Biomedical subjects
G Winchester
Publications and source records attributed to G Winchester.
The structural gene for F liver protein (Flp) maps to chromosome 5 of the mouse.
The BXD and AKXL panels of recombinant inbred mouse strains have been typed for the F liver protein alloantigen. The structural gene for F liver protein gene (Flp) is placed on the distal part of chromosome 5, between the known markers Bcd-1 and Gus-s. This excludes the possibility that F liver protein is a major histocompatibility complex molecule, and in turn raises a question about the uniqueness of F and certain other proteins as purgers of self-reactivity among T but not B cells. The typed RI strains have then been used for the immunogenetic studies presented in the succeeding article.
Results of reminding family physicians about administration of flu vaccine.
Explore the source record for details and available documents.
Antigen-presenting cells do not discriminate between self and nonself.
The immune response to F protein in mice provides a system in which the capacity of antigen-presenting cells to present autologous protein to T cells can be examined. When we used the F-type 1 (F.1) and F-type 2 (F.2) combination, these cells proved equally able to present autologous and foreign protein in both an in vivo adoptive transfer and an in vitro proliferation assay. This formally excludes the possibility that these cells themselves discriminate between self and nonself, while still allowing the possibility that their uptake of antigen may be regulated by lymphocyte products.
More on testing relative density of urine with a reagent strip.
Explore the source record for details and available documents.
In vitro responses to the liver antigen F.
In this paper we describe the first in vitro response to the liver alloantigen F. The anti-F response serves as a valuable model for autoimmune phenomena since priming appropriate strains of mice (responders) with allogeneic but not syngeneic type F leads to autoantibody production. The in vitro system is based on the proliferation of T cells, from mice primed in vivo with F, when coincubated with splenic adherent cells (SAC) prepulsed with F in vivo. The system displays two important correlates of the in vivo antibody response to F:1.T cells from mice primed with syngeneic F do not proliferate when incubated with SAC prepulsed with syngeneic F and 2. Mice that do not make antibody responses to allo F in vivo (DBA/2) do not show in vitro proliferative responses. These findings indicate that the proliferative assay is a good in vitro model for the F response.
Evidence that autoimmunity in NZB mice is caused by a defect in immune specificity rather than a generalized defect in tolerance of self-antigens.
Explore the source record for details and available documents.
p53 protein and control of growth.
Explore the source record for details and available documents.
Immunology. The T-cell receptor completed.
Explore the source record for details and available documents.
New ideas about self-tolerance and auto-immunity.
Recent advances in our understanding of B cell ontogeny strengthen the theory that self-tolerance is generated principally by clonal deletion. B cells pass through a stage: the "baby B cell", during which they are particularly susceptible to receptor cross-linking. Further evidence of clonal deletion comes from studies on the maintenance of the liver differentiation alloantigen F. In spite of this accumulating evidence room can still be found for the concept of immunological silence: it is a prediction of the dual recognition theory of T cell receptors that differentiation macromolecules which occur only on the surface of Ia negative cells cannot be seen by T helper cells.