Cherie Martina

Arizona State University, Phoenix, Arizona, United States

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Publications (3)7.86 Total impact

  • Cherie Martina, Jay Wayne, Anthony Bell, Yung Chang
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    ABSTRACT: Several studies have shown that the developmental arrest of severe combined immune deficiency (scid) thymocytes during the CD4(-)CD8(-) double negative (DN) to CD4(+)CD8(+) double positive (DP) transition can be overcome by a sub-lethal dose of ionizing radiation (IR). Concurrent with this developmental progression, IR also induces variable (diversity) joining (V(D)J) recombination at T cell receptor (TCR), delta, beta, and gamma, but not alpha loci. In addition, all irradiated scid mice succumb to thymic lymphoma. In this study, we demonstrate that scid neonates treated with anti-CD3 epsilon antibody become more resistant to the development of thymoma upon exposure to IR. It is known that the anti-CD3 epsilon antibody treatment induces T cell progression to the DP stage bypassing TCRbeta rearrangement. We show here that the resistance to tumor development is correlated with a reduction of TCRbeta rearrangements that are induced by IR. However, TCRgamma rearrangements were not altered by the antibody treatment. The particular effect of anti-CD3 epsilon antibody on TCRbeta rearrangements is likely attributed to a decline of the double negative thymocyte subset (DN3), in which TCRbeta rearrangements predominantly occur. These results suggest that the developmental stage of scid thymocytes can influence the effect of IR on TCR rearrangements as well as lymphomagenesis.
    Immunology Letters 03/2003; 85(3):279-86. · 2.34 Impact Factor
  • Cherie Martina, Jay Wayne, Anthony Bell, Yung Chang
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    ABSTRACT: Several studies have shown that the developmental arrest of severe combined immune deficiency (scid) thymocytes during the CD4−CD8− double negative (DN) to CD4+CD8+ double positive (DP) transition can be overcome by a sub-lethal dose of ionizing radiation (IR). Concurrent with this developmental progression, IR also induces variable (diversity) joining (V(D)J) recombination at T cell receptor (TCR), δ, β, and γ, but not α loci. In addition, all irradiated scid mice succumb to thymic lymphoma. In this study, we demonstrate that scid neonates treated with anti-CD3ε antibody become more resistant to the development of thymoma upon exposure to IR. It is known that the anti-CD3ε antibody treatment induces T cell progression to the DP stage bypassing TCRβ rearrangement. We show here that the resistance to tumor development is correlated with a reduction of TCRβ rearrangements that are induced by IR. However, TCRγ rearrangements were not altered by the antibody treatment. The particular effect of anti-CD3ε antibody on TCRβ rearrangements is likely attributed to a decline of the double negative thymocyte subset (DN3), in which TCRβ rearrangements predominantly occur. These results suggest that the developmental stage of scid thymocytes can influence the effect of IR on TCR rearrangements as well as lymphomagenesis.
    Immunology Letters - IMMUNOL LETT. 01/2003; 85(3):279-286.
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    ABSTRACT: There is evidence for both physiological functions of the natural neurotransmitter, acetylcholine, and pharmacological actions of the plant alkaloid, nicotine, on the development and function of the immune system. The effects of continuous exposure to nicotine over a 12-day course of fetal thymus organ culture (FTOC) were studied, and thymocytes were analyzed by flow cytometry. In the presence of very low concentrations of nicotine many more immature T cells (defined by low or negative TCR expression) and fewer mature T cells (intermediate or high expression of TCR) were produced. In addition, the numbers of cells expressing CD69 and, to a lesser extent, CD95 (Fas) were increased. These effects took place when fetal thymus lobes from younger (13-14 days gestation) pups were used for FTOC. If FTOC were set up using tissue from older (15-16 days gestation pups), nicotine had little effect, suggesting that it may act only on immature T cell precursors. Consistent with an increase in immature cells, the expression of recombinase-activating genes was found to be elevated. Nicotine effects were partially blocked by the simultaneous addition of the nicotinic antagonist d-tubocurarine. Furthermore, d-tubocurarine alone blocked the development of both immature and mature murine thymocytes, suggesting the presence of an endogenous ligand that may engage nicotinic acetylcholine receptors on developing thymocytes and influence the course of normal thymic ontogeny.
    The Journal of Immunology 10/2002; 169(6):2915-24. · 5.52 Impact Factor