W. Leonard

Immunology · Journal of Experimental Medicine · 2000–2013

A researcher in the Science corpus: 17 papers; trusts 19 researchers and is trusted by 14 researchers here, as inferred from the citation graph.

Subfields

Whom W. Leonard trusts overall

Their strongest outbound trust, strongest first, inferred from their citations.

  1. Long-Cheng Li
  2. E. Shevach
  3. Shane Crotty
  4. Hyoung-Pyo Kim
  5. O. Boyman
  6. Matthew A. Williams
  7. J. O’Shea
  8. Ye Zheng
  9. T. Malek
  10. Rajvir Dahiya

Who trusts W. Leonard overall

  1. W. Liao
  2. Alexander Y. Rudensky
  3. Steven Z. Josefowicz
  4. Sylvia M. Lee
  5. Jian-Xin Lin

Papers from W. Leonard's perspective

Ordered by how strongly the researchers W. Leonard trusts endorse each paper. Same corpus, a different order for every researcher.

  1. A function for interleukin 2 in Foxp3-expressing regulatory T cells (Nature Immunology)
  2. Inducing and expanding regulatory T cell populations by foreign antigen (Nature Immunology)
  3. Interleukin 27 negatively regulates the development of interleukin 17–producing T helper cells during chronic inflammation of the central nervous system (Nature Immunology)
  4. A novel transcription factor, T-bet, directs Th1 lineage commitment. (Cell)
  5. Selective regulatory function of Socs3 in the formation of IL-17-secreting T cells. (Proceedings of the National Academy of Sciences of the United States of America)
  6. IL-23 drives a pathogenic T cell population that induces autoimmune inflammation
  7. Interleukin-23 Promotes a Distinct CD4 T Cell Activation State Characterized by the Production of Interleukin-17*
  8. Interleukin 27 limits autoimmune encephalomyelitis by suppressing the development of interleukin 17–producing T cells (Nature Immunology)
  9. IL-2 regulates FOXP3 expression in human CD4+CD25+ regulatory T cells through a STAT-dependent mechanism and induces the expansion of these cells in vivo. (Blood)
  10. TGFbeta in the context of an inflammatory cytokine milieu supports de novo differentiation of IL-17-producing T cells. (Immunity)

Their papers