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E S Vitetta

Publications and source records attributed to E S Vitetta.

At least 235 records · Page 13Linked to original sources
PubMed1982

Characterization of a monoclonal antibody reactive with a subset of human breast tumors.

Fusion of spleen cells, from mice immunized against the human hormone-dependent breast cancer cell line ZR-75-1, with murine myeloma cells resulted in the establishment of a hybridoma cell line, HY59-H10 (H59). The purified monoclonal IgM produced by the hybridoma reacts with the most differentiated human breast tumor cell lines but not with cells derived from normal breast secretions or with numerous other malignant cell lines. Of 106 biopsy specimens examined, H59 bound to 54% of malignant breast specimens, to 83% of fibroadenomas, and to 82% of specimens containing fibrocystic disease.

Adenofibroma↗
PubMed1982

Interleukin-2 does not induce murine B cells to secrete Ig.

We previously defined two T cell-derived lymphokines, BDCF mu and BCDF gama, which induce B cell differentiation in the absence of IL 2. Although these studies indicated that IL 2 was not required to induce Ig secretion, the effect of IL 2 on B cell differentiation was not established. In the present studies we have assessed the ability of purified IL 2 to induce IgM or IgG secretion. Our results demonstrate that IL 2 does not induce IgM secretion by BCL1 tumor cells, nor does it enhance BCDF mu-induced IgM secretion by these cells. Similarly, IL 2 had no effect on LPS or BCDF gamma-induced IgG secretion by normal B cells. Thus, we conclude that IL 2 does not act directly on B cells to induce differentiation.

Animals↗
PubMed1982

Structural analysis of thymus-leukemia (TL) antigens in the mouse.

Thymus-leukemia (TL) antigens have been sequentially immunoprecipitated from glycoprotein pools prepared from lysates of biosynthetically labeled ASL-1w leukemia cells with a monoclonal antibody and a standard alloantiserum. Results suggest that on leukemia cells from Tlaa mice, as previously reported for thymocytes from these mice, all the alloantiserum-defined TL specificities (TL.1, 2, 3, 5, 6) as well as the specificity defined by the monoclonal antibody (TL.m3) are carried by a single molecular species. The degree of structural homology between the 45,000-m.w. heavy chains of TL and H-2 was investigated by the technique of comparative tryptic peptide mapping. Results indicate that TL is more distantly related at the primary structural level to H-2 than H-2 antigens are to one another.

Amino Acid Sequence↗
PubMed1981

Cytotoxic T cells specific for antigens expressed on surface immunoglobulin-positive cells.

C.B-20 mice were immunized with splenocytes or B leukemia cells (BCL1) from Ig H chain allotype congenic strains. Spleen cells from these immunized mice were rechallenged in vitro to generate H-2-restricted cytotoxic T cells that were specific for target antigens controlled by genes linked to the Ig H chain locus. The anti-Ig H cytotoxic T cells detected an antigen(s) expressed only on surface Ig+ cells. Thus, T cell lymphoblasts, eight BALB/c myeloma cell lines, and a T cell lymphoma were not lysed by the effector cells. In contrast, B cell lymphoblasts and the surface Ig+ BCL1 cells were sensitive to lysis. A surface Ig- hybridoma (which secretes the IgM from the BCL1 cells) generated by fusing BCL1 cells to X63 myeloma cells was not killed by the effector cells. These data indicate that cytotoxic T cells specific for antigenic determinants on either surface IgM+ or IgD+ or on a molecule that is coordinately expressed on IgM+ or IgD+ cells can be generated and that such cells might play a role in regulating the growth of normal B cells or surface Ig+ tumor cells in vivo.

Alleles↗
PubMed1981

Qa-2, H-2K, and H-2D alloantigens evolved from a common ancestral gene.

The Tla region located on the murine 17th chromosome controls several serologically defined cell surface antigens. These antigens, referred to as Qa-1-5 and TL, are expressed on a variety of hematopoeitic cell populations. In the present studies we have immunoprecipitated isotopically labeled Qa-2 and H-2 molecules from mitogen-stimulated B6 spleen cells. Sequential immunoprecipitation experiments have shown that the determinants recognized by alpha Qa-2, alpha H-2Kb, and alpha H-2Db alloantisera reside on separate molecular species. Comparative mapping of the arginine-labeled tryptic peptides from Qa-2, H-2Kb, and H-2Db molecules indicate that Qa-2 is structurally distinct but that there is considerable structural homology; 21-43% of the Qa-2 peptides co-chromatograph with peptides derived from H-2Db and H-2Kb, respectively. Similar levels of homology are observed when Qa-2 is compared with H-2Kk or H-2Dd. The results show that the Qa-2 alloantigen is encoded by a locus separate from the loci encoding H-2K or H-2D alloantigens, but that the Qa-2, H-2K, and H-2D alloantigens are sufficiently related at the primary structural level to indicate that they evolved from a common primordial gene.

Amino Acid Sequence↗
PubMed1981

Role of glycosylation in the H-2-restricted cytolysis of virus-infected cells.

The role of the oligosaccharide portions of cell surface glycoproteins in the susceptibility of virus-infected cells to H-2-restricted cytolysis was investigated by using the antibiotic tunicamycin (TM). TM inhibits the addition of sugars to the polypeptides of glycoproteins. TM treatment of P815 cells before and during infection with vesicular stomatitis virus (VSV) inhibited glycosylation of proteins and reduced by about 50% the lysis of infected P815 cells by VSV-immune, H-2-identical killer cells. In contrast, TM treatment had a modest inhibitory effect on cytolysis of P815 cells by alloimmune effector cells. TM treatment did not inhibit the surface expression of either H-2 or VSV glycoprotein. Thus, glycosylation of H-2 and/or viral glycoprotein is a prerequisite for the lysis of infected cells by H-2-identical, VSV-immune cytotoxic cells.

Animals↗
PubMed1981

Biochemical analysis of an MHC-linked hematopoietic cell surface antigen, Qa-2.

The region of the murine 17th chromosome telomeric to H-2D encodes a group of serologically defined cell surface antigens termed Qa-1-5. These antigens are of interest because their expression is restricted to hematopoietic cells. In addition, the molecular weight and subunit structure (ie, association with beta-2 microglobulin) of Qa-2 molecules are similar to H-2 and TL antigens. In the present studies, we have prepared isotopically labeled Qa-2 and H-2 molecules from mitogen-stimulated C57BL/6 spleen cells. Comparative peptide mapping of tryptic peptides from Qa-2 and H-2 molecules (Kb, DbKk, Dd) reveal that Qa-2 has a unique primary structure. However, considerable homology is indicated since 30--40% of the Qa-2 peptides cochromatograph with peptides derived from H-2Kb, H-2Db, H-2Kk, and H-2Dd. Studies by other investigators have demonstrated that similar levels of structural homology are observed when H-2K, H-2D, and H-2L tryptic peptides are analyzed. We conclude from these studies that the Qa-2 alloantigen is structurally related to a class of cell surface molecules (ie, H-2) that play critical roles in immune recognition processes. These data further suggest that the genes encoding Qa-2 and H-2 molecules have arisen from a common primordial gene.

Animals↗
PubMed1981

Induction of proliferation and differentiation of neoplastic B cells by anti-immunoglobulin and T-cell factors.

Sepharose-bound anti-immunoglobulins, which are potent mitogens for normal adult B cells, are not mitogenic for tumor cells freshly isolated from mice carrying the B-cell leukemia BCL1. However, after 4 or more days of in vitro cultivation, BCL1 cells can be stimulated to divide by either anti-mu or anti-delta antibodies. These results suggest that in vitro cultivation of BCL1 cells results in their differentiation into more mature cells which can be triggered to proliferate by their interaction with anti-Ig antibodies. Addition of T-cell helper factors to anti-Ia treated BCL1 cells results in their differentiation into Ig-secreting cells. These results indicate that surface Ig molecules on BCL1 cells are capable of delivering an activation signal to the cells but that the cells require a second signal from T cells for induction of Ig secretion.

Animals↗
PubMed1981

Immunosuppression in a murine B cell leukemia (BCL1): role of an adherent cell in the suppression of primary in vitro antibody responses.

The ability of lymph node cells from mice bearing the BCL1 tumor to respond in vitro to mitogens, allogeneic cells, and both TI and TD antigens was investigated. The lymph nodes of such mice are not invaded with tumor cells and contain normal numbers of T and B cells. Nevertheless, at the peak of tumor burden in the spleen and blood (approximately 8 to 12 wk after injection with tumor cells), the lymph node cells from the tumor-bearing mice display markedly decreased responsiveness both to allogeneic cells and to antigens. In addition, small numbers of lymph node cells from the tumor-bearing mice suppress primary antibody responses of normal lymph node cells. This nonspecific suppression of antibody responses is mediated by a G-10 Sephadex adherent, non-T, non-B cell present in the nodes of the tumor-bearing mice. Since the BCL1 tumor model is in many respects similar to the prolymphocytic type of human chronic lymphocytic leukemia, the present results may be helpful in elucidating the mechanisms underlying the in vivo immunosuppression associated with lymphocytic neoplasms in humans.

Animals↗
PubMed1981

Increased susceptibility to lethal effects of bacterial lipopolysaccharide in mice with B-cell leukemia.

Susceptibility to the lethal effects of bacterial lipopolysaccharide (LPS) increased more than one hundredfold in BALB/c mice given syngeneic B-cell tumor transplants. The increased susceptibility to LPS that developed during the following weeks paralleled tumor growth in the liver and spleen. The tumor-bearing animals also developed an enhanced capacity to clear colloidal carbon from the blood, consistent with increased activity of the reticuloendothelial system. Although hypersusceptibility to LPS has been reported to a number of animal models, our experiment was th first demonstration in a tumor model that susceptibility correlates with tumor burden.

Animals↗
PubMed1981

BCL1, a murine model of prolymphocytic leukemia. II. Morphology and ultrastructure.

The transplantable murine B-cell leukemia, BCL1, was examined by light and electron microscopy. The results show that the BCL1 cell closely resembles the prolymphocyte of human prolymphocytic leukemia (PLL). The spleen of animals transplanted with BCL1 is diffusely infiltrated by BCL1-prolymphocytes. Splenectomized animals given transplants of BCL1 develop a lymphomalike disease with less leukemia and bone marrow involvement than the nonsplenectomized transplant recipients. Ultrastructural features of the BCL1 cell are identical in the splenectomized and nonsplenectomized animals.

Animals↗