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Biomedical subjects

E Martz

Publications and source records attributed to E Martz.

At least 37 records · Page 2Linked to original sources
PubMed1981

Lymphocyte function-associated antigen 1 (LFA-1): a surface antigen distinct from Lyt-2,3 that participates in T lymphocyte-mediated killing.

Monoclonal antibodies (MAb) have been used to probe the relationship of cytolytic T lymphocyte (CTL) surface molecules to CTL function. Rat MAb to mouse CTL were generated. Twelve MAb so obtained gave preferential binding to T cells as compared to B cells, and three of these recognized previously undescribed surface polypeptides. These Mab and more broadly reactive and previously obtained MAb were tested for their ability to block CTL-mediated killing in the absence of complement. To ensure that any observed blocking was due to binding of MAb to the effector cell rather than the target cell, a xenogeneic mouse CTL anti-rat BN lymphoma target cell system was utilized (MAb and target cells both of rat origin). Of 24 MAb tested here, 21 had little or no effect on CTL function, including those to H-2, Thy-1, Lyt-1, Ly 5, Ly 6, Lgp 100, and at least six other defined antigens. We confirmed inhibition of killing with two MAb to Lyt-2,3. Another MAb, M7/14, gave profound and consistent blockade of CTL function. It was confirmed that M7/14 MAb blocks killing by binding to the mouse CTL and does not bind to the rat lymphoma target cells used for the CTL assay. The findings suggest that the antigen defined by M7/14, termed a lymphocyte function-associated antigen, LFA-1, participates in or is closely associated with the mechanism of CTL-mediated killing. LFA-1 contains two polypeptide chains of 180,000 and 95,000 Mr and is distinct from other described lymphocyte glycoproteins. LFA-1 thus represents both a previously undescribed lymphocyte surface antigen and molecular site for blockade of CTL-mediated killing.

Animals↗
PubMed1981

T11: a new protein marker on activated murine T lymphocytes.

Murine lymphocytes were activated in vitro in mixed lymphocyte cultures (MLC) or by the addition of the mitogens concanavalin A (Con A), phytohemagglutinin (PHA), or E. coli lipopolysaccharide (LPS). Activated lymphocytes were internally labeled with 35S-methionine and then disrupted by hypotonic lysis. A plasma membrane-enriched fraction was isolated from each cell population, and the 35S-labeled proteins in this fraction were examined by SDS-polyacrylamide gel electrophoresis (SDS-PAGE). An intensely labeled band, the position of which indicated an apparent m.w. of 11,000, was observed when plasma membrane-enriched fractions from MLC- and Con A-activated cells were subjected to SDS-PAGE. In contrast, plasma membrane-enriched fractions from normal spleen cells, LPS-activated cells, PHA-activated cells, and EL4, RDM4, and P815 tumor cells possessed little or none of this protein, which we have designated T11. T11 was not found in the soluble cytoplasmic protein from MLC-activated cells. Hence the presence of T11 in the plasma membrane-enriched fraction from these cells cannot be attributed to contamination by cytoplasmic protein. Removal of T cells from populations of MLC-activated cells by treatment with monoclonal anti-Thy 1 and complement removed T11. These results suggest that T11 may represent a new protein marker on a subclass of activated T lymphocytes.

Animals↗
PubMed1981

A novel lymphocyte function-associated antigen (LFA-1): cellular distribution, quantitative expression, and structure.

We have previously described a monoclonal antibody (MAb), M7/14, which blocks a variety of T cell functions, including CTL-mediated killing, the mixed lymphocyte response, and antigen-specific proliferation. The antigen defined by M7/14 has been designated lymphocyte function-associated antigen one (LFA-1). In this report, LFA-1 has been studied as to cell distribution, surface abundance, structure, and in comparison to other CTL surface antigens, LFA-1 is expressed on lymphoid cells of both the T and the B lineages and on a large fraction of bone marrow cells, but not on exudate macrophages or nonlymphoid tissues. T cells express more LFA-1 than B cells, both in the unstimulated and stimulated states. Compared with unstimulated spleen cells, cytolytic T lymphocyte cell preparations (CTLP) and Con A blasts, but not LPS blasts, show increased LFA-1 expression relative to H-2, and for T cell-containing populations, Lyt-2. M7/14 MAb binds to about 1.5 X 10(4) and 7 X 10(4) LFA-1 sites per average spleen cell or CTLP cell, respectively. M7/14 Mab binds to cTLP in quantitites of 2.5-fold and ies 10.4-fold less than H-2 and Thy-1 Mab, respectively; since the latter have little or no effect on CTL function, inhibition of killing by M7/14 MAb is specific for the LFA-1 surface site. M7/14 MAb and a blocking Lyt-2 MAb are bound in similar quantities of CTLP. LFA-1 is a glycoprotein and consists of 2 noncovalently linked polypeptide chains of 180,000 and 95,000 Mr. The same molecular species as on CTL is present on other T cells and on B cells. The molecular structure and cell distribution of LFA-1 clearly distinguishes it from Lyt-2,3, Ly-5, T145, and T11, which were previously suggested to be either associated with the function of and/or present on the surface of CTL.

Animals↗
PubMed1980

Immune T lymphocyte to tumor cell adhesion. Magnesium sufficient, calcium insufficient.

The prelytic adhesion of immune cytolytic thymus-derived lymphocytes to specific antigen-bearing ascites tumor target cells has been studied. A new assay was used in which adhesions are permitted to form for 2.5 min; the cells are then dispersed to prevent further adhesion, and the predispersion adhesions are quantitated by subsequent 51Cr release from the tumor cells as a result of cytolytic activity of the adhering lymphocytes. There were the following new findings: (a) magnesium is sufficient to support optimal adhesion formation even when EGTA is added to remove contaminating traces of calcium; (b) calcium supports no adhesion formation when traces of contaminating magnesium are removed by pretreating the medium with a chelating ion exchange resin; (c) calcium synergizes with suboptimal magnesium, increasing the apparent adhesion-supporting potency of magnesium 20-fold in the presence of 50 microM calcium; (d) in the presence of optimal magnesium (2--4 mM), calcium has not effect on the properties of the adhesion by any of six criteria; and (e) manganese supports adhesion better than magnesium, and strontium is ineffective. A survey of previous literature indicates that these results are remarkably similar to the predominant pattern for nonimmunologic cell adhesion (e.g., fibroblasts) involving cells from a variety of tissues in late embryonic and adult avians and mammals. This suggests that a "magnesium sufficient, calcium insufficient" mechanism may be found among the latter types of cell adhesions when appropriately examined. Moreover, it seems that the present lymphocyte-tumor cell adhesion, although evoked by specific receptor-antigen recognition, relies predominantly on mechanisms common to nonimmunologic intercellular adhesion processes.

Animals↗
PubMed1978

Cell movements in a confluent monolayer are not caused by gaps: evidence for direct contact inhibition of overlapping.

According to the hypothesis of contact inhibition of movement, cells in a confluent monolayer are restrained from major overlapping by a directional inhibition of locomotion. This explanation of monolayering proposes that contact between 2 cells locally paralyses the locomotory function, preventing movement in the direction that would lead to overlapping. Consequently, a cell in contact on all sides with neighbouring cells should be immobilized. Yet in strictly monolayered cultures of confluent chick liver or mouse 3T3 cells, we have previously observed both translational cell movements and re-shufflings of relative cell positions. The 'confluence' was not perfect, however, and it seemed possible that the movements observed were due to release from contact inhibition by occasional transitory gaps seen to open up between cells. In the present study, detailed gap experiences and cell movements were recorded for 31 cells over a total of 1637 cell-hours. There was no significant correlation between frequency of gaps experienced and the extent of cell movement measured as neighbour-exchanges. We conclude that gaps are not a major cause of the movements observed. The hypothesis based on contact inhibition of motion, which attempts to explain monolayering indirectly by imposing a restraint on cell locomotion, cannot explain the substantial cell movements seen in the confluent cell monolayer studied here. To explain contact inhibition of overlapping, the evidence favours a more direct hypothesis which places no restriction on cell movement other than that overlapping be avoided. Such direct avoidance of overlapping could result from differences in the strengths with which cells adhere to one another and to the substratum.

Cell Movement↗