Curriculum Vitae et Studiorum Ennio Carbone 2009
Curriculum Vitae et Studiorum Ennio Carbone 2009
Curriculum Vitae et Studiorum Ennio Carbone 2009
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class I homologue UL18 affect its binding to the inhibitory receptor LIR-<br />
1/ILT2/CD85j. Eur J Immunol. 2006 Mar;36(3):732-41.<br />
This study represent the evolution of the research reported in paper 5) providing<br />
molecular basis for the differences observed b<strong>et</strong>ween CMV clinical and laboratory<br />
strains in protecting infected cells to NK recognition. Here we show the UL-18 viral<br />
protein cloned from CMV clinical isolates have a higher affinity for the NK inhibitory<br />
receptor LIR-1 than the laboratory counterpart. The structural differences were<br />
resolved structurally and surprisingly we found that UL18 alpha1 domain contribute<br />
to the higher binding efficiency of the clinical isolates molecules. This data add new<br />
insight in the association kin<strong>et</strong>ics of the viral molecule with he inhibitory<br />
immunoreceptor.<br />
2) <strong>Carbone</strong> E, Neri P, Mesuraca M, <strong>et</strong> al.<br />
HLA class I, NKG2D, and natural cytotoxicity receptors regulate multiple<br />
myeloma cell recognition by natural killer cells<br />
Blood 105 (1): 251-258. 2005<br />
This paper describe for the first time that autologous NK cells recognize and eliminate<br />
multiple myeloma early stages cell targ<strong>et</strong>s. Moreover we demonstrate that the disease<br />
progression leads to tumor variant selection expressing high levels of MHC class-I<br />
levels and weak or no expression of NKG2D ligands.<br />
3) Berg L, Riise GC, Cosman D, Bergstrom T, Olofsson S, Karre K, <strong>Carbone</strong> E.<br />
LIR-1 expression on lymphocytes, and cytomegalovirus disease in lungtransplant<br />
recipients. Lanc<strong>et</strong>. 2003 Mar 29;361(9363):1099-101.<br />
Here we show that one of the inhibitory NK receptor (LIR-1, CD85J) is upregulated<br />
in heart and lung transplanted patient developing CMV disease. LIR-1 was previous<br />
reported to recognize UL-18 a CMV MHC class I coded molecule. Our study was of<br />
interest for a wide reader plate since it can be exploited to develop a b<strong>et</strong>ter diagnostic<br />
tool/kit for the early d<strong>et</strong>ection of CMV infection in transplanted patients.<br />
4) <strong>Carbone</strong> E, Terrazzano G, Melian A, Zanzi D, Mor<strong>et</strong>ta L, Porcelli S, Karre K,<br />
Zappacosta S. Inhibition of human NK cell-mediated killing by CD1 molecules. J<br />
Immunol. 2000 Jun 15;164(12):6130-7.<br />
This work was analysing:1) The NK-DC interaction molecular regulation focusing on<br />
MHC-I like molecules CD1 and their role in presing Mycobacterium Tubercolosis<br />
glycolipid antigens to NK cells. Our data demonstrate that CD1 molecules family<br />
inhibit NK cell recognition of autologous DC and their presentation of lipid antigen<br />
further inhibit NK cell cytotoxicity.<br />
5) Cerboni C, Mousavi-Jazi M, Linde A, Soderstrom K, Brytting M, Wahren B, Karre<br />
K, <strong>Carbone</strong> E. Human cytomegalovirus strain-dependent changes in NK cell<br />
recognition of infected fibroblasts. J Immunol. 2000 May 1;164(9):4775-82.<br />
This is the first evidence that CMV clinical strain not the laboratories infection inhibit<br />
NK recognition of the infected cells. This paper help a lot the other investigator to
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