000 03477nam a22004095i 4500
001 978-1-4419-7219-4
003 DE-He213
005 20140220083722.0
007 cr nn 008mamaa
008 101109s2011 xxu| s |||| 0|eng d
020 _a9781441972194
_9978-1-4419-7219-4
024 7 _a10.1007/978-1-4419-7219-4
_2doi
050 4 _aRC261-271
072 7 _aMJCL
_2bicssc
072 7 _aMED062000
_2bisacsh
082 0 4 _a614.5999
_223
100 1 _aMarincola, Francesco M.
_eeditor.
245 1 0 _aImmunologic Signatures of Rejection
_h[electronic resource] /
_cedited by Francesco M. Marincola, Ena Wang.
264 1 _aNew York, NY :
_bSpringer New York :
_bImprint: Springer,
_c2011.
300 _aVII, 300p. 21 illus., 19 illus. in color.
_bonline resource.
336 _atext
_btxt
_2rdacontent
337 _acomputer
_bc
_2rdamedia
338 _aonline resource
_bcr
_2rdacarrier
347 _atext file
_bPDF
_2rda
520 _aThis book collects salient observational data, derived predominantly from human studies, regarding the mechanism(s) of rejection in various pathologic conditions; the premise is that immune rejection, better defined as “immune-mediated, tissue-specific destruction” (TSD), comprises a broad range of phenomena ranging from tumor regression, to clearance of pathogen through destruction of infected cells, autoimmunity, allograft rejection by the host and host versus graft reactions. Like different hands can turn on or off a switch, distinct mechanisms can trigger TSD; however, a convergent pathway is ultimately observed when TSD occurs consisting of a dramatic switch from chronic to acute inflammation leading to the activation of a restricted number of genes that we comprise in the immunologic constant of rejection (ICR) model. Although the ICR model does not address “why” rejection occurs but rather “how”, and it may not contribute an explanation for the determinism of rejection, it provides, if correct, a simplified road map about the convergent pathways leading to TSD. This offers the opportunity to identify a common target for immune manipulation with therapeutic purposes since ICR-related pathways are restricted in expression to the tissues in which TSD occurs while are shut off in the rest of a normal organism. The book includes chapters from outstanding basic and/or observational scientists that have contributed to this area either by defining mechanisms relevant to the understanding of the inflammatory switch or by describing how this occurs in human tissues under different pathological conditions. We would like to entice our reader(s) to test with us, through, the readings, whether our hypothesis is correct; we predict that common themes will emerge particularly if attention will be paid to the general phenomenon of TSD rather than the peculiarities of individual pathologies. With the hope of having contributed with this book something novel and important and we wish our reader a pleasant journey in the wondrous land of immune-mediated, tissue-specific destruction.
650 0 _aMedicine.
650 0 _aOncology.
650 1 4 _aBiomedicine.
650 2 4 _aCancer Research.
700 1 _aWang, Ena.
_eeditor.
710 2 _aSpringerLink (Online service)
773 0 _tSpringer eBooks
776 0 8 _iPrinted edition:
_z9781441972187
856 4 0 _uhttp://dx.doi.org/10.1007/978-1-4419-7219-4
912 _aZDB-2-SBL
999 _c105712
_d105712