Graft-versus-host disease pathophysiology: Difference between revisions

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==Pathophysiology==
==Pathophysiology==
 
The pathophysiology involves donor alloreactive T lymphocytes mount an immune attack against recipient tissue.<ref name="pmid23593203">{{cite journal| author=Al-Chaqmaqchi H, Sadeghi B, Abedi-Valugerdi M, Al-Hashmi S, Fares M, Kuiper R et al.| title=The role of programmed cell death ligand-1 (PD-L1/CD274) in the development of graft versus host disease. | journal=PLoS One | year= 2013 | volume= 8 | issue= 4 | pages= e60367 | pmid=23593203 | doi=10.1371/journal.pone.0060367 | pmc=3617218 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23593203  }} </ref> The most common tissues affected are the skin, liver, and gastrointestinal tract.<ref name="pmid23593203">{{cite journal| author=Al-Chaqmaqchi H, Sadeghi B, Abedi-Valugerdi M, Al-Hashmi S, Fares M, Kuiper R et al.| title=The role of programmed cell death ligand-1 (PD-L1/CD274) in the development of graft versus host disease. | journal=PLoS One | year= 2013 | volume= 8 | issue= 4 | pages= e60367 | pmid=23593203 | doi=10.1371/journal.pone.0060367 | pmc=3617218 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23593203  }} </ref> Tissues of cardiac, skeletal muscle, or neurologic origin are typically not affected.<ref name="pmid23593203">{{cite journal| author=Al-Chaqmaqchi H, Sadeghi B, Abedi-Valugerdi M, Al-Hashmi S, Fares M, Kuiper R et al.| title=The role of programmed cell death ligand-1 (PD-L1/CD274) in the development of graft versus host disease. | journal=PLoS One | year= 2013 | volume= 8 | issue= 4 | pages= e60367 | pmid=23593203 | doi=10.1371/journal.pone.0060367 | pmc=3617218 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23593203  }} </ref> The process begin with Th1-type cells and their cytokines TNF-alpha, IL-2, and interferon-gamma. A Th2-type profile can suppress GvHD.<ref name="pmid23593203">{{cite journal| author=Al-Chaqmaqchi H, Sadeghi B, Abedi-Valugerdi M, Al-Hashmi S, Fares M, Kuiper R et al.| title=The role of programmed cell death ligand-1 (PD-L1/CD274) in the development of graft versus host disease. | journal=PLoS One | year= 2013 | volume= 8 | issue= 4 | pages= e60367 | pmid=23593203 | doi=10.1371/journal.pone.0060367 | pmc=3617218 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23593203  }} </ref> The programmed death-1 (PD-1) pathway is an immune checkpoint pathway that functions to suppress alloreactive T cells.


==References==
==References==

Revision as of 16:46, 12 June 2017

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Shyam Patel [2]

Overview

The pathophysiology of GvHD is based upon immune activation and inflammation due a T cell responses, ultimately resulting in organ damage.[1]

Pathophysiology

The pathophysiology involves donor alloreactive T lymphocytes mount an immune attack against recipient tissue.[1] The most common tissues affected are the skin, liver, and gastrointestinal tract.[1] Tissues of cardiac, skeletal muscle, or neurologic origin are typically not affected.[1] The process begin with Th1-type cells and their cytokines TNF-alpha, IL-2, and interferon-gamma. A Th2-type profile can suppress GvHD.[1] The programmed death-1 (PD-1) pathway is an immune checkpoint pathway that functions to suppress alloreactive T cells.

References

  1. 1.0 1.1 1.2 1.3 1.4 Al-Chaqmaqchi H, Sadeghi B, Abedi-Valugerdi M, Al-Hashmi S, Fares M, Kuiper R; et al. (2013). "The role of programmed cell death ligand-1 (PD-L1/CD274) in the development of graft versus host disease". PLoS One. 8 (4): e60367. doi:10.1371/journal.pone.0060367. PMC 3617218. PMID 23593203.

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