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Biomedical subjects

A H Hale

Publications and source records attributed to A H Hale.

At least 19 recordsLinked to original sources
PubMed1985

Effects of tumor status on the regulation of natural killer cell activity by tumor-associated fetal antigens.

In the present study we examined the effects of a tumor-associated fetal antigen (TAFA-II) on the activity of natural killer (NK) cells isolated from human cancer patients. TAFA-II suppressed the NK cell response of some patients, and the level of suppression appeared to be independent of tumor type or stage of cancer therapy. No significant correlations were found between lymphocyte, neutrophil, monocyte, or eosinophil populations and TAFA-induced suppression of NK cell activity. TAFA-II effects were also not attributable to Ia+ cells or to OKT3, OKT4, or OKT8 positive cells. This work confirmed results obtained in the rat model, in which suppression appeared to be directly mediated on the NK cell.

Adult↗
PubMed1982

Effect of prostaglandins on elicitation of anti-viral-cytolytic activity.

We have studied the modulating effect of prostaglandins (PG) on the elicitation of secondary anti-vesicular stomatitis virus (VSV) cytotoxic T-lymphocytes (CTL) with viral antigens. The results indicate that PGE1 and PGE2 both inhibit the induction of anti-VSV CTLs by ultraviolet-inactivated VSV. Consistent with the result was the augmentation of anti-VSV CTL activity when VSV-primed spleen cells were cultured in the presence of indomethacin. These results suggest that PGs may modulate anti-viral CTL responses.

Alprostadil↗
PubMed1981

Cross-reactive anti-vesicular stomatitis virus (VSV) cytotoxic T lymphocytes recognize the major surface glycoprotein.

The major surface glycoprotein (G) of vesicular stomatitis virus (VSV) was purified and incorporated into lipid vesicles containing the purified hemagglutinin-neuraminidase (HN) and fusion (F) glycoproteins of Sendai Virus. These lipid vesicles were then used to modify the render target cells susceptible to lysis by anti-VSV cytotoxic T lymphocytes. The results obtained provide direct evidence that the G protein is a target antigen for specific and cross-reactive anti-VSV cytotoxic T lymphocytes. The significance of this work is discussed.

Animals↗
PubMed1981

Phagocytosis-induced 51Cr release from activated macrophages and blood mononuclears. Effect of colchicine and antioxidants.

The chromium-release test was adapted to the measurement of the cellular injury induced when activated macrophages phagocytose particulates. Macrophages obtained from rabbit lungs undergoing BCG-induced chronic inflammation released more chromium when incubated in the presence of phagocytosable particles than when incubated under resting conditions. Blood mononuclear cells, 40-60% monocytes, procured from the same BCG-injected animals, were less susceptible to phagocytosis-induced injury than the macrophages obtained from the lungs. The amount of chromium released by the activated macrophages was proportional to the number of particles present during incubation. In the presence of catalase, the amounts of chromium released by phagocytosing and resting macrophages were similar; in the presence of superoxide dismutase and cytochrome c, the amount of chromium released by phagocytosing macrophages was 13-35% less than the amount of chromium released by macrophages incubated without the antioxidants. In addition, colchicine, an inhibitor of degranulation also exerted partial inhibition of the chromium release. These results suggest that oxygen radicals and lysosomal contents contribute to the cellular injury that results from phagocytosis.

Animals↗
PubMed1981

The involvement of Lyt-2 antigens in the lysis of virus-infected target cells by antigen specific anti-vesicular stomatitis virus cytotoxic T-lymphocytes.

The involvement of cell surface components associated with anti-viral cytotoxic T-lymphocytes (CTLs) in the specific lysis of virus-infected target cells was analyzed by the ability of different monoclonal antibodies to specifically inhibit CTL lytic activity. Utilizing monoclonal anti-Lyt antibodies, we showed that Lyt-2 antigens are closely associated with the CTL lytic event. The nature and limitations of this association are discussed.

Animals↗
PubMed1981

Elicitation of natural killer cells in beige mice by infection with vesicular stomatitis virus.

Vesicular stomatitis virus (VSV) infection of beige (bg/bg) mice induced levels of natural killer cytolytic activity comparable to that of uninfected normal bg/+ controls, but considerably less than natural killer activity in VSV-infected bg/+ mice. In contrast, VSV-infected bg/bg and bg/+ mice had essentially equivalent amounts of anti-VSV cytotoxic T-lymphocyte and antibody activity. VSV infection induced comparable levels of interferon in both bg/bg and bg/+ mice. Therefore, the decreased natural killer activity in bg/bg mice could not be attributed to an inability to produce interferon.

Animals↗
PubMed1981

Elicitation of anti-vesicular stomatitis virus cytotoxic T lymphocytes by using purified viral and cellular antigens incorporated into phospholipid vesicles.

We evaluated the minimal molecular and cellular requirements for elicitation of anti-vesicular stomatitis virus (VSV) cytotoxic T lymphocytes (CTL). The results indicated that lipid vesicles containing the purified major surface glyco-protein of VSV (G protein) and purified H-2K(k) glycoproteins elicited specific H-2K(k)-restricted anti-VSV CTL. These antiviral CTL were shown to be Ly 1(-),2(+). However, both Ly 1(+),2(-) and Ly1(-),2(+) T-cell subpopulations were shown to be required for elicitation of these CTL.

Animals↗
PubMed1981

Lysis of target cells infected with vesicular stomatitis virus (VSV) in the presence of tunicamycin by anti-VSV cytotoxic T lymphocytes.

We have analyzed the requirement for the expression of the major surface glycoprotein (G protein) of vesicular stomatitis virus (VSV) on target cells for recognition and lysis by anti-VSV cytotoxic T lymphocytes (CTL). In addition, we have attempted to determine if the carbohydrate moieties on the G protein are required for recognition and lysis by anti-VSV CTL. When VSV (Orsay) is grown at 30 degrees C in the presence of tunicamycin (TM), glycosylation of G protein is inhibited; however, nonglycosylated G protein is found on the surface of the cell and active virus particles are produced. In contrast, VSV (Orsay) grown at 39 degrees C in the presence of TM produces low titers of virus and the presence of G protein on the surface of cells is not detectable. The susceptibility of these target cells to lysis by anti-VSV CTL was analyzed. The results suggest that expression of the G protein is required for target cell lysis by anti-VSV CTL. However, the presence of the carbohydrate moieties on the G protein are nt an absolute requirement for recognition by anti-VSV CTL. VSV-infected target cells incubated in the presence of TM were lysed by anti-VSV CTL up to 50 to 80% of the infected target cell control. This result suggests either that some clones of anti-VSV CTL recognize carbohydrate moieties or that carbohydrate moieties play some as yet undefined nonantigenic role in the recognition of the target antigen by the CTL receptor.

Animals↗
PubMed1981

Elicitation of anti-H-2 cytotoxic T lymphocytes with antigen-modified H-2 negative stimulator cells.

By a newly developed technique, we have modified H-2k-negative cells in such a way as to render them capable of elicitation of anti-H-2 CTL. Purified H-2Kk and/or partially purified Iak glycoproteins were incorporated into lipid vesicles that contained the hemagglutinin-neuraminidase (HN) glycoprotein and the fusion (F) glycoprotein of Sendai virus. These lipid vesicles were incubated with H-2-negative tumor cells (R1-) in a manner that resulted in rendering these cells capable of eliciting anti-H-2Kk CTL. The presence of Iak on the surface of the modified stimulator cell had a significant effect on the proportion of anti-H-2Kk CTL possessing a particular Lyt phenotype. Primary effector cells elicited by an H-2Kk-Iak difference were primarily Lyt 1-, 2+, whereas primary anti-H-2Kk CTL elicited by an H-2Kk difference alone were predominantly Lyt 1+, 2+.

Animals↗