Ras-related C3 Botulinum Toxin Substrate (Rac) and Src Family Kinases (SFK) Are Proximal and Essential for Phosphatidylinositol 3-Kinase (PI3K) Activation in Natural Killer (NK) Cell-mediated Direct Cytotoxicity against Cryptococcus neoformans.
Abstract
The activity of Rac in leukocytes is essential for immunity. However, its role in NK cell-mediated anti-microbial signaling remains unclear. In this study, we investigated the role of Rac in NK cell mediated anti-cryptococcal killing. We found thatCryptococcus neoformansindependently activates both Rac and SFK pathways in NK cells, and unlike in tumor killing,Cryptococcusinitiated a novel Rac → PI3K → Erk cytotoxicity cascade. Remarkably, Rac was not required for conjugate formation, despite its essential role in NK cytotoxicity againstC. neoformans Taken together, our data show that, unlike observations with tumor cells, NK cells use a novel Rac cytotoxicity pathway in conjunction with SFK, to killC. neoformans.
추출된 의학 개체 (NER)
| 유형 | 영어 표현 | 한국어 / 풀이 | UMLS CUI | 출처 | 등장 |
|---|---|---|---|---|---|
| 시술 | botulinum toxin
|
보툴리눔독소 주사 | dict | 1 |
MeSH Terms
Cell Line, Tumor; Class Ia Phosphatidylinositol 3-Kinase; Cryptococcus neoformans; Cytotoxicity, Immunologic; Gene Expression Regulation; Host-Pathogen Interactions; Humans; Killer Cells, Natural; Mitogen-Activated Protein Kinase 1; Mitogen-Activated Protein Kinase 3; Phosphorylation; Primary Cell Culture; Pyrones; Quinolines; RNA, Small Interfering; Signal Transduction; rac GTP-Binding Proteins; rac1 GTP-Binding Protein; src-Family Kinases; RAC2 GTP-Binding Protein
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