Abstract
The complexity underlying a pathologic process does not necessarily require a complex explanation. The biology determining allograft or cancer rejection, autoimmunity or tissue damage during pathogen infections is complex; however, common patterns are emerging that lead to a common final outcome. For instance, tissue destruction occurs with resolution of the pathogenic process (cancer, infection) or tissue damage and organ failure (autoimmunity, allograft rejection). Observations in humans based on transcriptional profiling converge into what we call an 'immunologic constant of rejection' that characterizes such occurrences. This constant includes the coordinate activation of interferon-stimulated genes (ISGs) and immune effector functions (IEFs). Understanding this final effector pathway may suggest novel strategies for the induction or inhibition of tissue-specific destruction with therapeutic intent in cancer and other immune pathologies.
| Original language | English |
|---|---|
| Pages (from-to) | 256-262 |
| Number of pages | 7 |
| Journal | Trends in Immunology |
| Volume | 29 |
| Issue number | 6 |
| DOIs | |
| Publication status | Published - Jun 2008 |
| Externally published | Yes |
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ASJC Scopus subject areas
- Immunology and Allergy
- Immunology
Cite this
The immunologic constant of rejection. / Wang, Ena; Worschech, Andrea; Marincola, Francesco M.
In: Trends in Immunology, Vol. 29, No. 6, 06.2008, p. 256-262.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - The immunologic constant of rejection
AU - Wang, Ena
AU - Worschech, Andrea
AU - Marincola, Francesco M.
PY - 2008/6
Y1 - 2008/6
N2 - The complexity underlying a pathologic process does not necessarily require a complex explanation. The biology determining allograft or cancer rejection, autoimmunity or tissue damage during pathogen infections is complex; however, common patterns are emerging that lead to a common final outcome. For instance, tissue destruction occurs with resolution of the pathogenic process (cancer, infection) or tissue damage and organ failure (autoimmunity, allograft rejection). Observations in humans based on transcriptional profiling converge into what we call an 'immunologic constant of rejection' that characterizes such occurrences. This constant includes the coordinate activation of interferon-stimulated genes (ISGs) and immune effector functions (IEFs). Understanding this final effector pathway may suggest novel strategies for the induction or inhibition of tissue-specific destruction with therapeutic intent in cancer and other immune pathologies.
AB - The complexity underlying a pathologic process does not necessarily require a complex explanation. The biology determining allograft or cancer rejection, autoimmunity or tissue damage during pathogen infections is complex; however, common patterns are emerging that lead to a common final outcome. For instance, tissue destruction occurs with resolution of the pathogenic process (cancer, infection) or tissue damage and organ failure (autoimmunity, allograft rejection). Observations in humans based on transcriptional profiling converge into what we call an 'immunologic constant of rejection' that characterizes such occurrences. This constant includes the coordinate activation of interferon-stimulated genes (ISGs) and immune effector functions (IEFs). Understanding this final effector pathway may suggest novel strategies for the induction or inhibition of tissue-specific destruction with therapeutic intent in cancer and other immune pathologies.
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UR - http://www.scopus.com/inward/citedby.url?scp=44549086338&partnerID=8YFLogxK
U2 - 10.1016/j.it.2008.03.002
DO - 10.1016/j.it.2008.03.002
M3 - Article
C2 - 18457994
AN - SCOPUS:44549086338
VL - 29
SP - 256
EP - 262
JO - Trends in Immunology
JF - Trends in Immunology
SN - 1471-4906
IS - 6
ER -