A novel chemokine receptor for SDF-1 and I-TAC involved in cell survival, cell adhesion, and tumor development
A specific, high affinity small molecule antagonist to CXCR7 impedes in vivo tumor growth in animal models, validating this new receptor as a target for development of novel cancer therapeutics.
IL-10 inhibits cytokine production by activated macrophages.
- D. Fiorentino, A. Zlotnik, T. Mosmann, M. Howard, A. O’Garra
- Biology, MedicineJournal of Immunology
- 1 December 1991
The potent action of IL-10 on the macrophage, particularly at the level of monokine production, supports an important role for this cytokine not only in the regulation of T cell responses but also in acute inflammatory responses.
IL-10 acts on the antigen-presenting cell to inhibit cytokine production by Th1 cells.
IL-10 may inhibit macrophage accessory cell function which is independent of TCR-class II MHC interactions, as well as inhibits IL-2-induced IFN-gamma production by Th1 cells in an Ag-free system requiring only the presence of accessory cells.
CXCR7 (RDC1) promotes breast and lung tumor growth in vivo and is expressed on tumor-associated vasculature
- Z. Miao, K. Luker, T. Schall
- Biology, MedicineProceedings of the National Academy of Sciences
- 2 October 2007
It is established that CXCR7 promotes growth of tumors formed from breast and lung cancer cells and enhances experimental lung metastases in immunodeficient as well as immunocompetent mouse models of cancer.
Formation and hydrolysis of cyclic ADP-ribose catalyzed by lymphocyte antigen CD38.
Soluble CD38 catalyzed the formation and hydrolysis of cadPR when added to NAD+.
Cyclic ADP-ribose production by CD38 regulates intracellular calcium release, extracellular calcium influx and chemotaxis in neutrophils and is required for bacterial clearance in vivo
It is demonstrated that neutrophil chemotaxis to bacterial chemoattractants is dependent on Ca++ mobilization mediated by cyclic ADP-ribose, and CD38 acts as a critical regulator of inflammation and innate immune responses.
Interleukin 10 protects mice from lethal endotoxemia
- M. Howard, T. Muchamuel, S. Andrade, S. Menon
- Biology, ChemistryJournal of Experimental Medicine
- 1 April 1993
The protective effect of IL-10 was reversed by prior injection of neutralizing anti-IL-10 antibodies, and correlated with a substantial decrease in endotoxin-induced TNF-alpha release, which implicate IL- 10 as a candidate for treatment of bacterial sepsis, and more generally as an effective antiinflammatory reagent.
Ly‐1 B (B‐1) cells are the main source of B cell‐derived interleukin 10
- A. O’Garra, R. Chang, N. Go, Robin Hastings, G. Haughton, M. Howard
- BiologyEuropean Journal of Immunology
- 1 March 1992
Since IL 10 is a potent regulator of in vitro immune function, its production by Ly‐1 lineage B (B‐1) cells raises the possibility that this subset of B cells may regulate their own development and/or the function of other immunocompetent cells.
Immunoglobulin signal transduction guides the specificity of B cell-T cell interactions and is blocked in tolerant self-reactive B cells
It is indicated that Ag-specific B cells require two signals for mounting a T cell-dependent Ab response and regulation of sIg signaling as a mechanism for controlling self-reactive B cells is identified.
Pre-Clinical Development of a Humanized Anti-CD47 Antibody with Anti-Cancer Therapeutic Potential
Hu5F9-G4 induced potent macrophage-mediated phagocytosis of primaryhuman AML cells in vitro and completely eradicated human AML in vivo, leading to long-term disease-free survival of patient-derived xenografts.