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Biomedical subjects

M J Sheehy

Publications and source records attributed to M J Sheehy.

At least 37 records · Page 2Linked to original sources
PubMed1985

A particular subset of HLA-DR4 accounts for all or most of the DR4 association in type I diabetes.

Two human T-lymphocyte clones, derived from a mixed leukocyte culture (MLC) with stimulating cells from a type I diabetic patient, define a subset of HLA-DR4, tentatively called "DR4S." In testing of 69 random type I diabetic subjects and 69 random controls, 79% (37/47) of DR4-positive patients, but only 44% (8/18) of DR4-positive controls, had DR4S (P less than 0.01). The relative risk of type I diabetes for DR4S+ individuals was 8.8, while that for DR4+ DR4S- individuals was only 1.0. Thus, in the population tested, DR4S accounts for all or most of the increased frequency of HLA-DR4 in type I diabetes.

Clone Cells↗
PubMed1984

HLA antigens of insulin-dependent diabetics. I. PLT colonies detecting Dw10 and a new class II determinant distinct from HLA-D, DR, MB(DC), MT, and SB.

We describe three human proliferating T cell colonies, derived from mixed leukocyte culture with a non-diabetic individual (DR3 + 4) as the source of responding cells and an insulin-dependent diabetic patient (also DR3 + 4) as the source of stimulating cells. One colony detects HLA-Dw10 or a closely related antigen, and two detect an antigen that we call BO1 (Boston 1). BO1 is found so far on cells of all persons with DR5, about half of those with DRw6, and a particular subset of those with DR3. Among DR3-positive subjects, BO1 is positively correlated with HLA-B18 and BfF1, and negatively correlated with HLA-B8. These findings suggest that BO1 occurs in linkage disequilibrium with DR5, DRw6, and the haplotype B18, BfF1, DR3, the latter being common in southern Europe and reported previously to be a marker for insulin-dependent diabetes. In limited testing (21 subjects), BO1 was completely included in the supertypic specificity MT2, BO1 is a Class II HLA antigen, as demonstrated by blocking with monoclonal antibodies, but is distinct from all known antigens of the DR, MB(DC), MT, and SB series. It could be located on the same polypeptide chain as one or more of these antigen groups, however, particularly DR and/or MT.

Adult↗
PubMed1984

Specificity of hemin action in vivo at early stages of hematopoietic cell differentiation.

The effects of a single injection of hemin on murine marrow BFU-E and CFU-S were assessed to determine whether hemin is as effective in augmenting primitive (day 7) BFU-E levels in situ as it is in vitro and to assess hemin's action on transplantable pluripotent stem cells (CFU-S). The results show that hemin exerts a cell-specific enhancement of both BFU-E marrow levels and cell cycling within 6 h of its administration in vivo. No such effect on CFU-S was observed.

Animals↗
PubMed1983

Morphology of human T lymphocyte clones.

Six human T lymphocyte clones, characterized as to cytolytic activities and several surface markers, were investigated for possible morphologic correlates of function. Cytotoxic T lymphocyte clones and natural killer-like clones had basically similar morphology, but cytotoxic T lymphocytes tended to cluster in groups and had many more lipid bodies, whereas natural killer-like cells had fewer intercellular contacts and had more and larger electron-dense bodies. Dense bodies were also quite prominent in noncytotoxic clones. The latter were distinctive in having a minority of very large cells (10 to 16 microns) with many microvilli, scattered among the majority of 5- to 8-microns diameter cells.

Antibodies, Monoclonal↗
PubMed1981

A patient with post-hepatitis B immune deficiency: nonspecific helper factor partially restores the in vitro immune response.

A patient with severe post-hepatitis B aplastic anemia had depressed B and T cell responses. In mixed leukocyte culture, her cell were unresponsive to unrelated control stimulating cells, but responded well to a pool of cells from the same unrelated controls. She had reduced production of lymphocyte mitogenic factor (MF), suggesting a helper cell defect, and she had few or no cells reactive with the monoclonal anti-T cell antibodies OKT3, OKT4 or OKT5. Her cells proliferated in response to MF produced by a pool of cells without mitogen, however. Furthermore, her cells became specifically cytotoxic when stimulated by cells plus MF, but not when stimulated by either cells or MF alone. Thus her T cell deficiency was correctable by nonspecific helper factor in vitro.

Adolescent↗
PubMed1980

Determining antigenic relationships on the basis of MLC testing. I. A matrix approach for listing all possible antigenic assignments.

We present an approach for determining all possible antigenic relationships among a group of individuals, on the basis of MLC results. We assume that the researcher or tissue typer has a criterion for classifying responses into positives and negatives, and that this classification has already been done for the data set being considered. Given any set of positive and negative MLC responses, our technique produces all antigenic assignments consistent with the assumption that a response occurs if and only if the stimulator has antigen(s) foreign to the responder. No genetic assumptions are made.

Antigens↗
PubMed1980

Determining antigenic relationships on the basis of MLC testing. II. Mechanical algorithms.

We describe mechanical algorithms, involving manipulations of matrices, for listing all possible antigenic relationships among individuals tested in MLC. We also describe an algorithm for determining whether an MLC result can be interpreted in line with our assumption of the preceding paper, that stimulation occurs if, and only if, the stimulator has antigen(s) foreign to the responder.

Antigens↗
PubMed1979

Specific inhibition of human lymphocyte responses by primed autologous lymphocytes. I. Evaluation of MLR inhibition as a model for suppression.

Human lymphocytes from person A, primed for 10 to 14 days in MLC against lymphocytes from person B, inhibit specifically the proliferative response to B by fresh (i.e., unprimed) lymphocytes of A. Gamma-irradiated (2000 R) primed lymphocytes likewise inhibit specifically, although less strongly. Cells of A, primed with cells of B and then irradiated, usually can inhibit the response of A to cells of any individual sharing HLA-D antigens with B, and the effect tends to be independent of the number of stimulating cells. We also often see inhibition of responses to cells sharing HLA-A and -B antigens with person B, but this effect tends to be lost when the number of stimulating cells is increased. Similarly, at low doses, cells primed for HLA-D antigen a appear not to inhibit the response to an irrelevant HLA-D antigen b on the same stimulating cell. At higher doses of primed cells, even the response to the irrelevant antigen is inhibited. These data suggest to us that at least two mechnaisms may be involved: one directed at the stimulating cell (most likely cell-mediated cytolysis), and predominant at high ratios of primed cells to stimulating cells; the other directed at specific clones of responding cells, and predominant at low ratios.

Dose-Response Relationship, Immunologic↗
PubMed1977

Lack of restimulation by non-HLA antigens in primed lymphocyte typing.

We have studied the role of non-HLA antigens in restimulation of PLT cells by the following protocols. Responder cells were sensitized to cells from family members differing by one HLA haplotype. The PLT cells were restimulated by family members HLA- or HLA-D-identical to the responder. In none of these cases did we find significant restimulation, indicating that it is unlikely that there is a restimulatory non-HLA locus with even two alleles (p less than 0.05) of equal frequency. Other protocols we have used are consistent with this interpretation. This indicates that antigens determined by genes segregating independently of HLA do not play a major role in the PLT restimulation.

Antigens↗
PubMed1976

Three HLA-D region antigens defined by primed LD typing.

We have recently described a new method, primed LD typing or PLT, for specific identification of HLA-D antigens. Highly discriminatory PLT cells have been developed which clearly differentiate between cells of individuals that restimulate strongly and those that restimulate weakly. Seven such discriminatory PLT cells have been used to define three antigens called PL1, PL2, and PL3; two more PLT cells may define antigen(s) PL4.

Genes↗