An Overview to cGVHD: Disease Pathophysiology and Manifestations

Opinion
Video

Panelists discuss how chronic graft-vs-host disease (cGVHD) results from complex biological mechanisms involving inflammation, loss of peripheral tolerance, and fibrotic pathways affecting multiple organ systems.

Overview and Pathophysiology of cGVHD

The panel featured Dr Catherine Lee (Fred Hutch Cancer Center), Dr Michael Bishop (University of Chicago), and Dr Paul Shaughnessy (Sarah Cannon Transplant cellular therapy program). Dr Lee opened with the pathophysiology of cGVHD, describing it as resulting from three biologic phases:

  1. Early inflammation from pre-transplant conditioning that causes tissue damage and activates host antigen-presenting cells (APCs)
  2. Activated APCs secrete pro-inflammatory cytokines and increase MHC and co-stimulatory molecules, initiating alloreactive T-cell responses
  3. In cGVHD specifically, loss of peripheral tolerance occurs due to thymic injury and emergence of alloreactive B and T cells, leading to chronic inflammation

The NIH consensus criteria define diagnostic features and severity scoring in 8 classical organ systems (skin, mouth, eyes, lung, musculoskeletal, GI tract, genitourinary tract, liver). However, there are also "suspected" or "atypical" cGVHD manifestations outside these classical systems, including hematopoietic system, endothelium, central/peripheral nervous systems, kidneys, and serous membranes.

Newsletter

Stay up to date on practice-changing data in community practice.

Recent Videos
3 experts are featured in this series.
1 expert in this video
1 expert in this video
3 experts are featured in this series.
1 expert is featured in this series.
1 expert in this video
1 expert in this video
3 experts are featured in this series.
3 experts are featured in this series.
1 expert in this video
OSZAR »