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Division of Vaccine Discovery
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Division of Cell Biology
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Division of Developmental Immunology
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    ABSTRACT: Protein kinase C (PKC) proteins are a group of well-conserved, intracellular signaling enzymes expressed in all cells and tissues, including immune cells. Much of the molecular insight into PKC immunobiology has been gleaned from studies using PKC gene (Prkc) knockout mice and the analysis of different disease models in these animals. More-recent studies have revealed that PKCs also have crucial roles in the pathogenesis of human immune disorders. Therefore, strategies to modulate the functions of PKC enzymes could have a major impact on the treatment and therapies of autoimmune diseases and other immune disorders.
    Drug Discovery Today 05/2014;
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    ABSTRACT: The recent increase in whooping cough in vaccinated populations has been attributed to waning immunity associated with the acellular vaccine. The Immune Epitope Database (IEDB) is a repository of immune epitope data from the published literature and includes T cell and antibody epitopes for human pathogens. The IEDB conducted a review of the epitope literature, which revealed 300 B. pertussis-related epitopes from 39 references. Epitope data are currently available for six virulence factors of B. pertussis: pertussis toxin, pertactin, fimbrial 2, fimbrial 3, adenylate cyclase and filamentous hemagglutinin. The majority of epitopes were defined for antibody reactivity; fewer T cell determinants were reported. Analysis of available protective correlates data revealed a number of candidate epitopes; however few are defined in humans and few have been shown to be protective. Moreover, there are a limited number of studies defining epitopes from natural infection versus whole cell or acellular/subunit vaccines. The relationship between epitope location and structural features, as well as antigenic drift (SNP analysis) was also investigated. We conclude that the cumulative data is yet insufficient to address many fundamental questions related to vaccine failure and this underscores the need for further investigation of B. pertussis immunity at the molecular level.
    Human immunology 05/2014;
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    ABSTRACT: The pathogenesis of inflammatory bowel disease (IBD) is associated with a dysregulated mucosal immune response. Expression of the tumor necrosis factor (TNF) superfamily member 14 (TNFSF14, also known as LIGHT) on T cells is involved in their activation; transgenic expression of LIGHT on T cells in mice promotes inflammation in multiple organs, including intestine. We investigated the roles for LIGHT in recovery from intestinal inflammation in mice. We studied the role of LIGHT in intestinal inflammation using Tnfsf14(-/-) and wild-type mice. Colitis was induced by transfer of CD4(+)CD45RB(high) T cells into Rag1(-/-) or Tnfsf14(-/-)Rag1(-/-) mice, or by administration of dextran sulfate sodium salt (DSS) to Tnfsf14(-/-) or wild-type C57BL/6J mice. Mice were weighed; colon tissues were collected and measured, and histology analyses were performed. We measured infiltrating cell populations and expression of cytokines, chemokines, and LIGHT. Following administration of DSS, Tnfsf14(-/-) mice developed more severe colitis than controls, based on their reduced survival, accelerated loss of body weight, and histologic scores. LIGHT protected mice from colitis via the lymphotoxin β receptor and was expressed mainly by myeloid cells in the colon. Colons of Tnfsf14(-/-) mice also had increased accumulation of innate immune cells and higher levels of cytokines than colons from control mice. LIGHT therefore appears to regulate inflammation in the colon. Tnfsf14(-/-) mice develop more severe colitis than control mice. LIGHT signals through the lymphotoxin β receptor in the colon to regulate the innate immune response and mediate recovery from intestinal inflammation.
    Gastroenterology 02/2014;


  • Address
    9420 Athena Cir, 92037, La Jolla, CA, United States
  • Head of Institution
    Dr. Mitchell Kronenberg
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Top publications last week by downloads

Current Protein and Peptide Science 09/2007; 8(4):329-51.
Nature Immunology 01/2004; 4(12):1191-8.

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