Search PubMed⌕ Search

Biomedical subjects

R B Corley

Publications and source records attributed to R B Corley.

68 records · Page 4Linked to original sources
PubMed1980

The relationship between alloantigen responses in nude mice injected with a low number of congenic thymus cells.

BALB/c-nu mice were injected with 10(6) normal congenic thymocytes. This number of cells permits only partial reconstitution and in individual mice some functions were restored and others were not. The relationships between the functions of skin graft rejection, circulating alloantibody production and the ability to generate, in vitro, cytotoxic T cells were studied with regard to the strains CBA and C57BL/6.

Animals↗
PubMed1979

In vivo activity of a nonspecific T cell-replacing factor.

Nonspecific T cell-replacing factors prepared as supernatants from mixed lymphocyte cultures or concanavalin A-stimulated spleen cells are active in vivo iv injected into nude mice at least 3 days before antigen. The supernatants appear to act by enhancing the week IgM responses that occur in untreated nudes. Secondary responses and IgG antibody were not found.

Animals↗
PubMed1978

Specificity of helper T cells for different antigens.

BALB/c nude mice have been injected with 10(6) congenic thymus cells, a number which allows some, but not all mice to respond to any particular T-dependent antigen. These mice have been tested for their ability to respond to three bacteriophages, T4, T7 and phiX, sheep and horse erythrocytes, and alloantigens of C3H and C57BL/6 mice. The number of mice able to respond to each of these antigens was of the same order of magnitude. Sheep and horse erythrocytes showed cross-reactivity at the T cell level, i.e. the responses to these two antigens were not independent. The same was observed for C3H and C57BL/6. Otherwise, the responses were independent showing that the antigens are recognize by different populations of specific helper T cells.

Animals↗
PubMed1977

In vivo responses of alloreactive lymphocytes stimulated in vitro. Skin graft rejection mediated by MLR-Primed lymphocytes.

Mouse lymphocytes that have been primed in vitro against alloantigens show a specific increase in cells reactive to the priming antigens in mixed lymphocyte response (MLR) and include cells that are specifically cytotoxic in vitro. The primed population also contains cells capable of causing rejection of skin grafts when injected into nude mice. Functional enrichment of cells capable of rejecting skin grafts bearing specific alloantigens and depletion of cells capable of rejecting a third-party graft have been shown. Priming the cells a second time in vitro may result in a moderate enrichment of cells capable of rejecting the specific graft and depletion of cells reactive to third-party skin compared with once-primed cells. These findings support the prediction that the MLR is an in vitro model of allograft responses in vivo.

Animals↗
PubMed1977

In vivo responses of alloreactive lymphocytes stimulated in vitro. Helper-cell activity of MLR-primed lymphocytes.

Populations of mouse lymphocytes enriched in specific alloreactive cells by priming in a mixed lymphocyte response (MLR) include cells which, when injected into congenic nude mice, enable them to make alloantibody after immunization. Helper cells for the priming H-2 alloantigens (H-2b or H-2k) were enriched relative to helper cells for the other H-2 type. Furthermore, the alloantibody responses of nude mice reconstituted with lymphocytes primed twice in vitro were virtually monospecific for the priming alloantigens. These studies suggest that lymphocytes that proliferate in MLR include lymphocytes capable of giving specific help for H-2 antigens in vivo. Nude mice reconstituted with MLR-primed lymphocytes made less antibody to bacteriophage T4 and phix than mice reconstituted with unprimed cells, and fewer mice responded. Priming of cells a second time in MLR further depleted the population of phage helper cells. Similar results were sometimes, but not always, obtained when testing reconstituted nude mice for their ability to make anti-sheep erythrocyte (SRBC) responses. These results suggest that lymphocytes primed against H-2b or H-2k alloantigens do not have specificity for antigens of T4 or phix. These alloreactive cells may also lack specificity for SRBC. However, the results do not allow a definitive conclusion to be drawn.

Animals↗
PubMed1977

Responses of alloantigen-primed lymphocytes in vitro. The specificity of secondary responses assayed by titration of primed lymphocyte populations.

Maximal proliferative responses were observed at lower responder cell densities in alloantigen-primed lymphocyte populations when restimulated with the specific priming cell than when restimulated with other allogeneic cells. This relationship was due to the larger number of lymphocytes within the primed population which responded to the specific sensitizing cell than to unrelated stimulator cells. As a result, at high responder cell densities, stimulator cells unrelated to the specific sensitizing cells elicited a disproportionately high response relative to the response stimulated by the specific cells. Restimulation of decreasing numpacity of different cells. Because primed populations contain a larger number of lymphocytes that responde to the specific stimulator than to other stimulators, responses of primed lymphocytes could be made operationally monospecific. Limiting dilution analysis demonstrated that low numbers of primed cells were stimulated by the specific sensitizing cells but not by unrelated stimulator cells.

Cells, Cultured↗
PubMed1977

Responses of alloantigen-primed lymphocytes in vitro. The contribution of increased frequencies of responding lymphocytes to differences between reactivity of normal and primed lymphocyte populations.

Sensitization of lymphocytes against allogeneic cells in vitro results in significant enrichment of alloreactive lymphocytes. Such enrichment was found to profoundly influence the conditions for measuring proliferative responses. Fewer primed lymphocytes than unprimed ones had to be cultured to favor optimal proliferation. Second, proliferative responses could be detected using 10 to 20 times fewer primed responding cells than when using unprimed responders. Finally, although responses of both unprimed and primed lymphocytes were dependent on the number of stimulator cells in culture, the primary mechanism(s) through which this dependence was expressed appeared to differ. The results demonstrate that, under the same conditions, comparisons of responses of two populations that contain different proportions of reactive lymphocytes may not be justified.

Cells, Cultured↗
PubMed1976

Stimulation of lymphocytes by allogeneic lymphocytes and lymphoblasts in the presence of anti-HLA antisera.

Anti-HLA alloantisera inhibit mixed lymphocyte responses in which normal lymphocytes are used as stimulator cells. These same antisera are unable to inhibit lymphocyte proliferative responses stimulated by lymphoblastoid cells from cultured lymphoid cell lines. They also fail to inhibit either the generation of cytotoxic effector cells by lymphoblastoid cells or lymphocyte-mediated cytotoxicity against the lymphoblasts. Although the number of HLA antigens on the surface of lymphoblasts is reported to be greater than on normal lymphocytes, the failure of alloantisera to inhibit lymphoblast-induced responses in vitro does not appear to be due to insufficient amounts of antiserum to react with the antigenic sites. Rather, the data are interpreted to suggest that antigens which are not HLA and are not closely associated with HLA on the lymphocyte membrane are responsible for the stimulation of allogeneic lymphocytes by lymphoblastoid cells. Although lymphoid cell lines are known to contain the genome of the Epstein-Barr virus, antisera against products of the viral genome fail to inhibit proliferative responses to lymphoblastoid cells, suggesting that these antigens do not directly participate in lymphocyte activation.

Antibodies, Viral↗
PubMed1973

HL-A-linked human immune-response genes.

Genetic control of the response to specific natural-product antigens has been documented in three informative families. Families were selected on the basis of probands with tuberculosarcoidosis, chronic cutaneous moniliasis, and rheumatoid arthritis. An increased incidence of delayed cutaneous unresponsiveness was observed in each family. Positive associations were identified between HL-A haplotypes and immediate cutaneous hypersensitivity responses to 5, 8, and 11 of 23 test antigens in the three respective families. HL-A-associated differences in averaged responses of cutaneous hypersensitivity were excluded. These significant associations are consistent with linkage between HL-A haplotypes and genes responsible for the immune response to various natural-product antigens.

Antigens↗