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Biomedical subjects

C L Reinisch

Publications and source records attributed to C L Reinisch.

At least 37 records · Page 2Linked to original sources
PubMed1985

Selective activation of immunoregulatory T-cell circuits by an Ia+ antigen-presenting cell line.

ORA I-a, a cloned Ia+ monocyte tumor line, interacts with distinct immunoregulatory T-cell subsets. ORA cells present soluble and alloantigen to primed lymph node T cells and alloantigen to antigen-activated T-cell clones. However, they induce dose-dependent suppression during primary mixed lymphocyte cultures. Activation of a mixed lymphocyte response (MLR) suppressor pathway is mediated by Ly 1+ T cells. This T-cell subset proliferates in response to ORA when Ly 2+ cells are depleted. Furthermore, once activated, Ly 1+ T cells induce effectors of suppression within fresh T-cell populations. These studies indicate that antigen presentation to distinct T-cell subsets during different stages of an immune response may be mediated by unique antigen-presenting cell subpopulations. Immune homeostasis may thus be controlled not only by regulatory T cells, but also by unique antigen-presenting cells which are responsible for their selective activation.

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PubMed1985

T-cell regulation of erythropoiesis during acute lymphoblastic leukemia.

How and where erythropoiesis is maintained during advanced leukemic disease is an important and, as yet, unresolved question in hematology. To address the potential role of T-lymphocytes as cells that regulate CFU-E differentiation during leukemogenesis, an experimental model of disease has been developed in inbred Balb/c mice. Specifically, three-week-old Balb/c By mice were injected with murine sarcoma virus-murine leukemia virus-Moloney (MSV-MuLV-M), which resulted 6-8 months later in the development of immunoblastic T-cell sarcomas with a leukemic phase. Splenic T cells from either normal or tumor-bearing mice were assessed for their relative ability to modulate erythroid differentiation. Quantitatively, T cells, Ly1 or Ly 2,3 T-cell subsets isolated from tumor-bearing animals significantly enhanced erythropoiesis when compared with comparable normal T-cell subsets. These data suggest that the compensatory shift of erythropoiesis from the bone marrow to the spleen observed during leukemogenesis was facilitated by splenic T cells. In this circumstance, the enhanced erythropoietic function may be mediated by splenic T cells, which are selectively activated by virus.

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PubMed1984

Regulation of B cell lymphomagenesis by a malignant Qal+ inducer T cell clone.

A series of Thy-1.2+ Ly-1+ Qa-1+ malignant T cell clones have been isolated from murine sarcoma virus-murine leukemia-Moloney (MSV-MuLV-M)-induced B cell lymphomas or from MSV-MuLV-M-infected B6 mice. These T cell clones enhance both antigen-independent and -dependent lymphocyte differentiation and function. They also induce the differentiation of granulocytes and erythrocytes in the stem cell compartment, a function that parallels the immunopathology of the disease in vivo. The malignant T cell appears to sustain B lymphoma growth in vivo by releasing a factor (BCGF) that promotes B cell proliferation.

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PubMed1984

Induction of T-cell proliferation by an Ia+ monocytic tumor clone.

Ia+ immature malignant monocyte clones were isolated from retrovirus-induced lymphomas. These lymphomas contained a predominant population of Ly-1+ T cells. In order to explain this anomaly, the functional capacity of one of these clones, ORA I-a, was assessed. The results indicated that ORA I-a could present protein antigen to syngeneic and semisyngeneic antigen-primed lymph node T cells. Allogeneic stimulation, however, could not be induced. Furthermore, ORA I-a-conditioned medium could augment mitogen-dependent and -independent thymocyte proliferation. These studies suggest that the unique populations of malignant antigen-presenting cells can interact with distinct T-cell subpopulations. Functional analyses of these tumor cell lines may thus be useful in elucidating some of the cellular interactions which occur during the course of immunity.

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PubMed1984

The role of vascular smooth muscle cells in experimental autoimmune vasculitis. I. The initiation of delayed type hypersensitivity angiitis.

The destruction of vascular smooth muscle cells (VSMCs) in autoimmune arteritis is a poorly understood phenomenon. For evaluation of the cellular interactions that may contribute to vasculitis, the immunobiology of VSMCs and lymphocytes was explored in vitro. Primary VSMC cultures were established, and the interaction of these cells (from normal or autoimmune mice) with lymphocytes was then assessed. Specifically, splenocytes from MRL/lpr or C3H mice were cocultivated with MRL/lpr or C3H VSMCs. Massive mononuclear cell clusters from normal and autoimmune mice enveloped MRL/lpr VSMCs, which culminated in the detachment of MRL/lpr VSMCs from the culture plate. In contrast, the interaction of SPs from either normal or autoimmune mice did not encompass or destroy normal VSMCs. Further investigation indicated that MRL/lpr, but not C3H, VSMCs spontaneously expressed Ia and released Il-1 like factor(s), which may be at least two mechanisms by which MRL/lpr VSMCs stimulate the in vitro mononuclear cell influx. As a result of these studies, a novel mechanism for the induction of mononuclear cell autoimmune vasculitis is proposed. VSMCs derived from autoimmune mice may stimulate a mononuclear inflammatory cell phlogistic response which culminates in VSMC autodestruction.

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PubMed1984

The isolation and functional characterization of autoimmune clones expressing inappropriate Ia.

The MRL/lpr mouse is an inbred strain widely accepted as a model for autoimmune disease both in murine and human systems. Developed from a series of crosses involving four strains of mice, the MRL/lpr (H-2k) genome is a composite estimated to contain approximately 75% of its parental LG/J (H-2d) genome. To explore the cellular mechanism underlying lymphoproliferation in the MRL/lpr mouse, we have isolated a series of clones from the lymph nodes of MRL/lpr mice with autoimmune disease. Extensive immunofluorescent analyses of these clones, designated the PAC series, reveal expression of IAk and IEk (beta-chain) cell surface antigens, as well as inappropriate expression of IAd, IEd (beta-chain), and H-2d. PAC cells also express MAC-1, MAC-2, RA3-2C2, and RA3-6B2 and contain esterase-positive cytoplasmic granules. The capacity of PAC cells to present antigen was investigated by co-culturing PAC with IA-restricted, antigen-specific T cell hybridomas +/- antigen. These assays demonstrated the PAC inability to present antigen to IAk-restricted T cell hybridomas, as well as their capacity to present antigen to IAd-restricted T cell hybridomas. In addition, activation of MRL/lpr peritoneal macrophages using gamma-interferon resulted in increased fluorescent staining for IAd and IEd concomitant with decreased fluorescent staining for IAk. Based on these findings, we propose a model of lymphoproliferation in which Ly-1+, H-2K+ T cells proliferate to inappropriate d haplotype antigens expressed by a small subset of monocytes in the MRL/lpr lymph node. The major genomic contribution of the LG/J (H-2d) mouse may be in part responsible for inappropriate antigen expression either by age-dependent expansion of d haplotype cells or by age-regulated expression of Iad and H-2d genes.

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PubMed1983

Unique antigens on neoplastic cells of the soft shell clam Mya arenaria.

Soft shell clams (Mya arenaria) are commonly found in coastal waters of both the eastern and western United States. These invertebrates, which have an open circulatory system, may develop neoplasms of the haemolymph which ultimately kill the host. In this study we have 1) recorded the prevalence of hematopoietic neoplasms (HN) in Mya arenaria within a 50 mile radius of Woods Hole, Massachusetts and 2) utilized cells from one HN bearing clam to generate a series of monoclonal antibodies. Our data show that determinants are expressed on HN cells which are not detected on normal clam haemocytes, suggesting separate ontogenetic pathways of cell differentiation.

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PubMed1982

Syngeneic tumor immunizations produce Qa antibodies. Discovery of a new Qa antigen, Qa-6.

BALB/cBy (Qa-2-) mice injected with the syngeneic tumor, ORA I-a (Qa-2+), produced antibodies to Qa-2 and a newly discovered antigen, Qa-6. Specific antisera against Qa-6, in the presence of complement, lyses approximately 40% of lymph-node lymphocytes and splenocytes. Strain distribution analyses indicate that Qa-6 is specified by a gene within the TL subregion of the major histocompatibility complex. Thus, Qa-6 is the third member of the Qa/TL subset of cell surface antigens which is anomalously expressed on certain tumor cells. This finding suggests that the Qa and TL molecules may have a unique, functional role on the cell surface.

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PubMed1982

Repeated isolation of unique Qa2+ Ia+ clonally derived cell lines from Qa2- mice.

Qa2+ tumor cell lines were previously isolated from individual BALB/cBy (Qa2-) splenic lymphomas induced by murine sarcoma virus-murine leukemia virus-Moloney (MSV-MuLV-M). Two clonally derived cell lines, ORA I-a and Thorbly, and one noncloned cell line, BOMS, expressed Qa2, but neither Ly-1 nor Ly-2 were detected. In order to determine whether eight cloned and two noncloned tumor cell lines all represented a unique population of transformed cells, the presence of a series of surface differentiation antigens as studied. In addition to Qa2, each cell line examined expressed IAd, IEd, H-2Kd, H-2Dd, and receptors for C3b and the Fc portion of immunoglobulin (Ig). Neither Thy-1.2 nor Ig were detected on the cell surfaces, and cytoplasmic Ig was not precipitated from metabolically radiolabeled and detergent-solubilized cell extracts. However, monocyte specific alpha-napththyl acetate esterase-containing granules were present in all cell lines examined. Therefore, a unique Qa2+ monocytic cell is repeatedly isolated after chronic MSV-MuLV-M infection. Further analysis of these cells may provide insight into both the regulation of Qa2 expression and the interactions between monocytes and lymphocytes during leukemogenesis.

Animals↗
PubMed1981

Induction of surface Qa2 on lymphoid cells.

Three tumor cell lines isolated from individual murine sarcoma virus-infected BALB/cBy (Qa2-) mice were established. BOMS, ORA I, and Thorbly I were analyzed for the expression of Qa2 and Ly surface differentiation antigens. By Cytofluorograf analysis and absorption techniques, all 3 cell lines were found to be Qa2+, Ly1-, Ly2-. This cell surface phenotype suggests that immature lymphoid cells are uniquely susceptible to transformation by virus. Anomalous appearance of Qa2 on transformed lymphoid cells may be analogous to TL antigen induction.

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PubMed1980

The induction of immunoblastic T cell sarcomas by virus-transformed prothymocytes.

The ontogeny of thymus-dependent lymphoid tumors induced by murine sarcoma-murine leukemia virus (MSV-MuLV) was investigated. Tumors that developed in spleens of infected mice 6 or more months after the injection of virus were diagnosed as immunoblastic T cell sarcomas. Cells derived from the tumors and established as a continuous cell line expressed the thymus leukemia (TL), brain-associated theta (BAT), and Qa2 cell surface antigens but lacked either the Ly 1 or Ly 2, 3 mature T cell differentiation antigens. In addition, the tumor cell expressed c type viral antigens, and had receptors for the lectin peanut agglutinin. The tumor cells were inert when tested for their capacity to respond in several functional T cell assays. Taken together, these data support the hypothesis that the primary target of malignant transformation by MSV-MuLV is a prothymocyte.

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