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- A. Siletz, Kindra M Kelly-Scumpia, Steve Smale
- Tao te Ching
- 15 April 2015
MyD88-dependent expansion of an immature GR-1+CD11b+ population induces T cell suppression and Th2 polarization in sepsis
- M. Delano, P. Scumpia, L. Moldawer
- Biology, MedicineJournal of Experimental Medicine
- 11 June 2007
This work identifies a GR-1+CD11b+ population whose numbers dramatically increase and remain elevated in the spleen, lymph nodes, and bone marrow during polymicrobial sepsis and contributes to sepsi-induced T cell suppression and preferential Th2 polarization.
Type I Interferon Suppresses Type II Interferon–Triggered Human Anti-Mycobacterial Responses
- Rosane M. B. Teles, T. Graeber, R. Modlin
- Biology, MedicineScience
- 22 March 2013
In cultured cells, type I interferon and its downstream signaling cascade inhibited the antimicrobial response induced by type II interferons, providing a potential explanation for why robust disease rather than protection is seen in some cases of infection.
A Paradoxical Role for Myeloid-Derived Suppressor Cells in Sepsis and Trauma
- A. Cuenca, M. Delano, L. Moldawer
- Biology, MedicineMolecular Medicine
- 1 March 2011
Although clinical efforts are currently underway to suppress MDSC numbers and function in cancer to improve antineoplastic responses, such approaches may not be desirable or beneficial in other clinical conditions in which immune surveillance and antimicrobial activities are required.
Cecal Ligation and Puncture
- A. Cuenca, M. Delano, Kindra M Kelly-Scumpia, L. Moldawer, P. Efron
- Biology, MedicineCurrent Protocols in Immunology
- 1 November 2010
The cecum contains a high concentration of microbes, which are a combination of Gram‐negative and Gram‐positive flora, and this combination of ischemic/necrotic tissue and microbial infection distinguishes this multifactorial model from a number of other bacterial sepsis models.
TLR7-dependent and FcγR-independent production of type I interferon in experimental mouse lupus
- P. Lee, Y. Kumagai, W. Reeves
- Biology, MedicineJournal of Experimental Medicine
- 22 December 2008
It is shown that 2,6,10,14-tetramethylpentadecane induces a lupus-like disease in mice characterized by immune complex nephritis with autoantibodies to DNA and ribonucleoproteins by FcγRs and that TMPD elicits IFN-I production, monocyte recruitment, andAutoantibody production exclusively through a Toll-like receptor (TLR) 7– and myeloid differentiation factor 88 (
Neutrophil Mobilization from the Bone Marrow during Polymicrobial Sepsis Is Dependent on CXCL12 Signaling
- M. Delano, Kindra M Kelly-Scumpia, P. Efron
- Medicine, BiologyJournal of Immunology
- 15 July 2011
It is concluded that changes in the pattern of CXCL12 signaling during sepsis are essential for neutrophil bone marrow mobilization and host survival but have little impact on bone marrow granulopoiesis.
Type I interferon signaling in hematopoietic cells is required for survival in mouse polymicrobial sepsis by regulating CXCL10
- Kindra M Kelly-Scumpia, P. Scumpia, L. Moldawer
- Biology, MedicineJournal of Experimental Medicine
- 15 February 2010
A critical role is identified of type I IFN–dependent CXCL10 in host defense during polymicrobial sepsis by increasing neutrophil recruitment and function.
Deficiency of the type I interferon receptor protects mice from experimental lupus.
- D. Nacionales, Kindra M Kelly-Scumpia, W. Reeves
- Medicine, BiologyArthritis & Rheumatism
- 1 November 2007
The clinical and serologic manifestations observed in TMPD-treated mice were strongly dependent on IFNAR signaling, which is consistent with the association of increased expression of ISGs with lupus-specific autoantibodies and nephritis in humans.
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