Joost J. Oppenheim
National Institutes of Health
466 Papers
12.1K Citations
Joost J. Oppenheim is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Chemokine & Interleukin. The author has an hindex of 130, co-authored 454 publications. Previous affiliations of Joost J. Oppenheim include Science Applications International Corporation & University of Birmingham.
Chat about Author
Papers
Interview with Dr. Yoshiro Kobayashi regarding Pivotal Advance: A suppressive role of nitric oxide in MIP-2 production by macrophages upon coculturing with apoptotic cells.
TL;DR: It is concluded that nitric oxide can inhibit the synthesis of soluble inflammatory mediators produced in macrophage culture in response to apoptotic cells.
3
2000 Dolph Adams Award and the State of the Journal
TL;DR: Five years ago, the Council of the Society of Leukocyte Biology initiated $1000 cash awards in honor of Dolph Adams, based on the number of citations over the past 5 years, and serves as a measure of the impact of the papers on the scientific community.
3
Bi-Directional Macrophage-Lymphocyte Interactions Modulate Immune Responses
Joost J. Oppenheim,P S Steeg,R N Moore +2 more
- 01 Jan 1981
TL;DR: The multiplicity of endogenous pathways by which lymphocytes and macrophages mutually augment each other’s reactions in their effort to eliminate bacteria or other non-self antigens are discussed.
3
•Journal Article
Nanoparticle [Gd@C82(OH)22]n induces dendritic cell maturation and promotes Th1 immune responses
TL;DR: It is reported that [Gd@C82(OH)22]n could induce phenotypic maturation of dendritic cells (DC) by stimulating DC production of cytokines including IL-12p70, upregulating DC costimulatory molecules, and switching DCs from CCL5-responsive to CCL19-responsive phenotype.
3
Human lymphoproliferative reaction to food products. Possible role in periodontal inflammation.
TL;DR: Findings suggest that foods such as corn and nuts may be responsible for some periodontal abscesses and may be contributing factors to the development of intrabony alveolar lesions and chronic periodontitis.
3