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S Tognella

Publications and source records attributed to S Tognella.

17 recordsLinked to original sources
PubMed1979

Interference of levamisole with inhibition of E-rosette formation by Hodgkin's disease and systemic lupus erythematosus cytotoxic sera.

A new system has been used to test the influence of levamisole on T-cell function. Evidence has been produced that prior exposure to the drug "protects" normal human peripheral blood lymphocytes from the inhibition that cytotoxic sera from patients with Hodgkin's disease and systemic lupus erythematosus exhibit on their E-rosette-forming capacity. Also, damage of this T-cell function already induced by Hodgkin's sera may be partially corrected.

Cytotoxicity, Immunologic↗
PubMed1976

[Comparison between anti-lymphocyte antibodies in systemic lupus erythematosus and in Hodgkin's disease].

Anti-lymphocyte antibodies of cold-reactive IgM-type in Systemic Lupus Erythematosus (SLE) and IgG-type in Hodgkin's disease (HD) by means of immunofluorescent technique have been demonstrated. The contemporaneous attachment of SLE and HD sera on selected peripheral lymphocytes demonstrate that the target cell is T-lymphocyte and that the two kinds of antibodies coat the same cell. Co-capping experiments have shown that the phenomenon has the same behaviour as regard to SLE and HD antibody, indicating that the antigen is the same. Hypothesis about the meaning of these antibodyies have been made.

Antibody Formation↗
PubMed1976

[Presence of alpha-2-macroglobulin on the membrane of peripheral human blood lymphocytes : a new lymphocyte maker].

The presence of alpha-2-macroglobulin (alpha-2-M) on the surface of peripheral blood lymphocytes from normal human subjects and from patients with chronic lymphatic leukaemia (CLL) and with ataxia-teleangectasia was studied by indirect immunofluorescence technique. Same experiments were done on purified subpopulations of normal blood peripheral lymphocytes (B and T). The percentage of alpha-2-M bearing lymphocytes is 17 +/- 6% as regard to normal subjects (Ig-bearing cells are 14%): in CLL the percentage of alpha-2-M bearing cells generally is significantly lower than that of Ig-bearing cells (IgM-IgD). On selected subpopulations, 90% of alpha-2-M bearing cells are present among non T-cells and only 5% among T-cells (probably due to not absolute purification). Blocking experiments using anti-Ig sera did not affect significantly the percentage of alpha-2-M bearing cells and using anti-alpha-2-M sera did not affect that of Ig-bearing cells. The percentage of E-rosette forming cells is not affected by pretreatment of peripheral lymphocytes with anti-Ig and/or anti-alpha-2-M sera. Hypothesis is set forth that alpha-2-M bearing cells could be a lymphocytes subpopulation made by a subgroup of B-cells and by K-cells, taking part in that immunoregulatory system in which collaborate many serum alpha-globulins and T-suppresor cells.

Antibody Formation↗
PubMed1976

Anti-lymphocyte antibodies in systemic lupus erythematosus and in Hodgkin's disease: a comparison by immunofluorescence.

Anti-lymphocyte antibodies of IgM type (cold reactive) in systemic lupus erythematosus and of IgG type (not cold reactive) in Hodgkin's disease have been demonstrated by immunofluorescence to attach the same target cell (T-lymphocyte.) The same behaviour of both kinds of antibodies in "co-capping" experiments confirm that the antigen on the cell surface is the same. Hypothesis about the meaning of this phenomenon are made.

Antilymphocyte Serum↗
PubMed1975

[Electrophoretic mobility of peripheral lymphocytes and Hodgkin's erythrocytes. Correlation with some clinical, hematological and immunological parameters of the disease].

In 32 patients with Hodgkin's disease the electrophoretic mobility of peripheral blood lymphocytes and, at the same time, some clinical, hematological, and immunological parameters of the disease were determined. The mean mobility of lymphocytes was normal; nevertheless, the lymphocytic mobility of 8/32 patients was significantly decreased. No correlation with clinical, hematological, and immunological parameters of the disease was detected. However, the functional deficiency of hodgkinian T lymphocytes seems to play a role in their abnormal electrophoretic behaviour. In 9 out of these 32 patients the electrophoretic mobility of peripheral erythrocytes was also determined. The average mobility was significantly (P less than 0.05) decreased. No correlation with clinical, hematological, and immunological parameters nor with electrophoretic mobility of lymphocytes was detected.

Antibodies, Neoplasm↗
PubMedDate not supplied

[Effects of Hodgkin cytotoxic serum on electrophoretic mobility of normal and Hodgkin peripheral blood lymphocytes. (author's transl)].

The effect of Hodgkin patient cytotoxic sera on the electrophoretic mobility of normal and Hodgkin peripheral blood allo-lymphocytes has been studied. Contact with cytotoxic serum determined a significant decrease in the electrophoretic mobility of lymphocytes, due to the presence of cytotoxic antibody on the lymphocyte surface. The antibody seems to be directed against T-lymphocytes. The results are discussed in the light of the preceding data by the authors on the role of anti-T-autoantibodies in Hodgkin's disease.

Antilymphocyte Serum↗
PubMedDate not supplied

[Effects of Hodgkin cytotoxic serum on blast transformation of normal and Hodgkin human peripheral blood lymphocytes].

The PHA-resposiveness of normal and Hodgkin patient human peripheral blood lymphocytes has been studied before and after incubation with Hodgkin cytotoxic sera. The following conclusions have been reached: (a) Hodgkin cytotoxic serum is capable of decreasing the PHA-responsiveness of normal lymphocytes and of furtherly impairing the already defective PHA-responsiveness of Hodgkin lymphocytes. (b) The impaired PHA-responsiveness can be restored to the original levels by eluting the cytotoxic antibody. Control experiments in which normal and Hodgkin lymphocytes were put in contact with normal and Hodgkin non-cytotoxic serum showed no decrease of PHA-responsiveness. These data are in agreement with the hypothesis that the presence of serum cytotoxin is at least partly responsible for the immuno-incompetence of T-lymphocytes characteristic of Hodgkin's disease.

Antilymphocyte Serum↗