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Seminars in Immunology

Print ISSN
1044-5323
Electronic ISSN
1096-3618
Impact factor
8.337
Publisher
Sciencedirect
URL
http://www.sciencedirect.com/science/journal/10445323
Usage rank
1634
Article count
1065
Free count
24
Free percentage
0.0225352
PDFs via platforms
Sciencedirect from 1993, CSA, Proquest, Gale, Rcgp, and Ingenta

  1. Insights from the worm: the C. elegans model for innate immunity.

    Seminars in Immunology 26(4):303 (2014) PMID 24856329

    The nematode worm Caenorhabditis elegans comprises an ancestral immune system. C. elegans recognizes and responds to viral, bacterial, and fungal infections. Components of the RNA interference machinery respond to viral infection, while highly conserved MAPK signaling pathways activate the innate im...
  2. TWEAK/Fn14 axis: the current paradigm of tissue injury-inducible function in the midst of complexities.

    Seminars in Immunology 26(3):229 (2014) PMID 24636536

    TNF-like weak inducer of apoptosis (TWEAK), a TNF family ligand, and its only known signaling receptor, FGF-inducible molecule-14 (Fn14), have emerged as a key molecular pathway regulating tissue responses after acute tissue injury and in contexts of chronic injury and disease, including autoimmunit...
  3. Ectodysplasin research--where to next?

    Seminars in Immunology 26(3):220 (2014) PMID 24928340

    Ectodysplasin (Eda) is the most studied tumor necrosis ligand in the field of developmental biology. In all vertebrates studied so far, inactivating germline mutations in Eda lead to the genetic disease called hypohidrotic ectodermal dysplasia (HED). In humans, HED is a life-threatening condition in...
  4. The role of chemokines and chemokine receptors in alloantigen-independent and alloantigen-dependent transplantation injury
    Author(s) unavailable

    Seminars in Immunology 2012

    Transplantation injury and rejection involves the interplay of innate and acquired immune responses. Immune-related injury manifests itself in three temporal phases: early innate immune driven alloantigen-independent injury, acquired immune driven alloantigen-dependent injury, and chronic injury. Seq...
  5. Cancer vaccines: the state of the art.

    Seminars in Immunology 22(3):103 (2010) PMID 20552730

  6. The CD94/NKG2C+ NK-cell subset on the edge of innate and adaptive immunity to human cytomegalovirus infection.

    Seminars in Immunology 26(2):145 (2014) PMID 24666761

    We originally reported that HCMV infection promotes, to a variable degree in healthy individuals, a redistribution of the NK-cell receptor (NKR) repertoire which persists under steady-state conditions. Its hallmark is an expansion of a mature NK-cell subset displaying high surface levels of the CD94...
  7. Stratification and compartmentalisation of immunoglobulin responses to commensal intestinal microbes.

    Seminars in Immunology 25(5):358 (2013) PMID 24238818

    The gastrointestinal tract is heavily colonized with commensal microbes with the concentration of bacteria increasing longitudinally down the length of the intestine. Bacteria are also spatially distributed transversely from the epithelial surface to the intestinal lumen with the inner mucus layer n...
  8. Identity crisis of Th17 cells: Many forms, many functions, many questions

    Seminars in Immunology 25(4):263 (2013) PMID 24239567

    • Th17 cells are potent regulators linked to induction and persistence of inflammation. • The human Th17 compartment is heterogeneous with pro- and anti-inflammatory c...
  9. CD4 CTL: living up to the challenge.

    Seminars in Immunology 25(4):273 (2013) PMID 24246226 PMCID PMC3886800

    I restricted precursor cells and promotes the lineage commitment of CD8αβ(+) cytolytic T lymphocytes (CTL). ThPOK continues to repress the CTL gene program in mature CD4(+) T cells, even as they differentiate into effector Th cell subsets. The Th cell fate however is not fixed and two recent studies...
  10. T cell metabolism and the immune response.

    Seminars in Immunology 24(6):399 (2012) PMID 23313070

    As T cells respond to pathogens, they must transition from a quiescent, naïve state, to a rapidly proliferating, active effector state, and back again to a quiescent state as they develop into memory cells. Such transitions place unique metabolic demands on the differentiating cells. T cells meet th...