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J M Plate

Publications and source records attributed to J M Plate.

35 records · Page 2Linked to original sources
PubMed1981

Major histocompatibility complex restriction of soluble helper molecules in T cell responses to altered self.

Evidence for major histocompatibility complex (MHC) restriction of soluble helper effects was observed in the generation of syngeneic killer T cells to trinitrophenyl-altered self. Ia-bearing T cells obscure the observation of such interactions, thus, must be removed to detect MHC restriction of nonspecific soluble helper factor supernates (HFS). Genetic mapping studies demonstrated that the strain producing HFS must be compatible in the H-21A region with the strain utilizing the helper molecules for optimal helper signals to be delivered.

Animals↗
PubMed1980

Genetic mapping of an H-2-associated antigen expressed on regulatory T cells.

T lymphocytes that serve regulatory functions in the generation of effector T cells to alloantigen and to altered syngeneic cells express a distinguishing H-2-associated cell surface marker that we have termed Ha. Genetic mapping studies with the B10.A(2R), B10.A(4R), B10.A(5R), and LG/Ckc lines of mice have delineated the locus determining the expression of Ha to the right of H-2K and left of H-2IB or within the I-A region. Thus these regulatory T lymphocytes express Ia antigens.

Absorption↗
PubMed1978

Kidney transplants in mice. An analysis of the immune status of mice bearing long-term, H-2 incompatible transplants.

Kidney transplants between strains of mice which are incompatible at either the K or the D end of the H-2 complex usually function for prolonged periods supporting the lives of nephrectomized recipients. This occurs with no recipient treatment. With multiple H-2 and non-H-2 determined incompatibilities, transplants may be rejected but more slowly than skin grafts. In the strain combination studied most extensively in these experiments (B10.D2 to B6AF(1)) in which the incompatibility was confined to the K end of the H-2 region, about 70 percent of recipients survived for many weeks with normal blood urea nitrogen levels. Skin grafts between untreated members of these strains were rejected promptly (mean survival time of 13.5 +/- 1.1 days) as were kidney transplants to recipients of prior skin grafts. Donor strain skin grafts to recipients of kidney transplants after kidney transplantation enjoyed greatly prolonged survival whereas skin grafts from a third party (A.SW) were rejected normally. If kidney tissue was transferred in the form of free grafts without primary vascular union, it was rejected promptly leaving its recipient highly immunized. Cellular and humoral immunity to donor antigens declined over the first few weeks after transplantation, and the spleens of long-term recipients contained no "killer cells." Recipient lymphoid cells could mount active graft versus host reactions to donor strain antigens on transfer to neonatal mice. Nevertheless, they were distinctly less able to respond specifically by the production of killer cells to donor strain antigens after sensitization in vitro. No evidence that this defect was associated with the presence of suppressor cells was forthcoming from several types of in vivo and in vitro tests.

Animals↗
PubMed1976

Cellular responses to murine alloantigens of the major histocompatibility complex: the role of cell subpopulations that express different quantities of H-2 associated antigenic markers.

Subsets of lymphoid cells that function in the initiation and differentiation of cell-mediated responses to H-2-coded alloantigens were defined with an antiserum raised between congenic resistant lines of mice that differed for a limited number of components of the H-2 complex. Only those cells that express "Ia markers" can stimulate responses to H-2K, D and/or I region antigens in mixed lymphoid cell cultures, even though all lymphoid cells apparently express the H-2K and H-2D-coded private antigens. Ia markers, therefore, serve to distinguish the subset of cells which includes as its members the stimulating cells. The Ia marker(s) is expressed on the cell membrane of at least one of the two T cell subsets that collaborate in the development of T effector cells to H-2-associated alloantigens, i.e. precursors and helpers. The cells remaining after lysis with our antiserum plus complement no longer can respond in the MLR. Syngeneic non-T cells cannot reconstitute the response. Most activated and proliferating cells express the Ia determinant(s). A proportion of T effector or killer cells, however, does not express the Ia markers. We suggest, therefore, that the MLR-responsive cell in normal lymph nodes is an "activated" cell and the "Ia markers" are involved in the differentiation of T precursor to T effector cells. The end stage T effector probably is devoid of the Ia marker.

Animals↗
PubMed1975

Characterization of immune response and mixed lymphocyte reactions in selected intra-H-2 recombinant strains.

The genes controlling the immune response to the random linear terpolymers GAT and GLpro have been mapped in the Ir-1A or Ir-1B subregions with five lines of H-2-s/H-2-a recombinant mice. The I region also contains a third subregion, I-C, which codes for a lymphocyte-activating determinant, Lad2, controlling mixed lymphocyte reactivity. The mixed lymphocyte responses associated with I-C region disparity are compared with the stimulation noted with other H-2 region differences. Unidirectional lymphocyte activitation was associated with the Lad2 determinants in selected combinations.

Animals↗
PubMed1974

Mixed lymphocyte culture responses of mice. Genetic analysis of the responses to H-2Dd specificities.

Cellular responses in vitro to H-2D region histocompatibility antigens were demonstrated to be under the genetic control of two or three (P = 0.013) independently segregating loci. The H-2 region itself accounts for one of these loci, however, its activity appears to be dependent upon an association with other non-H-2-associated genetic information. The ability to stimulate a response and to respond to that stimulus are two separate genetic functions in certain MLR combinations. The stimuli in our studies were products of the H-2D region and cell donors must differ at that region in order for a response to occur. The control of the level of responses was determined by other genetic material. Differences at these "response loci" were not necessary for the induction of a proliferative response in the mixed lymphocyte cultures.

Alleles↗