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Biomedical subjects

W Ptak

Publications and source records attributed to W Ptak.

At least 109 records · Page 6Linked to original sources
PubMed1980

Macrophage suppressor factor in contact sensitivity. Mechanisms of its release and action.

An antigen-specific suppressor factor (TSF) produced by mouse T lymphocytes prevents immune cells from conferring adoptive immunity on normal recipients. This TSF attaches easily to the macrophage surface, and these 'armed' macrophages in the presence of a corresponding antigen manufacture (in vitro) a non-specific macrophage suppressor factor (MSF) which impairs the activity of cells sensitized to homologous or heterologous antigens. Our experiments show that MSF is temperature- and trypsin-sensitive, and is not a prostaglandin. Its molecular weight is in the range of 10 kD. MSF is synthesized by macrophages de novo subsequent to triggering by TSF and antigen. MSF impairs only the activity of cells mediating contact sensitivity reaction (Ly 1) but has no influence on T-suppressor cells (Ly 23). The possibility that MSF is an enzyme is discussed.

Animals↗
PubMed1979

Ontogeny of cells involved in the suppressor circuit of the immune response.

Some macrophage (M phi) cell surface structures which bind T cell-derived factors remain intact after the M phi are killed by heating at 56 degrees C (but not 72 degrees C) for 45 min. As a result, appropriately killed M phi (HK M phi) can act as competitive antagonists for those M phi functions which are involved in binding and active presentation of T cell-derived regulatory signals. By blocking the transmission of these signals with HK M phi, we have found that the spleens of newborn mice contain considerable numbers of "latent" helper cells whose activity is not ordinarily seen because it is overridden by suppressor mechanisms. Similarities between these neonatal helper cells and a subset of adult T helper "inducer" cells (cell surface phenotype Ly-1+; Ly-2-, 3-; IJ+; Qa 1+), whose activity appears in significant numbers only after immunization, are described.

Animals↗
PubMed1978

Intermediary role of macrophages in the passage of suppressor signals between T-cell subsets.

We have examined the ability of macrophages (Mphi) to transmit T-cell derived suppressor signals to other T cells. The suppressor signal studied is an antigen-specific factor which suppresses the ability of adoptively transferred, sensitized lymphocytes to express contact hypersensitivity in normal recipients. We have found that this factor binds to peritoneal exudate Mphi via cell surface structures which can be blocked with heat-aggregated gamma globulin. Dead (HK) Mphi bind the factor but fail to present it in a functional way to assay (immune) T cells, whereas live (L) Mphi perform both functions. Further, L Mphi can retrieve the factor in an active form from the surfaces of HK Mphi. Based on these and other findings (1-5), we discuss the possibility that Mphi may play as important a role in presenting T-cell communication signals to the cells of the immune system as they do in presenting antigen.

Animals↗
PubMed1978

Splenic suppressor cells in fetal and newborn mice.

Newborn mice are refractory to sensitization with picryl chloride and the graft versus host reaction (GvHR) in F1 fetal mice injected with parental lymphocytes is markedly reduced. Moreover, spleen cells (but not thymic lymphocytes) of fetal or newborn animals are able to suppress the cell-mediated immune responses, contact sensitivity (CS) and GvHR in a variety of experimental situations. The inhibitory cells are thy-positive and their suppressive activity wanes early after birth.

Animals↗
PubMed1978

Modification of the activity and surface topography of peritoneal macrophages by cytophilic antibody.

Cytophilic antibody (Cab) attached to the macrophage surface substantially changes the cell surface relief as tested in the scanning electron microscope. Diffuse loss of surface structure is accompanied by diminished ability to interiorize opsonized sheep erythrocytes and to damage non-specifically bystanding target cells (chicken erythrocytes). Cross-linking of Cab on the macrophage surface by antigen or antibody partially restores macrophage membrane activity.

Animals↗
PubMed1978

Split unresponsiveness to trinitrophenyl (TNP) determinant. Suppression of anti-TNP antibody responses by sensitization with picryl chloride.

Contact sensitization by epicutaneous application of picryl chloride causes in mice a significant reduction of the antibody responses to immunogenic TNP-conjugates. This split unresponsiveness is along-lasting. It was found that hapten applied on the skin became attached to the serum proteins and the transfer of such a serum into normal recipients, while not influencing the ability of these animals to become contact-sensitized to PCl, rendered them unable to mount the anti-TNP antibody response. Possible mechanisms of split unresponsiveness to the TNP determinant induced by PCl treatment are suggested.

Animals↗
PubMed1977

The immunopotentiating effect of thiosulphate in vivo.

Sodium thiosulphate injected i.v. into mice causes a marked increase in concentration of several serum proteins, particularly immunoglobulins. When given together with antigen, it significantly potentiates the T-dependent humoral responses.

Animals↗
PubMed1977

Split unresponsiveness to the trinitrophenyl determinant. I. Manoeuvers which suppress either humoral or cell-mediated immune responses.

2,4,6-Trinitrobenzene sulfonic acid (TNBS) injected intravenously (i.v.) makes mice fully tolerant to the trinitrophenyl (TNP) determinant. Administration of in vitro TNP-labeled syngeneic erythrocytes or thymocytes renders mice unable to develop contact sensitivity to picryl chloride, while the humoral anti-TNP responses seem to be unaffected. The reverse was found after pretreatment of mice with TNP-labeled isologous IgG (MGG) since only anti-TNP antibody responses, but not contact sensitivity to picryl chloride, were significantly reduced. TNP-coupled macrophages given to animals suppressed both the cell-mediated and humoral responses, and this might be due to the presence on their surface of TNP-labeled cytophilic antibody. TNBS administered i.v. binds to circulating proteins and formed blood elements. Thus the split unresponsiveness affecting either humoral or cell-mediated compartments after the injection of TNP-MGG or of haptenated cells respectively, is presumably due to dissecting events which in vivo after the injection of TNBS, occur simultaneously. These results may be interpreted to indicate that split unresponsive states to TNP determinants are mediated two independent mechanisms which require different tolerogen presentations to be triggered.

Animals↗
PubMed1977

Inhibitory effect of alpha-globulins of different origin on the cell-mediated immune responses in mice.

alpha-Globulins prepared from different biological sources (human and bovine sera, mouse ascitic fluid, human ovarian cyst fluid) were separated by ion exchange chromatography on DEAE-cellulose into fractions A, B and C. Whereas fractions A and B had no immunosuppressive activity, fraction C injected into mice shortly before antigen administration, but not after, significantly inhibited the contact sensitivity to oxazolone. Single high doses were preferential over divided doses given on several occasions. In transfer experiments when cells of animals sensitized to oxazolone were injected into recipients treated previously with fraction C, the response was also inhibited. Fraction C, when administered into F1 hybrid mice before injection of parental splenocytes, prevented the development of GVH reaction. The authors point out that the critical concentration of alpha-globulins at the time of antigen administration is necessary to make T-lymphocytes hyporesponsive, and when once triggered by antigen they become refractory to alpha-globulins action.

Alpha-Globulins↗
PubMed1977

Interference with the transmission of T cell-derived messages by macrophage membranes.

Heat-killed macrophages (HK Mphi) and/or semi-purified Mphi membranes interfere with primary thymus-dependent but not thymus-independent in vitro immune responses. In addition, they can absorb out and render inactive the helper activity found in mixed lymphocyte culture supernatants which augments the primary in vitro response of normal spleen cells. They do not, however, inactivate the helper activity which augments the response of thymus-deprived spleen cells. Both the immunologic interference and the absorbing activity of the HK Mphi are eliminated by treatments which inactivate or block Fc receptors. We suggest that HK Mphi or their membranes can act as competitive antagonists for live Mphi functions and in so doing block communication networks between T cell subclasses. Thus they can serve as useful probes both for studying some of the roles live Mphi might play in mediating immunologic functions as well as dissecting out some of the many arcane T cell interactions which normally occur.

Animals↗
PubMed1977

Fetal suppressor cells. Their influence on the cell-mediated immune responses.

The cell-mediated immune responses are significantly reduced in fetal and newborn mice, furthermore, spleen cells of these animals are able to suppress the immune responses of adult lymphocytes in a variety of situations. Newborn mice sensitized to picryl chloride within 24 hr after birth fail to develop contact sensitivity reaction when tested several weeks later, and fetal mice do not develop graft-versus-host reaction when given injections of parental lymphocytes. Spleen cells of fetal or newborn mice are able to suppress the passive transfer of contact sensitivity and the local graft-versus-host reaction elicited by immunized parental cells in F1 hybrid mice, and reduce significantly the severity of graft-versus-host reaction and mortality rate in cyclophosphamide-treated F1 recipients. In no experiment were thymus cells of either fetal or newborn mice found to be inhibitory. The possible mechanisms of action and biological significance of fetal suppressor cells are discussed.

Aging↗
PubMed1977

Impaired antibody responses in alloxan diabetic mice.

Alloxan diabetic BALB/C mice with high hyperglycaemia levels (larger than or equal to 600 mg/100 ml) when immunized either with T-dependent (SRCB) or T-independent (TNP-LPS) antigens show a significant decrease in the number of specific PFC when compared with normo-glycaemic controls. Moderate diabetes (greater than 350 mg/100 ml) does not affect the immune response and in some experiments a slight increase of anti-SRBC plaques was seen. In transfer experiments primed spleen cells of either diabetic or normal doners gave much better responses when transferred to normal rather than diabetic X-irradiated recipients. In Mishell-Dutton (MD) cultures anti-SRBC response of CBA spleen cells was moderately reduced only when the blood glucose level of cell donors exceeded 500 mg/100 ml. Glucose added to MD cultures of normal spleen cells diminished significantly the number of SFC when in concentrations exceeding 600 mg/100 ml. The data indicate that in diabetic animals B-lymphocyte function may be affected but give no clear-cut answer to whether this is also true for T-helper cells. Disabled lymphocytes, whatever population they represent, may partially recover when transferred into normo-insulinic milieu. It may be inferred that under conditions tested neither hyperglycaemia nor excess of corticosteroid accounted significantly for the impaired humoral responses in diabetic animals. These experiments imply, however, that in hypoinsulinaemia the lack of saturation of insulin receptors on the lymphocyte, and possibly also macrophage, membranes renders these cells functionally inactive presumably due to accumulation of cyclic AMP in the cell membrane.

Adrenalectomy↗
PubMed1977

Feedback inhibition of IgM memory cells by high antigen dose.

The ability of high and low antigen doses (SRBC) to recruit IgM memory cells has been compared in several strains of mice. In intact animals priming with low doses was more efficient than priming with high doses. If, however, mice of different strains were X-irradiated two days after priming and repopulated, regardless of whether syngeneic or allogeneic splenocytes were used, they fell into two categories--those in which more memory cells were found after low antigen priming and those in which the reverse was true (Swiss mice). Two possible explanations are offered to explain these interstrain differences--antibody mediated suppression, and generation of suppressor T cells. Our data favor the latter, and we assume that suppressor T cells appear at different intervals after priming in different strains of mice, and that these cells are radioresistant.

Animals↗
PubMed1977

Inflammatory giant cells: immunophagocytosis and rosette formation.

Mouse inflammatory giant cells formed after subcutaneous implantation of coverslips were exposed to sheep red blood cells opsonized with isologous antibodies. The maximal number of engulfed erythrocytes in numerous multinuclear cells exceeded that encountered in subcutaneous macrophages, but, on a per nucleus basis, the giant cells appeared less phagocytic.

Animals↗