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Biomedical subjects

J Forman

Publications and source records attributed to J Forman.

At least 163 records · Page 9Linked to original sources
PubMed1977

Inability of choleragenoid-sensitized cells to induce T cell-mediated cytolysis.

Murine splenocytes and tumor cells bind cholera enterotoxoid (choleragenoid). Four hours after sensitization, choleragenoid-coated cells were lysed in the presence of anti-cholergenoid serum and complement, indicating that the binding was stable. Choleragenoid-coated cells were unable to sensitize spleen cells from normal or choleragenoid primed syngeneic mice into displaying a cytotoxic effect against choleragenoid-coated target cells in the T cell-mediated cytotoxicity assay. Cells coated with both choleragenoid and trinitrophenyl (TNP) groups did sensitize syngeneic spleen cells to display a cytotoxic effect against target cells bearing choleragenoid and TNP or TNP alone, but not choleragenoid alone. These data demonstrate that the mere binding of a foreign component to lymphoid cells is not sufficient to allow sensitization of cytotoxic T cells.

Animals↗
PubMed1977

T cell-mediated cytotoxicity against trinitrophenyl-modified cells: effect of glutaraldehyde treatment on the immunogenicity and antigenicity of trinitrophenyl-modified cells.

Cells treated with low concentrations of glutaraldehyde for a 10-sec interval were unable to incorporate 3H-leucine into TCA precipitable protein, respond to H-2 allogeneic cells in mixed lymphocyte reactions (MLR) and cell-mediated lympholysis (CML) assays, or display capping of cell surface immunoglobulin (Ig) with a fluoresceinated anti-Ig reagent. Such cells could stimulate and specifically block H-2 allogeneic CML activity but could not stimulate an H-2 allogeneic MLR response. Trinitrobenzenesulfonic acid (TNBS) treated spleen cells were used to sensitize syngeneic splenocytes into displaying a cytotoxic effect against trinitrophenyl (TNP)-modified target cells. Treatment of the stimulator cells with glutaraldehyde immediately after modification with TNBS did not impair their immunogenic activity. Similar treatment of TNP-modified concanavalin A-stimulated lymphoblasts that were used as inhibitors in a CML cold target competition assay allowed such cells to retain their antigenicity. Cells treated with glutaraldehyde before TNP-modification, however, were not antigenic in the cold target competition assay. These data are compatible with TNBS acting on plasma membrane molecules directly to cause cells to be antigenic and immunogenic in the CML assay rather than affecting internal cellular components.

Aldehydes↗
PubMed1977

[The stratified tuberculoma caused by Mycobacterium kansasii with cavitation (author's transl)].

Report on a 39 years old female textile worker with an acute cavity. M. kansasii was repeatedly isolated by cultivation from the sputum. The patient became negative by treatment with INH, SM, PAS, Ethionamide, but the cavity persisted. Therefore seven months after the onset of the disease the left upper lobe was resected. A colliquative Stratified tuberculoma and some lesions of caseated bronchitis and peribronchitis were found in the neigh bourhood. Clusters and microcolonies of M. kansasii could be observed as well in the wall of the cavity as in the centre of caseated bronchial lesions. The mycobacteria had a characteristic shabe of long segmentated rods. All about the microcolonies situated in the lumina of small bronchi and bronchioli caseated lesions were present, surrounded by specific granular tissue consisting of epithelial cells, some Langhans giant cells, lymphocytes and fibrocytes. The alterations caused by M. kansasii did not differ from those lesions caused by M. tuberculosis (human.) formerly described as stratified tuberculoma and caseated bronchial lesions with mycobacteria centrally located.

Adult↗
PubMed1977

Relationship between trinitrophenyl and H-2 antigens on trinitrophenyl-modified spleen cells. I. H-2 antigens on cells treated with trinitrobenzene sulfonic acid are derivatized.

Spleen cells were treated with TNBS in order to determine if cell surface H-2 antigens are derivatized with TNP. By labeling the cell membrane of the TNP-modified cells with 125I, followed by detergent lysis and immune precipitation with anti-TNP, it was determined that no H-2 antigenic activity remained in the supernatant. Further, by the use of an antibody-induced antigen redistribution assay it was found that previous exposure to TNP-modified cells to anti-TNP in the absence of complement rendered these cells resistant to lysis by anti-H-2 in the presence of complement. Together these data indicate that at the concentration of TNBS used for modification, H-2 antigens are derivatized with TNP. However, in addition to H-2, other proteins including immunoglobulin were also derivatized with TNP. Anti-TNP cytotoxic effector cells were blocked from their cytotoxic activity by anti-TNP antiserum. These data indicate that TNP directly couples to H-2 antigens on the cell surface of TNP-modified cells and that TNP is associated with the antigenic determinant that the cytotoxic T cell recognizes.

Animals↗
PubMed1977

Relationship between trinitrophenyl and H-2 antigens on trinitrophenyl-modified spleen cells. II. Correlation between derivatization of H-2 antigens with trinitrophenyl and the ability of trinitrophenyl-modified cells to react functionally to the CML assay.

Spleen cells were modified with varying concentrations of trinitrobenzene sulfonic acid and then assayed for both their ability to stimulate syngeneic spleen cells into displaying a cytotoxic effect against TNP-modified target cells and for the extent of TNP derivatization of H-2 antigens. It was found that there was a direct correlation between the extent of derivatization of H-2 antigens and the ability of such derivatized cells to act as stimulator cells in the TNP-CML assay. Thus, these data lend support to the altered self or interaction antigen hypothesis as the explanation for the H-2 gene restriction of syngeneic CML. Target cells were also modified with TNBS at varying concentrations to determine the optimal concentration required to permit lysis in the CML assay. The results of these experiments indicate that similar concentration ranges of TNBS are required to create antigenic determinants on the target cells as well as immunogenic determinants on the stimulator cells that can be recognized by cytotoxic T cells.

Animals↗
PubMed1976

Cell surface immunoglobulin. XVIII. Functional differences of B lymphocytes bearing different surface immunoglobulin isotypes.

Three populations of murine splenic B lymphocytes have been characterized previously (6, 7, 9) as those bearing only IgM, those bearing only IgD, and a population bearing both isotopes. These studies were designed to test the response of the IgM+ cells (IgM-only or IgM plus IgD) vs. the IgD-only cells to the B-cell mitogen, lipopolysaccharide. Results that after 1-4 days of culture, in the presence of mitogen, the IgM+ cells enlarge and elaborate an IgM polyclonal response. The IgD-only cells, in contrast, do not exhibit an IgM polyclonal response, but instead undergo blastogenesis and proliferation.

Animals↗
PubMed1976

Inability of normal and activated thymus-derived cells to act as cytotoxic effector cells against antibody-coated targets.

Thymus lymphocytes activated in vitro by a T cell mitogen (concanavalin A (Con A)) did not form Fc rosettes nor were they cytotoxic against untreated or antiserum-coated target cells. Con A activated spleen cells were cytotoxic against target cells, but they did not display an increased cytotoxic effect against antibody-coated YAC targets, when compared to normal spleen cells. Con A-activated spleen cells as well as cells activated by a mixed lymphocyte culture did not form Fc rosettes. Thus, activated cytotoxic T cells did not form Fc rosettes nor did they cause cytotoxicity on antibody-coated target cells. Antibody coating of the target cells did not suppress expression of cytotoxicity of activated T cells.

Animals↗
PubMed1975

On the role of the H-2 histocompatibility complex in determining the specificity of cytotoxic effector cells sensitized against syngeneic trinitrophenyl-modified targets.

Spleen cells cultured with syngeneic trinitrophenyl (TNP)-modified stimulator cells display a cytotoxic effect against syngeneic TNP-modified targets, but not against modified targets from unrelated H-2 haplotypes. Targets that share the K and I region of the H-2 complex with the stimulator (or effector) cell are lysed to the same extent as the specific targets, while targets that share the I region only are not. When only the D region is shared, a weak cytotoxic effect is observed. Therefore, the stimulator (or effector) and target cell must share the K or D but not the I region of the H-2 complex in order for optimal cytotoxicity to occur. Spleen cells sensitized to irradiated TNP-modified H-2-allogeneic cells are cytotoxic to these specific cells. Coculture of F1 hybrid cells with irradiated TNP-modified parental cells result in a cytotoxic effect against only those specific parental cells and not TNP-modified cells from the other parent. The cytotoxic effect of the F1 effector cells in the cell-mediated lympholysis test is blocked by the addition of unlabeled TNP-modified targets that are H-2 syngeneic with the sensitizing parental strain, but not H-2 syngeneic with the other parental strain. These data demonstrate that the specificity of the effector cell in this syngeneic cytotoxicity system is directed against altered self H-2-controlled-gene products, rather than a requirement for sharing of histocompatibility genes between effector and target cell in order for lysis to occur. The role of H-2 antigens in determining the sensitivity of a target cell to T-cell-mediated lysis is discussed.

Animals↗
PubMed1975

Absence of H-2 antigens capable of reacting with cytotoxic T cells on a teratoma line expressing a T/t locus antigen.

An established cell line of murine teratoma cells (F9), which lacks serologically detectable H-2 that is determined by a wild-type T/t locus gene. These cells are not killed and do not react with cytotoxic T cells sensitized to H-2 antigens in a cell-mediated lympholysis assay. Modification of spleen cells from the strain or origin (129) of this teratoma line with trinitrobenzene sulfonic acid allows the generation of syngeneic killer cells that display a cytotoxic effect against trinitrophenyl-modified splenic targets, but not against trinitrophenyl-modified F9 targets. Thus, the F9 antigen is structurally similar to H-2b but does not act as a target antigen in the cell-mediated lympholysis assay for anti-H-2b cytotoxic T cells, nor does it crossreact with H-2b antigens at the T cell level.

Animals↗
PubMed1975

Immunogeneic analysis of H-2 mutations. II. Cellular immunity to the H-2DA mutation.

The H-2da haplotype was derived from the H-2d haplotype by a mutation localized to the D end of the H-2 complex. Coculture of H-2d and H-2da spleen cells gives rise to bidirectional MLR. However, the H-2d anti-H-2da response is much stronger than that of H-2da anti-H-2d. Both haplotypes give rise to reciprocal CML. B10.D2(R103) strain spleen cells, which differ only at the D end of the H-2 complex from the H-2d haplotype, kill H-2da target cells in CML when sensitized to H-2d stimulators and vice versa. Therefore, both the mutant and strain of origin share a D end CML specificity. H-2d and H-2da reject skin grafts in both directions, although some H-2d grafts show prolonged acceptance on H-2da recipients. These data are consistent with a mutation in the D end of the H-2d haplotype resulting in gain-loss of an antigen(s) that gives rise to reciprocal MLR, CML, and skin graft rejection. Further, the mutant can be distinguished from the strain of origin on the basis of the strength of immune response in MLR.

Animals↗
PubMed1975

Immunogenetic analysis of H-2 mutations. III. Genetic mapping and involvement in immune reactions of the H-2ka mutation.

Mutation M523 (H-2ka) occurred spontaneously in strain CBA/CaLacSto and was discovered during routine skin graft testing for genetic homogeneity. By linkage and complementation tests, the mutation was previously mapped in the K end of the H-2 complex. We demonstrate that the mutation occurred in the K region, without affecting the I region in the K end of the complex. The mutant antigens cause rejection of skin grafts, stimulate cells in mixed lymphocyte culture, and function as stimulators as well as targets in cell-mediated lymphocytotoxicity. Yet, they are serologically indistinguishable from the antigens of the original strain and do not induce formation of humoral antibodies upon immunization of the CBA strain. Together with the results obtained on testing of other H-2 mutants, the data strongly support the notion that classical H-2 antigens (i.e., products of the H-2K and H-2D loci) can function as lymphocyte-stimulating determinants, and that I-region differences are not required for the induction of strong cell-mediated lymphocytotoxicity.

Animals↗
PubMed1975

[Unruptured aneurysms of Valsalva sinus of septal origin].

Aneurysms of Valvsalva sinus unruptured into a cavity, but developing into the membranous and even muscular interventricular septum are exceptional. Two cases illustrating this fact are reported. In one of them, a massive mitral incompetence by elongated chordae tendinae related to the presence of a voluminous intra-septal pouch. Atrio-ventricular and intraventricular conduction disturbances were present in both patients. The interest of supra-valvar angiography which makes it possible to advise operation before the eventual rupture is underlined.

Adult↗