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Professional Education


  • Doctor of Philosophy, University of California San Francisco (2011)

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Research & Scholarship

Lab Affiliations


Publications

Journal Articles


  • Reporter Alleles that Inform on Differences in Cre Recombinase Expression JOURNAL OF IMMUNOLOGY Klinger, M., Chmura, S. A., Killeen, N. 2010; 184 (11): 6170-6176

    Abstract

    Alleles that express reporters after Cre recombination allow for fate-mapping studies when used in combination with appropriate cre alleles. In this study, we describe two fluorescent reporter alleles that differentially mark populations of cells as a function of their level of expression of Cre recombinase. Mice carrying these alleles were generated and used to demonstrate the usefulness of the reporter alleles for informing on prior Cre recombinase expression in lymphocytes. The alleles expand the range of genetic tools available for understanding how differences in gene expression result in divergent developmental fates during the development and differentiation of lymphocytes and other cells.

    View details for DOI 10.4049/jimmunol.1000089

    View details for Web of Science ID 000278439600030

    View details for PubMedID 20427774

  • Macrophage- and Dendritic-Cell-Derived Interleukin-15 Receptor Alpha Supports Homeostasis of Distinct CD8(+) T Cell Subsets IMMUNITY Mortier, E., Advincula, R., Kim, L., Chmura, S., Barrera, J., Reizis, B., Malynn, B. A., Ma, A. 2009; 31 (5): 811-822

    Abstract

    Interleukin-15 receptor alpha (IL-15R alpha) is a pleiotropically expressed molecule that chaperones and trans-presents IL-15 to NK and T cells. To investigate whether IL-15R alpha presented by different cells perform distinct physiological functions, we have generated four lines of mice lacking IL-15R alpha in various cell types. We find that IL-15R alpha expression on macrophages but not dendritic cells (DCs) supports the early transition of antigen specific effector CD8(+) T cells to memory cells. After memory CD8(+) T cell differentiation, IL-15R alpha expression on DCs selectively supports central memory CD8(+) T cells, whereas IL-15R alpha expression on macrophages supports both central and effector memory CD8(+) T cells. By contrast, mice lacking IL-15R alpha on macrophages, DCs, or both, exhibit equivalent defects in NK cell homeostasis and activation. These studies define unique roles for macrophage expression of IL-15R alpha and show that NK cells rely upon distinct IL-15R alpha dependent IL-15 signals than memory CD8(+) T cells. Moreover, they demonstrate the diversity, specification, and geographic restriction of cytokine signals.

    View details for DOI 10.1016/j.immuni.2009.09.017

    View details for Web of Science ID 000272097900015

    View details for PubMedID 19913445

  • Thymic OX40 Expression Discriminates Cells Undergoing Strong Responses to Selection Ligands JOURNAL OF IMMUNOLOGY Klinger, M., Kim, J. K., Chmura, S. A., Barczak, A., Erle, D. J., Killeen, N. 2009; 182 (8): 4581-4589

    Abstract

    OX40 is a member of the TNF receptor family expressed on activated and regulatory T (Treg) cells. Using an Ox40-cre allele for lineage marking, we found that a subpopulation of naive T cells had also previously expressed OX40 in the thymus. Ox40-cre was induced in a small fraction of thymocytes that were OX40(+), some of which were CD25(high) Treg cell precursors. Thymic OX40 expression distinguished cells experiencing a strong signaling response to positive selection. Naive T cells that had previously expressed OX40 demonstrated a partially activated phenotype that was distinct from that of most naive T cells. The results are consistent with the selection of Treg cells and a minor subpopulation of naive T cells being dependent on strong signaling responses to thymic self ligands.

    View details for DOI 10.4049/jimmunol.0900010

    View details for Web of Science ID 000265004700015

    View details for PubMedID 19342632

  • A single class II myosin modulates T cell motility and stopping, but not synapse formation NATURE IMMUNOLOGY Jacobelli, J., Chmura, S. A., Buxton, D. B., DAVIS, M. M., Krummel, M. F. 2004; 5 (5): 531-538

    Abstract

    Upon encountering an antigen, motile T cells stop crawling, change morphology and ultimately form an 'immunological synapse'. Although myosin motors are thought to mediate various aspects of this process, the molecules involved and their exact roles are not defined. Here we show that nonmuscle myosin heavy chain IIA, or MyH9, is the only class II myosin expressed in T cells and is associated with the uropod during crawling. MyH9 function is required for maintenance of the uropod and for T cell motility but is dispensable for synapse formation. Phosphorylation of MyH9 in its multimerization domain by T cell receptor-generated signals indicates that inactivation of this motor may be a key step in the 'stop' response during antigen recognition.

    View details for DOI 10.1038/ni1065

    View details for Web of Science ID 000221101100018

    View details for PubMedID 15064761

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