Cupressus sempervirens extract inhibited human basal cell carcinoma tumorigenesis, local invasion, and angiogenic property
Mehdi AmirniaFatemeh MokhtariAysa RezabakhshElaheh NabatEffat KhodaianiSajad KhalilzadehAli Akbar MovassaghpourAbbas DelazarAnali SadeghiReza Rahbarghazi
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In a mixed leukocyte culture (MLC) reaction of allogenic mouse spleen cells differing for H-2K or H-2D, only a weak cytotoxic response is generated. This cytotoxic response is augmented significantly if bacterial lipopolysaccharide (LPS), 5 microgram/ml, or polyadenylic acid (poly A):polyuridylic acid (poly U), 20 microgram/ml, is present in the culture. The cytotoxic cells generated in the presence of these two agents are specific for sensitizing H-2K or H-2D antigen. Two lines of evidence suggest that these two agents exert their effect at different steps in the development of cytotoxic lymphocytes: (a) the effect of poly A:U depends on the presence of adherent cells, whereas the effect of LPS is independent of the presence of adherent cells and (b) LPS promotes the development of cytotoxic cells when ultraviolet light-treated stimulating cells are used in the MLC whereas poly A:U does not.
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Abstract The main conclusion from these experiments is that the antigen‐specific suppressor T cell of mice which inhibits the induction of cytotoxic T lymphocytes is not itself a cytotoxic T cell. This conclusion is supported by two main observations: first, a certain cell number from first‐step cultures which was suppressive in the presence of a high dose of antigen actually helped the cytotoxic response at a lower antigen dose. This observation is difficult to reconcile with the hypothesis that suppression is due to the killing of the stimulator or the responder cells in the second‐step culture by cytotoxic T cells. Second, cells from first‐step cultures of cortisone‐treated mice displayed cytotoxic activity but had no suppressive effect on the generation of killer cells. It was further demonstrated that these cells failed to influence in any way the suppressive effect, however weak, of cells from first‐step cultures of normal spleen. We therefore favor the view that the suppression observed in this system is due to a regulatory signal which occurs as a result of the ability of both inhibitory cells and responder cells to recognize and respond to allogeneic determinants expressed on the surface of stimulator cells. The suppressor T cells described here act by linked associative recognition of antigen. That is, suppressor T cells only inhibit the induction of a precursor cytotoxic T cell in the presence of an antigen to which both the precursor cell and the suppressor cell can bind. In this sense, suppressors act in a manner analogous to helper T cells in T‐B cell cooperation; carrier‐specific helper T cells only enhance an anti‐hapten B cell response in the presence of hapten‐carrier conjugates. Similarly, alloantigen a (carrier)‐specific suppressor T cells only inhibit alloantigen b (hapten)‐specific cytotoxic responses in the presence of (a × b)F 1 stimulator cells (hapten‐carrier conjugate), not in the presence of a mixture of parental stimulator cells (a + b).
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Sir: A number of investigators have recently reported that cell membranes, or solubilized proteins derived from them, are capable of inducing cytotoxic responses in secondary cultures (1–6). They have implied thereby that they are gaining insight into the specificity of the structures recognized by cytotoxic T cells. An alternative interpretation seems equally plausible: that the membrane preparations act not directly on cytotoxic memory cells, but rather on helper T cells, which, by secreting soluble mediators, “trigger” cytotoxic cell differentiation. This interpretation is supported by several recent reports. Thus, Ryser et al. (7), Wagner and Rollinghoff (8), and this laboratory (Okada et al. , in press) have shown that cell mediators secreted by primed Lyt I+ T cells can cause the direct differentiation of cytotoxic T cells in secondary (memory) cultures. Moreover, the specificity of the cytotoxic cells induced by these mediators is that of the antigen initially used for priming.
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Abstract Sir: A number of investigators have recently reported that cell membranes, or solubilized proteins derived from them, are capable of inducing cytotoxic responses in secondary cultures (1–6). They have implied thereby that they are gaining insight into the specificity of the structures recognized by cytotoxic T cells. An alternative interpretation seems equally plausible: that the membrane preparations act not directly on cytotoxic memory cells, but rather on helper T cells, which, by secreting soluble mediators, “trigger” cytotoxic cell differentiation. This interpretation is supported by several recent reports. Thus, Ryser et al. (7), Wagner and Rollinghoff (8), and this laboratory (Okada et al., in press) have shown that cell mediators secreted by primed Lyt I+ T cells can cause the direct differentiation of cytotoxic T cells in secondary (memory) cultures. Moreover, the specificity of the cytotoxic cells induced by these mediators is that of the antigen initially used for priming.
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Abstract Cytotoxic T lymphocytes in the responding cell population recognize allogeneic target antigens on ultraviolet light (uv)‐treated stimulating cells in a mixed leukocyte culture. However, under these conditions no cytotoxic response is generated unless the responding cells are also stimulated with x‐irradiated or mitomycin C‐treated cells differing by the H‐2 I region‐determined LD antigens. We refer to the signal given to the cytotoxic T lymphocyte by its target antigen as signal 1, and to the help which the cytotoxic T lymphocyte receives presumably from the LD‐responsive T helper cell as signal 2. We have developed a method in which different cell populations are separated by an agar layer to demonstrate that a soluble “factor(s)” can both potentiate a weak cytotoxic reaction as well as allow the development of cytotoxicity against uv‐treated stimulating cells. These results support the two‐signal model in which a “factor”, presumably produced by helper T cells responding to LD antigens, can give signal 2 to the cytotoxic T lymphocyte that has recognized target determinants.
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Beta-2 microglobulin
Clinical Significance
Grading (engineering)
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Allograft rejection represents a cytotoxic response mediated to a large degree by thymus-derived T lymphocytes (1). The study of such cell-mediated cytotoxic phenomena has been greatly facilitated by the discovery first noted by Hayry and Defendi (2) and Wunderlich and Cany (3), that a natural consequence of allogeneic stimulation in an unidirectional mixed lymphocyte culture (MLC) was the appearance of cytotoxic lymphocytes specific for antigens present on the stimulator cells. Subsequent studies have shown that such in vitro generation of cytotoxic lymphocytes was dependent on the proliferative response in an MLC (4), was genetically determined (5), and possibly required the interaction of several subpopulations of T cells (6). We now report that the surface active agent chlorpromazine: (a) inhibits allogeneic stimulation of the proliferative response in an MLC; (b) inhibits the MLC generation of cytotoxic lymphocytes, (c) has no effect on the recognition, binding, or lysis of target cells by already sensitized lymphocytes; and (d) blocks a postproliferative membrane-mediated event, independent of proliferation, and necessary for the MLC generation of cytotoxic lymphocytes.
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Abstract Targeted disruption of β 2 ‐microgobulin gene results in deficient major histocompatibility complex class I expression and failure to develop CD4 − 8 + T cells. Despite this, β 2 M −/− mice reject skin grafts and cope with most viral infections tested. We asked whether CD4 + 8 − cytotoxic T cells could play a role in compensating for the defect in CD4 − 8 + cytotoxic T cell function. We found that the cytotoxic activity against class II + targets is significantly higher among CD4 + 8 − T cells of β 2 M −/− than among those of β 2 M +/+ mice. In the limiting dilution experiment, we showed that the precursor frequency for the cytotoxic, CD4 + 8 − , class II‐specific T cells is at least fivefold higher in β 2 M −/− than in β 2 M +/+ mice. These results suggest that CD4+8 − cytotoxic T cells could play a major role in carrying out cytotoxic function in β 2 M −/− mice.
Beta-2 microglobulin
Histocompatibility
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