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Biomedical subjects

M A Barcinski

Publications and source records attributed to M A Barcinski.

At least 37 records · Page 2Linked to original sources
PubMed1987

Effect of hydroxyurea on the concanavalin-A proliferative response of Trypanosoma cruzi infected mice.

Mice infected with Trypanosoma cruzi develop immunosuppression with a deficient production of interleukin-2 (IL-2). In this situation the deficient concanavalin A (Con A) T-cell response is not corrected by addition of exogenous IL-2. Here we show that elimination of cycling cells by treatment of infected mice with hydroxyurea (HU) fully restored the ability of spleen cells to respond to IL-2. Further, capacity for IL-2 production was restored to HU treated infected mice, but not as completely as the response to IL-2.

Animals↗
PubMed1987

The cellular immune response to a purified antigen from Leishmania mexicana subsp. amazonensis enhances the size of the leishmanial lesion on susceptible mice.

Immunization of BALB/c mice with gp10/20, a glycoconjugate purified from Leishmania mexicana subsp. amazonensis, induced a delayed-type hypersensitivity response to the antigen, and a significant increase was elicited in the size of the lesion induced by a subcutaneous infection with this parasite. The increase in the lesion size was observed when mice were immunized by the subcutaneous and the intraperitoneal routes. The subcutaneous immunization with gp10/20 was unable to reverse the prophylactic effect of an intravenous injection of irradiated promastigotes. An L3T4+ T-cell line specific for gp10/20 was able to transfer this lesion-enhancing effect and specific delayed-type hypersensitivity reactivity to normal syngeneic recipients. The same T-cell line was a good producer of a hematopoietic growth factor, granulocyte-macrophage colony-stimulating factor.

Animals↗
PubMed1986

Autologous induction of the human T-cell-dependent monocyte procoagulant activity: a possible link between immunoregulatory phenomena and blood coagulation.

Activated monocytes acquire the ability to induce clot formation in platelet-poor citrated human plasma. The generation of this procoagulant activity (PCA) is dependent upon an interactive pathway between monocytes and T lymphocytes. Here we show that an ongoing autologous mixed lymphocyte reaction (AMLR) can elicit a T-cell-instructed PCA. PCA was measured by the ability of the cells to accelerate the clotting time of pooled citrated platelet-poor human plasma. AMLR was measured by tritiated thymidine incorporation. PCA and AMLR had very similar kinetics. Correlation coefficients between both reactions ranged from 0.59 to 0.99. Addition of an anti-DR monoclonal antibody blocked both reactions. T-Lymphocyte-depleted cell populations did not increase their level of PCA after 6 days in culture. Addition of autologous T cells to the T-depleted population restored its ability to produce PCA. Cyclosporin A blocked the peripheral blood mononuclear cell ability to generate PCA. A lymphokine generated during the AMLR was able to induce PCA in normal mononuclear cells. The results indicate that self recognition activates monocytes to produce PCA and suggests that this mechanism may represent a link between immunoregulatory phenomena and blood coagulation.

Antibodies, Monoclonal↗
PubMed1986

Characterization of the T-cell proliferative response to a purified glycopeptide antigen (GP-25) present on the Trypanosoma cruzi cell surface.

A glycoconjugate (GP-25) was previously purified from Trypanosoma cruzi and shown to be a major immunogenic constituent of the parasite cell surface, capable of inducing specific humoral responses in the vast majority of patients with Chagas' disease. In the present study, the T-cell proliferative response to GP-25 was studied in mice immunized with T. cruzi fractions or whole parasites. Recognition of GP-25 by proliferating T cells requires the participation of syngeneic, accessory spleen cells and is specifically blocked by anti-la antibodies. Furthermore, recognition of GP-25 is influenced by the MHC haplotype of accessory antigen-presenting cells. Short-term, GP-25-specific T-cell lines were used to demonstrate the specificity of anti-GP-25 T cells and to show that this glycoconjugate is not involved in T-cell cross-reactivity with heart antigens. T cells primed with nonpathogenic trypanosomatids are able to recognize the purified T. cruzi GP-25 molecule, indicating that T cells recognize a GP-25 epitope which is shared among trypanosomatids.

Animals↗
PubMed1986

Characterization of cellular immune response to chemically defined glycoconjugates from Leishmania mexicana subsp. amazonensis.

Two defined glycoconjugates (GP-10/20 and FR II Phe) purified from Leishmania mexicana subsp. amazonensis were analyzed with respect to their ability to induce cellular responses in immunized and infected mice. Each glycoconjugate was recognized by specific immune cells, as assessed by the proliferative response of lymph node cells of immunized mice. The response to GP-10/20 depended on helper T cells and antigen-presenting cells and was restricted by a major histocompatibility complex class II gene product. A specific anti-GP-10/20 T-cell line was established, and it was able to transfer a delayed-type hypersensitivity (DTH) response to normal mice. Both antigens were also recognized during an ongoing disease, as assessed by DTH response of infected mice. By this response, it was possible to distinguish susceptible from resistant strains of mice. In the course of the disease in resistant mice a correlation between the size of the primary lesion and the DTH response to GP-10/20 was observed. The presence of the glycoproteins on both promastigote and amastigote forms of the parasite, the antigenic similarities between both fractions, and the distribution of the GP-10/20 antigen in other trypanosomatids were studied. The results showed that both antigens were present on promastigotes and amastigotes. GP-10/20 shared no epitopes with FR II Phe, was included as part of the crude preparation leishmanin, and had some cross-reactive determinants with Leishmania donovani and Crithidia deanei.

Animals↗
PubMed1986

Monocyte procoagulant activity induced by concanavalin A is decreased in a population of chronic chagasic patients.

1. The ability of peripheral blood mononuclear cells (PBMC) from Chagas' disease patients to induce monocyte procoagulant activity (PCA) in response to concanavalin A (Con A) and to a Con A induced lymphokine was studied. 2. In spite of the variability of PCA levels among both chagasic patients and normal controls, statistical analysis of the data permitted us to draw the following general conclusions. 3. The Con A-induced monocyte PCA measured in 17 assays of 15 chagasic patients was significantly lower than the PCA response of 18 normal controls or of 11 patients with non-chagasic myocardiopathies. 4. The response of PBMC from chagasic patients to lymphokine was also lower than that observed for normal controls. 5. These results suggest that monocytes from chagasic patients are deficient for the generation of PCA which is an in vitro correlate of the delayed-type hypersensitivity reaction.

Adult↗
PubMed1984

Lymphocyte subpopulations in chronic Chagas' disease.

Monoclonal antibodies of the Orthoclone series were used to identify total T lymphocytes (OKT3) and their helper-inducer (OKT4) and cytotoxic-suppressor (OKT8) subsets in 25 patients with chronic Chagas' disease and 25 healthy controls. No significant difference in the number of total T cells (OKT3+) circulating in the peripheral blood of patients and controls was found. However, in contrast to normal subjects, chagasic patients show quantitative alterations in both helper (OKT4+) and suppressor (OKT8+) T cell subsets. The chagasic patients have abnormal helper/suppressor ratios, with low and high values scattered around the mean. Surprisingly, high ratios were found within females while almost all males have low ratio values. These findings suggest that the putative immunoregulatory disfunctions in patients with chronic chagasic cardiomyopathy may involve both helper and suppressor T cell subsets.

Antibodies, Monoclonal↗
PubMed1982

Induction of the acute-phase protein serum amyloid P in experimental Chagas' disease.

Serum amyloid P protein (SAP), which shares several structural properties with C-reactive protein, has been recently identified as an acute-phase reactant in mice. In this study, the systemic inflammatory response of mice to infection with Trypanosoma cruzi was characterized with respect to induction of SAP as well as to stage-specific alterations on complement C3 and C4 levels. The SAP response depended on the dose and infectivity of the parasites. Kinetic data indicated a close temporal relationship between the onset of parasitemia and induction of SAP. The levels of SAP were maximally enhanced (1,050%) by the time parasitemia started to regress, and the response remained elevated as the infection entered the latency phase. The decline in parasitemia was paralleled by a significant reduction in C3 levels. A reciprocal relationship between the extent of parasitemia and SAP/C3 levels became apparent when these parameters were compared in individual inbred mice during the time of decreasing parasitemia.

Amyloid↗
PubMed1982

Immune recognition in the streptococcal carditis of mice: the role of macrophages in the generation of heart-reactive lymphocytes.

The role of immune T cells and of streptococcus-pulsed M phi in the production of cardiac lesions, as well as the ability of M phi to present streptococcal antigens to mouse lymphocytes, was investigated. Cells of mice infected with extracts of group A streptococcus were able to induce the appearance of heart lesions when transferred to syngeneic receptors as well as to transfer DTH reactions to syngeneic heart extracts. Streptococcus-pulsed M phi were also able to induce heart lesions and an increase in the serum CPK activity when injected into syngeneic receptors. This last phenomenon was only observed in mice aged 5 mo or more. Furthermore, it was shown in an in vitro model of T cell proliferation that peritoneal M phi pulsed with group A streptococci are able to induce a specific response to syngeneic cardiac extracts. M phi pulsed with group G streptococcus failed to induce such a response. Those findings are discussed as part of a model for the induction of rheumatic cardiac lesions in which M phi display a central role by selecting antigenic determinants from the pathogenic organism for presentation to immunocompetent cells.

Aging↗
PubMed1981

Dependence on macrophages of the guinea pig T-cell immune response to Herpetomonas samuelpessoai.

The specific in vitro activation of guinea pig T-lymphocytes by Herpetomonas samuelpessoai and its dependence upon macrophages was studied. Peritoneal exudate T-cells from guinea pigs sensitized against intact H. samuelpessoai organisms were activated specifically in vitro as measured by 3H thymidine incorporation. These same T-cells also were activated by Trypanosoma cruzi extracts, indicating cross reactivity at the cellular level between the two protozoan antigens. The T-cell specific response was found to be dependent on adherent cells. Moreover, macrophages that had been "pulsed" in vitro with H. samuelpessoai organisms were able to induce the specific T-cell activation.

Animals↗
PubMed1980

Role of macrophage-dependent determinant selection in induction phase of streptococcal carditis.

A genetically controlled antigen-presentation function in macrophages is proposed to explain the induction phase of streptococcal carditis. Antigenic determinants in strains of beta-haemolytic streptococci causing rheumatic fever are selected by macrophages, through the operation of immune response (Ir) genes, to be presented to T lymphocytes. Cross-reactivity between the selected determinants and heart tissue components generates clones of autoreactive T cells. Autoimmunity will develop if, coincidental with the presentation of the relevant antigenic determinant, regulation of T-cell production is disturbed. This hypothesis explains the capacity of different strains of streptococcus to produce rheumatic fever and also the variability in host susceptibility to the disease.

Animals↗
PubMed1979

Immune response gene control of determinant selection. II. Genetic control of the murine T lymphocyte proliferative response to insulin.

The genetic control of the murine T cell proliferative response to insulin was examined. It was found for two responder strains of mice that each recognizes a different determinant on the insulin molecule. H-2b mice recognize a determinant in the A chain loop of insulin whereas H-2d mice recognize a determinant that resides in the B chain, possibly in the last eight amino acids. Using H-2 recombinant strains of mice, the location of Ir gene control of the response to both determinants was mapped to the K region and/or I-A subregion of H-2. The possibility of non-MHC regulation of MHC-controlled immune responses is suggested by studies of recombinant inbred strains of mice.

Animals↗