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Biomedical subjects

F H Bach

Publications and source records attributed to F H Bach.

At least 379 records · Page 21Linked to original sources
PubMed1979

H-2 I-region encoded targets in allograft rejection.

Fresh thyroids transplanted to I-region disparate recipients are, in most cases, rejected; in some instances fresh thyroids undergo periods of crisis followed by functional recovery. Cultured thyroids that are taken from donor animals pretreated with lymphocytotoxic drugs, gamma radiation and cultured for 10 d in vitro are not rejected by any normal allogenic recipient. If the recipient is sensitized with lymphoid cells syngeneic with an I-region disparate cultured thyroid donor, the cultured thyroid is rejected if I-A-subregion differences are included. We interpret these data to indicate that there exist I-region encoded perenchymal cell target determinants which are not, by themselves, immunogenic.

Animals↗
PubMed1979

Elicitation of anti-leukemia cytotoxic responses.

We have presented the rationale for the in vitro approaches that we have taken for generating cytotoxic lymphocytes capable of lysing autologous leukemia cells or leukemia cells from HLA identical siblings. Two different approaches have been used, both of which are based on earlier findings concerning the antigenic and cellular interactions involved in the generation of strong cytotoxic responses to alloantigens in mixed leukocyte culture.

Cytotoxicity, Immunologic↗
PubMed1979

The availability for recognition of normal H-2 antigens by cytotoxic T lymphocytes on a Rauscher-virus-transformed cell, RBL-5A.

The availability for recognition of cell surface H-2Db antigenic determinants on RBL-5A cells in comparison to normal C57BL/L cells was investigated by an in vitro immunological assay. No differences in the immunological recognition of the H-2Db antigens on RBL-5A cells compared to normal C57BL/L cells were detected. This assay system, however, readily detected changes in the H-2Kb determinant profile on target cells from the C57BL/L H-2Kb region mutant strains H(zl) and H(zl70) when compared to normal C57BL/6 mice. The result obtained with RBL-5A target cells therefore suggests that Rauscher murine leukaemia virus transformation does not induce, either genotypically or phenotypically, an immunologically recognizable alteration of the H-2Db antigen profile on this cell.

Animals↗
PubMed1979

The major histocompatibility complex (HLA) as a genetic marker in human craniofacial anomalies.

Study of the incidence and segregation of the serologically detectable A and B products of the HLA complex in 140 family units in which one or more offspring was afflicted with a developmental craniofacial anomaly has uncovered no evidence of an association between HLA-A or B antigens or haplotypes and the malformations under study. Further analysis of HLA-D products in the same family units by the mixed leukocyte culture (MLC) technique has, however, uncovered a relatively high incidence of non-reactivity between the cells of one (or both) parent(s) and cells of some offspring in 41 of the 140 families included in this study. The parent couples involved in this finding were unrelated and generally did not share any HLA-SD haplotypes. When this finding was studied further by Primed LD Typing techniques, the results in six families suggested that such MLC non-reactivity is a consequence of the sharing of LD alleles by each pair of parents in these families. The known polymorphism of the HLA-D locus (or loci) and the low incidence of comparable findings in the normal population suggest that LD allele sharing in this particular population may be related to the selection of certain particular HLA-D products in families afflicted with developmental craniofacial anomalies. This result may be relevant to the possible existence in man of an analogue of the murine T/t complex which may occur in linkage with the HLA complex, in the same manner as the linkage disequilibrium which is been documented between the t complex and H-2 in chromosome 17 of the mouse.

Adult↗
PubMed1979

Lyt phenotypes of responding cells in secondary alloantigen responses.

Lymphocytes responding in a "secondary" MLC-CML system, after in vitro sensitization, apparently fall into two classes with regard to their Lyt phenotype. First, are the cells that form the majority of the proliferating cells after restimulation with either I or K + I differences, which are Lyt 1-2, and second, are Tc that are Lyt 1-2+. The Lyt 1-2- proliferating cells are not cytotoxic and are lysed by treatment with anti-Thy 1.2 serum in the presence of C.

Animals↗
PubMed1979

Past, present, and future aspects of histocompatibility.

We have stressed problems attendant on studies of the MHC, ignoring non-HLA factors and their role in allograft immunity. Many other topics could have been chosen for discussion is any such overview; our selection reflects our own interests. We felt assured, however, that excellent coverage by our many colleagues of the diverse and varied aspects of histocompatibility not approached in this summary has allowed us this freedom.

Cells, Cultured↗
PubMed1978

In vitro sensitization of thymocytes. Role of H-21 I region determinants and cell-free mixed leukocyte culture supernates in generation of cytotoxic responses.

Stimulation of thymocytes in vitro by spleen cells differing for the entire H-2 complex leads to a significant proliferative response without a significant cell-mediated lympholysis (CML) response. Addition of soluble cell-free supernates (SF), (taken from a 7-day mixed leukocyte culture) enables these cultures to develop CML response. For optimal CML response, the SF has to be added within 48 h of onset of cultures. Although with spleen cells as responding cells, SF could quantitatively replace I-region different stimulating cells for generation of CML responses, with thymocytes as responding cells, stimulation with I-region cells appeared obligatory for the generation of CML responses. The implications of these findings are discussed.

Animals↗
PubMed1978

T-cell-specific murine Ia antigens: serology of I-J and I-E subregion specificities.

(B10 X B10.D2)F1 mice were immunized with B10.A(5R) concanavalin A-stimulated thymocyte blasts. The genetic disparity between donor and recipient was restricted to the I-J and I-E subregions of the murine major histocompatibility (H-2) complex. A high-titered, T-cell-specific anti I-JkEk serum was obtained. The antiserum lysed 27-30% of haplotype k, q, or s lymph node cells, 5.3 +/- 2% of haplotype k spleen cells, and did not lyse thymocytes. Nylon wool-passed lymph node or spleen cells (H-2k) showed considerable reactivity with anti-I-JkEk serum (35-40% lysis); anti-Thy1.2 plus complement-treated spleen cells did not react (less than 5% lysis). I-Ek antibody was detected by B10.A(3R) lymph node cell reactivity (20% lysis), whereas reaction with H-2k lymph node cells after B10.A(3R) absorption demonstrated IJk antibody (12% lysis). Lymphocyte activation with alloantigen or mitogen led to increased anti-I-JkEk serum reactivity. These results, showing antibody production to at least two T-cell Ia antigenic determinants by concanavalin A thmocyte blast immunization, suggest that a group of I-region-encoded T-cell specificities may not have been detected using conventional immunization protocols because they would not have comprised a major antigenic component of the immunizing cell population. The existence of multiple Ia antigenic determinants unique to T lymphocytes would have important implications for serological and functional studies of T-cell subpopulations.

Animals↗
PubMed1978

Alternative pathways of T lymphocyte activation.

Data presented in this paper suggest that there may be two alternative pathways which T lymphocytes can use in generating a cytotoxic response to alloantigens in vitro. First, there is the pathway taken when stimulator and responder cells differ by an entire H-2 complex where Ly1+2- helper T lymphocytes respond to I region encoded lymphocyte defined differences and provide help to the Ly1-2+ cytotoxic T lymphocytes responsive primarily to K/D region encoded cytotoxicity defined determinants. Second, there is the pathway taken when stimulator and responder cells differ by only K or D region differences without an I region encoded difference; under these conditions, an Ly1+2+ cell, which does not appear to play a significant role in the development of a cytotoxic response to an entire H-2 difference, appears to play a pivotal role.

Cytotoxicity, Immunologic↗
PubMed1978

Involvement of fusion activity of ultraviolet light-inactivated Sendai virus in formation of target antigens recognized by cytotoxic T cells.

Mice inoculated with ultraviolet light-inactivated Sendai virus mount a cell- mediated immune response to the virus. Cytotoxic T cells specific for Sendai virus can be obtained by in vitro secondary stimulation of primed spleen cells with syngeneic stimulator cells coated with UV-inactivated Sendai virus. Neither in vivo nor in vitro stimulation alone is sufficient to generate specific cytotoxic T cells. Sharing of the H-2 haplotype between cytotoxic T cells and target cells is required for the Sendai virus-specific lysis to occur. The fusion (F) glycoprotein of Sendai virus has been implicated in target antigen formation (20). Ethanol treatment of Sendai virus causes complete inactivation of the cell-fusion and hemolytic activities of the envelope, but does not affect the antigenicity of the F glycoprotein; furthermore, hemagglutinin and neuraminidase activities of the envelope HANA glycoprotein are also left intact after ethanol treatment. Target cells can be prepared by coating them with various numbers of UV-inactivated Sendai virus that have been treated with ethanol or, as a control, phosphate-buffered saline (PBS). The amount of virus adsorbed to target cells during the cytotoxicity reaction time using either ethanol-treated or untreated (PBS "treated") virions is essentially identical, but target cells coated with ethanol-treated Sendai virus fail to serve as targets for cytotoxic T cells. These results indicate that fusion activity of the Sendai virus envelope is essential to the formation of the target antigen and that virus adsorption to cell surfaces without fusion of the envelope with cell membranes is not sufficient to allow killing by virus-specific cytotoxic T cells.

Animals↗