Graft-versus-host disease pathophysiology
Graft-versus-host disease |
Differentiating Graft-versus-host disease from other Diseases |
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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
- ↑ 1.0 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.