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Biomedical subjects

P de Paoli

Publications and source records attributed to P de Paoli.

14 recordsLinked to original sources
PubMed1996

Treatment of human immunodeficiency virus infection with hydroxyurea: virologic and clinical evaluation.

To assess the efficacy of the therapeutic use of inhibitors of ribonucleotide reductase for the treatment of human immunodeficiency virus (HIV) type 1 infection, 7 consecutive patients were enrolled in a clinical trial involving monotherapy with hydroxyurea for 8-19 weeks. During therapy, patients were evaluated for clinical status and immunologic, hematologic, and quantitative virologic parameters, including determinations of viremia and the number of provirus-containing cells by competitive polymerase chain reaction. In all patients, these parameters were not modified during the course of therapy. The number of CD4 cells remained generally unchanged or showed a tendency to further decline. No sign of improvement in HIV disease was detected in any patient. These observations indicate that monotherapy with hydroxyurea does not provide therapeutic benefit to HIV-1-infected patients.

Acquired Immunodeficiency Syndrome↗
PubMed1991

Long-term human B cell lines dependent on interleukin-4 and antibody to CD40.

CD40 is a 45- to 50-kilodalton transmembrane glycoprotein expressed on B lymphocytes, epithelial cells, and some carcinoma cell lines. Human resting B lymphocytes entered a state of sustained proliferation when incubated with both the mouse fibroblastic Ltk- cell line that had been transfected with the human Fc receptor (Fc gamma RII/CDw32) and monoclonal antibodies to CD40. In combination with interleukin-4, factor-dependent long-term normal human B cell lines were generated that were consistently negative for Epstein-Barr viral infection. Thus, cross-linking of CD40 is likely to represent an important phenomenon in the clonal expansion of B cells.

Antibodies, Monoclonal↗
PubMed1990

Phenotypic analysis of a CD2- CD3+ T cell receptor gamma delta lymphocyte subset.

We have identified, in a patient with atopic dermatitis, a consistent population of peripheral blood lymphocytes expressing a CD3+ gamma/delta TCR complex, while being unreactive with CD2. Further immunofluorescence studies showed that these cells almost completely co-express CD29 and CD45RA and have high membrane levels of CD11a compared to the alpha/beta TCR T cells. Neither a genetic influence nor an acute or reactivated herpesvirus infection were found to be related to the expanded gamma/delta T-cell subpopulation. Our data confirm the previous observations regarding the presence in the peripheral blood of an expanded gamma/delta TCR, CD2- subset and show that these cells have a peculiar phenotypic profile. The reasons for this expansion are, however, still unknown.

Adult↗
PubMed1986

Enzyme- and immunohistochemical study of a case of histiocytic necrotizing lymphadenitis.

A combined morphological, immunohistological, and enzyme histochemical analysis was performed on frozen and fixed lymph node tissue in a case of histiocytic necrotizing lymphadenitis (HNL) using conventional histology, a panel of monoclonal and polyclonal antibodies, and a series of common haematological enzyme reactions. Histology showed multiple paracortical necrotizing foci which, in a prominently necrobiotic background devoid of granulocytes, contained large numbers of foamy histiocytes and macrophages intermingled with cells resembling degenerating plasmacytoid T-cells. Most of the histiocytes were alpha1-antichymotrypsin positive and foamy cells were also distinctly Leu-M1 positive. Strong granular acid phosphatase (AP) positivity was present in the cytoplasm of the macrophages and histiocytes. The cells with plasmacytoid features showed weaker and homogeneously diffuse AP staining. Alpha-naphthyl acetate esterase (ANAE) activity was much less striking than AP in the necrotizing foci and most of the ANAE negative cells corresponded to those with plasmacytoid features. No cells with B-cell lineage markers were present within the necrotizing foci; most of the occasional T-cells (Leu-1+, Leu-4+) present in the foci were Leu-2a+ (OKT8+) whereas OKT10+ lymphoid cells were abundant and appeared to correspond with the cells with plasmacytoid features. Our combined data confirm that the special type of necrosis found in HNL develops within foci of plasmacytoid T-cells undergoing regressive changes and apparently exhibiting distinct immunohistological and enzyme histochemical features.

Adult↗
PubMed1986

Persistent generalized lymphadenopathy in Northeastern Italy: increased frequency of HLA-DR 5.

We undertake a study of Italian intravenous drug abusers and male homosexuals with the prolonged generalized lymphadenopathy syndrome (PGL). 75% of the subjects had the HLA-DR 5 antigen (relative risk 3.25). Only one patient was DR 2 positive. 14/20 subjects had anti-HTLV III antibodies and immunological malities were a rather constant finding.

Acquired Immunodeficiency Syndrome↗
PubMed1986

OKT4+ chronic lymphocytic leukaemia cells display different reactivity with selected monoclonal antibody combinations.

Four cases of chronic T lymphocytic leukaemia are characterized by selected monoclonal antibody combinations and double-fluorescence studies. We found 3 possible combinations: OKT4++ Leu8++ Leu9+, OKT4++ Leu8+ Leu9- and the OKT4++ Leu9++ Leu8- phenotypes are correlated with different biological aspects of the disease. No markers of T cell activation were found, and serological examinations did not reveal anti-HTLV-I antibodies. In considering a larger number of patients, multiparametric analysis could be useful to better classify this heterogeneous type of leukaemia.

Aged↗
PubMed1985

Expression and modulation of common acute lymphoblastic leukaemia antigen by B prolymphocytic leukaemia cells.

Leukaemic blood lymphocytes from patients with B prolymphocytic leukaemia express the common acute lymphoblastic leukaemia antigen (CALLA). The in vitro incubation of prolymphocytes with leucocyte conditioned medium produced the acquisition of plasma cell morphology, of intracytoplasmic immunoglobulins and the simultaneous reduction of CALLA expression. The presence of CALLA appears to be unrelated to different clinical courses. Our report demonstrates that the antigen is present also in relatively mature stages of B lymphocyte differentiation. The blastic appearance of prolymphocytes could suggest that CALLA may be related to active metabolism or function of these cells.

Antigens, Neoplasm↗
PubMed1984

Chronic T lymphocytic leukaemia: antigenic, morphological and functional properties of the neoplastic lymphocytes.

We describe 2 cases of T cell leukaemia. Both patients react with OKT 4 monoclonal antibody, while their clinical course, surface markers and in vitro immunological reactivity present opposite behaviour. The cells of 1 patient react with all pan T cell markers (OKT 3, OKT 11, Leu 1), from E and Ea rosettes and respond well to mitogens. This patient does not present liver, spleen or lymph node enlargement; white cell count is stable and no other haematological alterations are present. The cells from the 2 patient are unreactive with OKT 3 and are unable to form Ea rosettes. The response to mitogens is almost abolished. The disease has an aggressive clinical course with progressively increasing blood leucocyte count and infiltration of liver and spleen. These data suggest that the study of antigenic and functional properties of T CLL may be useful to better define the biologic characteristics and the prognostic criteria of the disease.

Aged↗
PubMedDate not supplied

CD8 lymphocytes during Epstein Barr virus (EBV) infection: A CD29 positive population is expanded in acute infectious mononucleosis.

The expression of phenotypic markers on CD4 and CD8 lymphocytes during the acute and convalescent phases of Epstein Barr virus (EBV) induced infectious mononucleosis was examined by two colour flow cytometry. Activated CD8 cells constitute the major population increased during acute infectious mononucleosis; in this phase we observed a preferential expansion of the CD8 CD29+ compared to the CD8 CD45RA+ cells. Serum soluble CD8 levels were also raised during the acute phase and a correlation with CD8 CD38+ and CD8 CD29+ cell numbers was found. The convalescent phase of infectious mononucleosis was characterized by a progressive return of CD8 subset and of soluble CD8 to baseline normal values. These results demonstrate that acute EBV infection induces the expansion of a CD8 subset with peculiar surface antigenic profile.

Acute Disease↗
PubMedDate not supplied

Effects of alpha-interferon and steroids on CD23 expression and release in B-cell chronic lymphocytic leukemia.

BACKGROUND: Since high CD23 expression and release have been reported in B-chronic lymphocytic leukemia (B-CLL), we investigated whether alpha-interferon or corticosteroids were able to modulate the expression and/or the release of this factor. METHODS: CD23 expression was determined with FITC-labelled anti-CD23 monoclonal antibody, and sCD23 release with a sandwich enzyme immunoassay. Twenty-one patients affected by B-CLL (stage A or B) were studied before and after three different treatment regimens (alpha-interferon, corticosteroids, alpha-interferon+corticosteroids). RESULTS: CD23 was highly expressed in the B-cells of all patients, and expression was not modified by any of the therapies, sCD23 release from leukemic cells was significantly greater (p < 0.00001) in untreated subjects than controls, and in vitro treatment with phorbol myristate acetate (PMA) led to a 10-fold increase (p < 0.0001) in sCD23 secretion. On the contrary, PMA did not increase sCD23 release in normal B cells. Treatment with corticosteroids (either alone or associated with alpha-interferon) reduced sCD23 secretion from leukemic cells, whereas alpha-interferon alone was not able to modify sCD23 release. CONCLUSIONS: Our data support the hypothesis that CD23 plays a role in the maintenance and progression of B-CLL and that the pharmacological modulation of this receptor/lymphokine could be useful in the therapy of B-CLL.

Aged↗