Burn Wound Infection-Induced Myeloid Suppression
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Publisher
Ovid Technologies (Wolters Kluwer Health)
Reference30 articles.
1. Modulation of Macrophage Hyperactivity Improves Survival in a Burn-Sepsis Model
2. Inhibition of the signaling pathways for macrophage proliferation by cyclic AMP. Lack of effect on early responses to colony stimulating factor-1.
3. Macrophage growth arrest by cyclic AMP defines a distinct checkpoint in the mid-G1 stage of the cell cycle and overrides constitutive c-myc expression.
4. MARROW GRANULOCYTE-MACROPHAGE PROGENITOR CELL RESPONSE TO BURN INJURY AS MODIFIED BY ENDOTOXIN AND INDOMETHACIN
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1. Single-cell Transcriptional Landscape of Temporal Neutrophil Response to Burn Wound in Larval Zebrafish;The Journal of Immunology;2024-06-26
2. Single-cell transcriptional landscape of temporal neutrophil response to burn wound in larval zebrafish;2024-04-02
3. Pathophysiology of Burn Injuries;Handbook of Burns Volume 1;2019-10-30
4. IL-15 Superagonist Expands mCD8+ T, NK and NKT Cells after Burn Injury but Fails to Improve Outcome during Burn Wound Infection;PLOS ONE;2016-02-09
5. Role of G-CSF in monophosphoryl lipid A-mediated augmentation of neutrophil functions after burn injury;Journal of Leukocyte Biology;2015-11-04
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