrand cross-links, melphalan, was tested in in vitro, ex vivo, and most notably in vivo models. Cell proliferation, induction of apoptosis, tumor growth and animal survival were assessed. The combination of ATM inhibition with a drug triggering double strand breaks, doxorucibin, was also probed. We found that ATR inhibition is strongly synergistic with melphalan, even in resistant cells. The combination was dramatically effective in targeting myeloma primary patient cells and cell lines reducing cell proliferation and inducing apoptosis. The combination therapy significantly reduced tumor burden and prolonged survival in animal models. Conversely, ATM inhibition only marginally impacted on myeloma cell survival, even in combination with doxorucibin at high doses. These results indicate that myeloma cells extensively rely on ATR, but not on ATM, for DNA repair. Our findings posit that adding an ATR inhibitor such as VX-970 to established therapeutic regimens may provide a remarkably broad benefit to myeloma patients.
- Published
- 2020
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8. A laboratory-based scoring system predicts early treatment in Rai 0 chronic lymphocytic leukemia.
- Author
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Cohen JA, Rossi FM, Zucchetto A, Bomben R, Terzi-di-Bergamo L, Rabe KG, Degan M, Steffan A, Polesel J, Santinelli E, Innocenti I, Cutrona G, D'Arena G, Pozzato G, Zaja F, Chiarenza A, Rossi D, Di Raimondo F, Laurenti L, Gentile M, Morabito F, Neri A, Ferrarini M, Fegan CD, Pepper CJ, Del Poeta G, Parikh SA, Kay NE, and Gattei V
- Subjects
- Humans, Italy, Laboratories, Mutation, Prognosis, United Kingdom, Leukemia, Lymphocytic, Chronic, B-Cell diagnosis, Leukemia, Lymphocytic, Chronic, B-Cell genetics, Leukemia, Lymphocytic, Chronic, B-Cell therapy
- Abstract
We present a laboratory-based prognostic calculator (designated CRO score) to risk stratify treatment-free survival in early stage (Rai 0) chronic lymphocytic leukemia (CLL) developed using a training-validation model in a series of 1,879 cases from Italy, the United Kingdom and the United States. By means of regression analysis, we identified five prognostic variables with weighting as follows: deletion of the short arm of chromosome 17 and unmutated immunoglobulin heavy chain gene status, 2 points; deletion of the long arm of chromosome 11, trisomy of chromosome 12, and white blood cell count >32.0x10
3 /microliter, 1 point. Low-, intermediate- and high-risk categories were established by recursive partitioning in a training cohort of 478 cases, and then validated in four independent cohorts of 144 / 395 / 540 / 322 cases, as well as in the composite validation cohort. Concordance indices were 0.75 in the training cohort and ranged from 0.63 to 0.74 in the four validation cohorts (0.69 in the composite validation cohort). These findings advocate potential application of our novel prognostic calculator to better stratify early-stage CLL, and aid case selection in risk-adapted treatment for early disease. Furthermore, they support immunocytogenetic analysis in Rai 0 CLL being performed at the time of diagnosis to aid prognosis and treatment, particularly in today's chemofree era., (Copyright© 2020 Ferrata Storti Foundation.)- Published
- 2020
- Full Text
- View/download PDF
9. Modeling multiple myeloma-bone marrow interactions and response to drugs in a 3D surrogate microenvironment.
- Author
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Belloni D, Heltai S, Ponzoni M, Villa A, Vergani B, Pecciarini L, Marcatti M, Girlanda S, Tonon G, Ciceri F, Caligaris-Cappio F, Ferrarini M, and Ferrero E
- Subjects
- Bioreactors, Bortezomib pharmacology, Cell Adhesion, Cell Survival, Coculture Techniques, Drug Resistance, Endothelial Cells, Gelatin, Humans, Multiple Myeloma drug therapy, Stromal Cells, Tumor Microenvironment, Bone Marrow pathology, Cell Communication, Cell Culture Techniques, Models, Biological, Multiple Myeloma pathology
- Abstract
Multiple myeloma develops primarily inside the bone marrow microenvironment, that confers pro-survival signals and drug resistance. 3D cultures that reproduce multiple myeloma-bone marrow interactions are needed to fully investigate multiple myeloma pathogenesis and response to drugs. To this purpose, we exploited the 3D Rotary Cell Culture System bioreactor technology for myeloma-bone marrow co-cultures in gelatin scaffolds. The model was validated with myeloma cell lines that, as assessed by histochemical and electron-microscopic analyses, engaged contacts with stromal cells and endothelial cells. Consistently, pro-survival signaling and also cell adhesion-mediated drug resistance were significantly higher in 3D than in 2D parallel co-cultures. The contribution of the VLA-4/VCAM1 pathway to resistance to bortezomib was modeled by the use of VCAM1 transfectants. Soluble factor-mediated drug resistance could be also demonstrated in both 2D and 3D co-cultures. The system was then successfully applied to co-cultures of primary myeloma cells-primary myeloma bone marrow stromal cells from patients and endothelial cells, allowing the development of functional myeloma-stroma interactions and MM cell long-term survival. Significantly, genomic analysis performed in a high-risk myeloma patient demonstrated that culture in bioreactor paralleled the expansion of the clone that ultimately dominated in vivo Finally, the impact of bortezomib on myeloma cells and on specialized functions of the microenvironment could be evaluated. Our findings indicate that 3D dynamic culture of reconstructed human multiple myeloma microenvironments in bioreactor may represent a useful platform for drug testing and for studying tumor-stroma molecular interactions., (Copyright© 2018 Ferrata Storti Foundation.)
- Published
- 2018
- Full Text
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10. Predictive value of beta2-microglobulin (beta2-m) levels in chronic lymphocytic leukemia since Binet A stages.
- Author
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Gentile M, Cutrona G, Neri A, Molica S, Ferrarini M, and Morabito F
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- Aged, Biomarkers, Tumor blood, Female, Humans, Integrin alpha4 blood, Kaplan-Meier Estimate, Leukemia, Lymphocytic, Chronic, B-Cell pathology, Male, Middle Aged, Neoplasm Staging, Predictive Value of Tests, Prognosis, Leukemia, Lymphocytic, Chronic, B-Cell blood, beta 2-Microglobulin blood
- Published
- 2009
- Full Text
- View/download PDF
11. Expression of CD10 by B-chronic lymphocytic leukemia cells undergoing apoptosis in vivo and in vitro.
- Author
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Morabito F, Mangiola M, Rapezzi D, Zupo S, Oliva BM, Ferraris AM, Spriano M, Rossi E, Stelitano C, Callea V, Cutrona G, and Ferrarini M
- Subjects
- ADP-ribosyl Cyclase immunology, ADP-ribosyl Cyclase metabolism, ADP-ribosyl Cyclase 1, Amino Acid Chloromethyl Ketones pharmacology, Antibodies pharmacology, Antibodies, Monoclonal pharmacology, Antigens, CD immunology, Antigens, CD metabolism, Apoptosis drug effects, Apoptosis genetics, Apoptosis immunology, B-Lymphocytes chemistry, B-Lymphocytes metabolism, Cell Line, Tumor, Etoposide pharmacology, Gene Expression Regulation, Neoplastic drug effects, Gene Expression Regulation, Neoplastic immunology, Humans, Immunoglobulin A pharmacology, Immunoglobulin D pharmacology, Immunoglobulin M pharmacology, Leukemia, Lymphocytic, Chronic, B-Cell genetics, Leukemia, Lymphocytic, Chronic, B-Cell pathology, Membrane Glycoproteins, Palatine Tonsil, Vidarabine pharmacology, Apoptosis physiology, Leukemia, Lymphocytic, Chronic, B-Cell metabolism, Neprilysin biosynthesis, Vidarabine analogs & derivatives
- Abstract
Background and Objectives: B-cell chronic lymphocytic leukemia (B-CLL) is an accumulating disease of slowly proliferating cells. CD10 is not normally expressed on the surface of B-CLL cells. The aim of this study was to ascertain whether B-CLL cells, induced into apoptosis, expressed surface CD10, since a correlation between apoptosis and CD10 expression has been demonstrated., Design and Methods: Peripheral blood cells from 31 untreated B-CLL patients were induced into apoptosis by etoposide, fludarabine or Ga(mu)-Ab treatment and tested for CD10 expression by flow cytometry. Normal CD5+ B cells were also induced into apoptosis and tested for CD10 expression., Results: CD10 positive cells were absent in B-CLL cell suspensions, but were detected following in vitro culture, and their appearance paralleled that of apoptotic cells. Treatment with etoposide, fludarabine or Ga(mu)-Ab enhanced both apoptosis and CD10 expression. Inhibition of apoptosis by VAD-fmk or Ga(delta)-Ab prevented CD10 expression. Cell separation tests following induction of apoptosis demonstrated that CD10+ cells were apoptotic. CD10+ cells were observed in the peripheral blood of two patients within a few hours following fludarabine infusion. In another patient, who failed to respond, no CD10+ cells were seen. Expression of CD10 was observed also in normal CD5+ B cells when these were induced into apoptosis., Interpretation and Conclusions: This study demonstrates that B-CLL cells, as well as normal CD5+ B cells, become CD10+ following apoptosis induction in vitro. Some of the data obtained also suggest a use for CD10 to monitor apoptosis of B-CLL in a clinical setting.
- Published
- 2003
12. Chromosome aberrations evaluated by comparative genomic hybridization in B-cell chronic lymphocytic leukemia: correlation with CD38 expression.
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Ottaggio L, Viaggi S, Zunino A, Zupo S, Rossi E, Spriano M, Abbondandolo A, and Ferrarini M
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- ADP-ribosyl Cyclase 1, Adult, Aged, Chromosomes, Human ultrastructure, Cytogenetic Analysis, Female, Humans, Immunophenotyping, Leukemia, Lymphocytic, Chronic, B-Cell classification, Male, Membrane Glycoproteins, Middle Aged, Nucleic Acid Hybridization, Prognosis, ADP-ribosyl Cyclase metabolism, Antigens, CD metabolism, Chromosome Aberrations, Leukemia, Lymphocytic, Chronic, B-Cell diagnosis
- Abstract
Background and Objectives: B-cell chronic lymphocytic leukemia (B-CLL) results from the accumulation of monoclonal CD5+ B cells. Despite its homogeneity at cellular level, B-CLL is clinically heterogeneous. Clinical studies indicate that CD38+ B-CLL are characterized by a more aggressive clinical course than are CD38- B-CLL. On the basis of these studies and considering the established correlation between specific chromosome aberrations and the clinical course of B-CLL, it is possible that CD38+ B-CLL cases are also characterized by specific subsets of chromosomal alterations., Design and Methods: Comparative genomic hybridization (CGH) was performed on purified B-cells from peripheral blood of 52 patients with B-CLL in order to detect chromosome imbalance. The immunophenotype of the patients, including CD38 expression, was also determined by flow cytometry. The results of CGH experiments were then compared with CD38 expression., Results: We found a clear correlation between the presence of chromosomal imbalances and CD38 expression: 13/16 CD38+ cases had chromosome imbalances, most of them (12/13) correlated with a poor prognosis. Among the CD38- B-CLL patients, only 8/36 displayed chromosome imbalances; the only three cases with loss in 13q as a single aberration, considered a good prognostic marker, were in this group. Moreover, we found that cytogenetic alterations were also more complex in the CD38+ B-CLL subset, since 9/10 with two or more aberrations were in the CD38+ group., Interpretation and Conclusions: Collectively, the data reinforce the value of CD38 as a prognostic factor and indicate that genotypic/phenotypic features distinguish B-CLL subsets.
- Published
- 2003
13. The patterns of IL2, IFN-gamma, IL4 and IL5 gene expression in Hodgkin's disease and reactive lymph nodes are similar.
- Author
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Serrano D, Ghiotto F, Roncella S, Airoldi I, Cutrona G, Truini M, Burgio VL, Baroni CD, Ferrarini M, and Pistoia V
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- Adolescent, Adult, Aged, Female, Hodgkin Disease genetics, Humans, Interleukin-2 genetics, Interleukin-4 genetics, Interleukin-5 genetics, Lymph Nodes metabolism, Male, Middle Aged, Polymerase Chain Reaction, Gene Expression, Hodgkin Disease metabolism, Interferon-gamma genetics, Interleukins genetics, Lymphatic Diseases metabolism
- Abstract
Background and Objective: The lymph nodes involved in classic Hodgkin's disease (HD), i.e. mixed cellularity (MC) and nodular sclerosis (NS) subtypes, usually contain few (1-2%) Reed-Sternberg (RS) cells scattered in a background of lymphocytes, eosinophils, plasma cells and neutrophils. CD4+ T-lymphocytes are increased in number, express activation markers and cluster around RS cells. The presence of eosinophilia in most HD patients and the presence of hyper-IgE in a subset of them may suggest that activated lymph node T cells release large amounts of IL5 and IL4, respectively., Methods: The expression of four T-cell-associated cytokine genes, i.e. interleukin (IL)2, IL4, IL5 and interferon (IFN)-gamma, in frozen sections of 14 HD (7 MC, 7 NS) and 10 reactive lymph nodes was investigated by qualitative and quantitative reverse transcriptase-polymerase chain reaction (RT-PCR). T-cell clones were also raised from purified CD4+ lymphocytes of one HD lymph node and one reactive lymph node and tested for IL2, IL4, IL5 and IFN-gamma secretion in culture supernatants by immunoassays., Results: The transcripts of all the cytokine genes were detected in every lymph node irrespective of the HD or reactive nature. HD or reactive lymph node-derived CD4+ T-cell clones released the four cytokines according to a predominant T-helper (Th)0-type pattern. In more than half of the lymph nodes of either HD or reactive nature, there was a predominance of IL4 over IFN-gamma mRNA production (Th2-type pattern). In the remaining HD or reactive lymphadenopathies, either a balanced IL4/IFN-gamma mRNA ratio (Th0-type pattern) or a predominance of IFN-gamma over IL4 mRNA expression (Th1-type pattern) was observed., Interpretation and Conclusions: The overall pattern of cytokine gene expression in classic HD is similar to that detected in reactive lymph nodes. Further studies are needed to determine whether differences in the absolute concentrations of cytokines released in HD versus reactive lymph nodes and the long-standing course of HD versus the self-limiting nature of reactive adenopathies may explain certain peculiar features of HD, such as eosinophilia, for example.
- Published
- 1997
14. [Antigenic analysis of immunoglobulins in lymphoproliferative diseases (author's transl)].
- Author
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Scolari L and Ferrarini M
- Subjects
- Humans, Antigens analysis, Immunoglobulins analysis, Lymphoproliferative Disorders immunology
- Published
- 1979
15. In vitro effects of adenosine induced supernatants on human T lymphocyte functions.
- Author
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Pardi R, Ferrarini M, Gromo G, Manfredi A, Memoli M, Zocchi MR, and Sabbadini MG
- Subjects
- Animals, Cells, Cultured, Lymphokines physiology, Rats, Receptors, Immunologic physiology, Receptors, Interleukin-2, T-Lymphocytes physiology, Adenosine pharmacology, Lymphocyte Activation drug effects, T-Lymphocytes drug effects
- Published
- 1987
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