The project involves characterization of how calprotectin regulates the activity of CD69+ tissue residents T cells in a murine model of periodontitis. The functional interaction of calprotectin with CD69 on T cells will be characterized as regulating the extent of inflammation in the initial and chronic phases of murine experimental periodontitis. The successful applicant will be responsible for analyzing, organizing, and presenting data, drafting manuscripts, and making presentations. Finalization of all data, manuscripts and presentations will be done collaboratively with lab members and with approval of the PI.
CD69+ resident-memory T cell regulation: The CD69 receptor on tissue-resident antigen-experienced T cells binds several membrane-bound and soluble ligands. For example, CD69 engagement on T regulatory cells was reported to induce immunosuppressive activities. A putative natural ligand for CD69-mediated activation of Tregs is calprotectin. When released from infected or desquamating keratinocytes or neutrophils, calprotectin may interact with CD69+ T regulatory or T helper 17 cells, ultimately suppressing the immune response.
Degree and/or credentials: Ph.D., DDS, DVM, MD or equivalent is required
Experience with murine models of infection, culture of bacteria and fungi, flow cytomety, confocal immunofluorescence microscopy, microdissection, genetic screening, immunoassays
Excellent record keeping, scientific writing as evidenced by published manuscripts and ability to work independent and in a team
Strong interpersonal and organizational skills
Doctorate in relevant field including 1 to 5 years of research experience preferred
Collaboration within and outside of the laboratory is strongly encouraged
Previous experience in mucosal immunology studies is an asset but not required
Preferred specialties and skills:
Preference will be given to individuals with research experience in Langerhans cell and tissue-resident T cell biology, T cell activation, and protein-protein interactions
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