Sickle cell vaso-occlusion causes activation of iNKT cells that is decreased by the adenosine A2A receptor agonist regadenoson

Blood

Volumn 121, Issue 17, 2013, Pages 3329-3334

  Field, Joshua J ^a,b   Lin, Gene ^c   Okam, Maureen M ^d,e   Majerus, Elaine ^f   Keefer, Jeffrey ^g   Onyekwere, Onyinye ^h   Ross, Ainsley ^d   Campigotto, Federico ⁱ   Neuberg, Donna ⁱ   Linden, Joel ^c   Nathan, David G ^e,i,j  

^a BLOOD RESEARCH INSTITUTE   (United States)

^b MEDICAL COLLEGE OF WISCONSIN   (United States)

^c LA JOLLA INSTITUTE FOR ALLERGY AND IMMUNOLOGY   (United States)

^d BRIGHAM AND WOMEN S HOSPITAL   (United States)

^e HARVARD MEDICAL SCHOOL   (United States)

^f WASHINGTON UNIVERSITY SCHOOL OF MEDICINE   (United States)

^g JOHNS HOPKINS UNIVERSITY SCHOOL OF MEDICINE   (United States)

^h HOWARD UNIVERSITY COLLEGE OF MEDICINE   (United States)

ⁱ DANA FARBER CANCER INSTITUTE   (United States)

^j BOSTON CHILDREN S HOSPITAL   (United States)

more..

Author keywords

[No Author keywords available]

Indexed keywords

GAMMA INTERFERON; REGADENOSON; SYNAPTOTAGMIN I; ADENOSINE A2 RECEPTOR AGONIST; ADENOSINE A2A RECEPTOR; PURINE DERIVATIVE; PYRAZOLE DERIVATIVE; TRANSCRIPTION FACTOR RELA;

ADULT; ARTICLE; BLOOD VESSEL OCCLUSION; BRADYCARDIA; CELL ACTIVATION; CLINICAL ARTICLE; CONTROLLED STUDY; DRUG DOSE ESCALATION; DRUG EFFECT; DRUG SAFETY; FEMALE; HUMAN; MALE; MULTICENTER STUDY; NATURAL KILLER T CELL; PHASE 1 CLINICAL TRIAL; PRIORITY JOURNAL; PROTEIN TARGETING; SICKLE CELL ANEMIA; STEADY STATE; TREATMENT RESPONSE; CASE CONTROL STUDY; CHEMISTRY; COMPARATIVE STUDY; FLOW CYTOMETRY; INTRAVENOUS DRUG ADMINISTRATION; METABOLISM; PATHOLOGY; PHOSPHORYLATION; PROGNOSIS; TISSUE DISTRIBUTION; VASCULAR DISEASE;

ADENOSINE A2 RECEPTOR AGONISTS; ADULT; ANEMIA, SICKLE CELL; CASE-CONTROL STUDIES; FEMALE; FLOW CYTOMETRY; HUMANS; INFUSIONS, INTRAVENOUS; INTERFERON-GAMMA; MALE; NATURAL KILLER T-CELLS; PHOSPHORYLATION; PROGNOSIS; PURINES; PYRAZOLES; RECEPTOR, ADENOSINE A2A; TISSUE DISTRIBUTION; TRANSCRIPTION FACTOR RELA; VASCULAR DISEASES;

MLCS; MLOWN;

EID: 84879350342     PISSN: 00064971     EISSN: 15280020     Source Type: Journal    
DOI: 10.1182/blood-2012-11-465963     Document Type: Article

References (26)

1. Wallace KL, Marshall MA, Ramos SI, et al. NKT cells mediate pulmonary inflammation and dysfunction in murine sickle cell disease through production of IFN-gamma and CXCR3 chemokines. Blood. 2009;114(3):667-676.
2. Wallace KL, Linden J. Adenosine A2A receptors induced on iNKT and NK cells reduce pulmonary inflammation and injury in mice with sickle cell disease. Blood. 2010;116(23):5010-5020.
3. Field JJ, Nathan DG, Linden J. Targeting iNKT cells for the treatment of sickle cell disease. Clin Immunol. 2011;140(2):177-183.
4. Lappas CM, Day YJ, Marshall MA, et al. Adenosine A2A receptor activation reduces hepatic ischemia reperfusion injury by inhibiting CD1d-dependent NKT cell activation. J Exp Med. 2006;203(12):2639-2648.
5. Astellas Pharma. Lexiscan [package insert]. Northbrook, IL: Astellas Pharma; 2009.
6. Rosin DL, Robeva A, Woodard RL, et al. Immunohistochemical localization of adenosine A2A receptors in the rat central nervous system. J Comp Neurol. 1998;401(2):163-186.
7. Van Kaer L, Parekh VV, Wu L. Invariant natural killer T cells: bridging innate and adaptive immunity. Cell Tissue Res. 2011;343(1):43-55.
8. Brennan PJ, Tatituri RV, Brigl M, et al. Invariant natural killer T cells recognize lipid self antigen induced by microbial danger signals. Nat Immunol. 2011;12(12):1202-1211.
9. Matsuda JL, Gapin L, Baron JL, et al. Mouse V alpha 14i natural killer T cells are resistant to cytokine polarization in vivo. Proc Natl Acad Sci USA. 2003;100(14):8395-8400.
10. Stetson DB, Mohrs M, Reinhardt RL, et al. Constitutive cytokine mRNAs mark natural killer (NK) and NK T cells poised for rapid effector function. J Exp Med. 2003;198(7):1069-1076.
11. Bendelac A, Savage PB, Teyton L. The biology of NKT cells. Annu Rev Immunol. 2007;25:297-336.
12. Ghosh S, Hayden MS. New regulators of NF-kappaB in inflammation. Nat Rev Immunol. 2008; 8(11):837-848.
13. Stanic AK, Bezbradica JS, Park JJ, et al. Cutting edge: the ontogeny and function of Va14Ja18 natural T lymphocytes require signal processing by protein kinase C theta and NF-kappa B. J Immunol. 2004;172(8):4667-4671.
14. Majumdar S, Aggarwal BB. Adenosine suppresses activation of nuclear factor-kappaB selectively induced by tumor necrosis factor in different cell types. Oncogene. 2003;22(8): 1206-1218.
15. Sands WA, Martin AF, Strong EW, et al. Specific inhibition of nuclear factor-kappaB-dependent inflammatory responses by cell type-specific mechanisms upon A2A adenosine receptor gene transfer. Mol Pharmacol. 2004;66(5):1147-1159.
16. Polanowska-Grabowska R, Wallace K, Field JJ, et al. P-selectin-mediated platelet-neutrophil aggregate formation activates neutrophils in mouse and human sickle cell disease. Arterioscler Thromb Vasc Biol. 2010;30(12):2392-2399.
17. Fadlon E, Vordermeier S, Pearson TC, et al. Blood polymorphonuclear leukocytes from the majority of sickle cell patients in the crisis phase of the disease show enhanced adhesion to vascular endothelium and increased expression of CD64. Blood. 1998;91(1):266-274.
18. Belcher JD, Marker PH, Weber JP, et al. Activated monocytes in sickle cell disease: potential role in the activation of vascular endothelium and vasoocclusion. Blood. 2000;96(7):2451-2459.
19. Wun T, Cordoba M, Rangaswami A, et al. Activated monocytes and platelet-monocyte aggregates in patients with sickle cell disease. Clin Lab Haematol. 2002;24(2):81-88.
20. Duits AJ, Schnog JB, Lard LR, et al. Elevated IL-8 levels during sickle cell crisis. Eur J Haematol. 1998;61(5):302-305.
21. Pathare A, Al Kindi S, Alnaqdy AA, et al. Cytokine profile of sickle cell disease in Oman. Am J Hematol. 2004;77(4):323-328.
22. Frenette PS. Sickle cell vaso-occlusion: multistep and multicellular paradigm. Curr Opin Hematol. 2002;9(2):101-106.
23. Frenette PS. Sickle cell vasoocclusion: heterotypic, multicellular aggregations driven by leukocyte adhesion. Microcirculation. 2004; 11(2):167-177.
24. Zhang Y, Dai Y, Wen J, et al. Detrimental effects of adenosine signaling in sickle cell disease. Nat Med. 2011;17(1):79-86.
25. Wen J, Jiang X, Dai Y, et al. Adenosine deaminase enzyme therapy prevents and reverses the heightened cavernosal relaxation in priapism. J Sex Med. 2010;7(9):3011-3022.
26. Wen J, Jiang X, Dai Y, et al. Increased adenosine contributes to penile fibrosis, a dangerous feature of priapism, via A2B adenosine receptor signaling. FASEB J. 2010;24(3):740-749.