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Biomedical subjects

M Zembala

Publications and source records attributed to M Zembala.

At least 181 records · Page 10Linked to original sources
PubMed1978

Migration inhibition of T lymphocytes from human peripheral blood by specific antigen and lymphokines.

The inhibition of migration of human peripheral blood cells in the presence of PPD was studied. It was found that migration inhibition of peripheral blood mononuclear cells (MN) from Mantoux-positive donors was far greater than the migration inhibition of peripheral blood leucocytes (PBL). Moreover, MN cells and T lymphocytes showed larger and more uniform areas of migration. In contrast, the migration of B lymphocytes and monocytes was poor. Further analysis using purified subpopulations of MN cells showed that PPD inhibited the migration of T lymphocytes but not of B lymphocytes and monocytes. Corresponding to these findings, lymphokine-containing supernatants also inhibited the migration of purified T cells from Matoux-negative donors. It was concluded that the T lymphocyte was the predominant cell in the MN cell population, which migrated, and was subject to inhibition by PPD or lymphokines. These results imply that the movement of human T lymphocytes may be influenced by soluble factors from antigen-activated sensitized cells.

Adult↗
PubMed1978

Suppression of anti-hapten (TNP) antibody response by suppressor T cells and their product. The role of macrophages.

The effect of the lymphocytes from picryl sulfonic acid treatment animals on primary and secondary humoral immune response to TNP hapten was investigated. These cells known to inhibit contract sensitivity reactions were also able to depress primary IgM response. When peritoneal exudate cells from normal mice incubated in suppressor supernatant were transferred into primed mice the suppression of IgM but no IgM secondary response was observed. In contrast peritoneal exudate cells incubated in control supernatant augmented IgM but didn't affect IgG response. It is postulated that normal peritoneal exudate cells (presumably macrophages) can stimulate IgM response. This enhancing activity could be partially blocked by soluble suppressor factor.

Animals↗
PubMed1978

Monocyte changes in cancer patients and their role in mitogen induced lymphocyte responses.

Monocyte Fc receptor expression and monocyte-mediated antibody dependent cell cytotoxicity (ADCC) was studied in a group of patients with stomach and colorectal carcinoma. Is was found that FC receptor expression and ADCC was increased in patients as compared to control subjects. These differences were more evident after trypsin pretreatment of monocytes. There was an inverse correlation between these changes and lymphocyte response to PHA. The role of monocyte functional changes in determining the magnitude of patients' lymphocyte response is discussed.

Antibody-Dependent Cell Cytotoxicity↗
PubMed1978

The in vitro migration inhibition of mononuclear cells in patients with colorectal carcinoma.

The response of peripheral blood mononuclear cells to PHA and PPD in migration inhibition test has been studied in patients with Duke's B-D colorectal carcinoma. It was found the response of patients cells to both stimulants was increased. This enhanced lymphokine release and/or production was closely connected with the tumor load. The implications of these findings to the regulatory mechanisms of the immune response in cancer patients are briefly discussed.

Adult↗
PubMed1977

Depressed in vitro peripheral blood lymphocyte response to mitogens in cancer patients: the role of suppressor cells.

The reactivity of peripheral blood lymphocytes from patients with advanced malignancy was assessed by mitogen-induced stimulation of protein synthesis as measured by 3H-leucine incorporation. It was confirmed that the lymphocyte response of patients was depressed. Furthermore, the lymphocytes of 15 out of 27 cancer patients, selected because of their low responses, inhibited the reactivity of normal lymphocytes in co-cultures. The lymphocytes from one patient with Hodgkin's disease were also inhibitory. In contrast, lymphocytes from healthy subjects, patients with chronic lymphocytic leukaemia, lymphosarcoma or multiple myeloma caused no suppression. Experiments with purified cell populations from patients with carcinoma indicated that purified T cells responded to mitogens while unseparated lymphocytes failed to respond and that the inhibitory activity was due to adherent cells, presumably monocytes. There was no evidence for B-cell-mediated suppression. However, in two cases inhibition was caused by isolated T cells of the patients and not by adherent cells. These experiments suggested that one mechanism for the depression of cell-mediated immunity seen in patients with advanced cancer may be the nonspecific suppresssion of certain T-cell functions by circulating monocytes.

Adult↗
PubMed1977

Suppressor T cell product, which depresses the passive transfer of contact sensitivity, shares epitope(s) with the major histocompatibility complex.

Specific suppressor T cell product appears in the supernatant of cultures of lymph node cells of mice injected with picryl sulphonic acid and then painted with picryl chloride. It is detected by its ability to depress the passive transfer of contact sensitivity by immune cells incubated in it. This communication shows that the product can be absorbed by antisera prepared against the major histocompatibility locus but not by antisera prepared against mouse immunoglobulin.

Animals↗
PubMed1977

Analysis of the induction phase of contact sensitivity by footpad transfer of regional lymph node cells. Macrophages and radioresistant T-lymphocytes induce immunity.

The skin of CBA mice was painted with the contact sensitizing agent 4-ethoxymethylene-2-phenyloxazolone (oxazolone). One day later the regional lymph node cells were injected into the footpads of normal recipients. The recipients were tested 6 days later for contact sensitivity by challenging the ears with oxazolone and measuring the increase of ear thickness at 24 h. T cells and macrophages in the regional lymph nodes each independently gave rise to contact sensitivity in the recipient following injection into the footpad. This activity of T cells and macrophages was found in lymph nodes taken 1, 3 and 4 days after painting the donors. The role of T cells in the injected population was shown by purifying T cells by nylon-wool filtration and rosetting with sheep red cells coated with antibody and complement (EAC rosetting) and by destroyed T cells with anti-0 serum and complement. The activity of purified T cells resisted 2000 rad in vitro. The activity of cells from T-deprived (B) mice showed that a second cell type was important in the footpad transfer. This cell behaved like a macrophage, and not like a B cell, on EAC rosetting in the presence or absence of divalent cations and on treatment with silica and carrageenan--agents which damage macrophages. Our working hypothesis is that the footpad transfer may be caused independently by macrophages or T cells with oxazolone (probably linked to major histocompatibility complex antigens) on their surface and that these cells act by collaborating with T cells in the recipient which give rise to the effector cells for contact sensitivity.

Animals↗
PubMed1976

Adult thymectomy prevention of the appearance of suppressor T cells which depress contact sensitivity to picryl chloride and reversal of adult thymectomy effect by thymus extract.

Suppressor cells, which depress the passive transfer of contact sensitivity appear in the lymph nodes and spleen of mice injected with picryl sulfonic acid (PSA). These cells produce a soluble suppressor T cell product (s-TCP), and immune lymph node cells incubated in s-TCP fail to transfer contact sensitivity. This paper shows that the appearance of suppressor T cells following the injection of PSA was prevented by adult thymectomy (ATx). ATx also limited the production of s-TCP. However, ATx had no effect on the DNA synthesis which occurs in the lymph nodes of mice injected with PSA. The adverse effect of ATx on suppressor cells was completely reversed by a neonatal thymus graft placed under the renal capsule and partially reversed by grafts given 600 r in vitro and to a limited extent by grafts given 1000 r. The injection of thymus extract also reversed the effect of ATx whereas splenic extract was inactive. It is suggested that the suppressor T cell which depresses contact sensitivity is dependent on the presence of the thymus because it requires a thymus hormone, and not primarily because it belongs to a short-lived population which is rapidly renewed by cells coming from the thymus.

Animals↗