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Printable Handouts
Navigable Slide Index
- Introduction
- Financial disclosures
- Acute graft-versus-host disease: Clinical presentation
- Response to steroids in patients with aGVHD
- Does GVHD impact survival?
- What could my group contribute to the understanding of aGVHD pathogenesis?
- Intestinal inflammation during aGVHD
- EBMT/ELN treatment guidelines for aGVHD
- Treatment of aGVHD: Grade I vs. grade II
- Treatment of aGVHD: High- vs. low-dose of methylprednisolone
- Treatment of aGVHD: Lower-dose steroids for grade II skin/upper GI disease
- Treatment of aGVHD
- Second line treatment of aGVHD
- ECP in aGVHD: Efficacy (Retrospective analyses)
- ECP in aGVHD: Efficacy (Retrospective and prospective analyses)
- Ruxolitinib + ECP for steroid-refractory aGVHD after allo-SCT: Safety
- Kinase targets in GVHD
- Can we reduce GVHD by JAK1/2 targeting?
- Prospective evaluation of ruxolitinib in aGVHD
- Safety and efficacy of ruxolitinib vs. BAT in patients with SR aGVHD
- Safety and efficacy of ruxolitinib vs. BAT in patients with SR aGVHD: REACH2 results
- REACH 2: 6-Mo follow-up duration of response and event-free survival
- Third line treatment of aGVHD
- Conclusions (Treatment of aGVHD)
- Colitis and other immune-related adverse events (irAEs) after immune checkpoint blockade
- ECP is an effective therapy for inflammatory diseases
- Long-term in vivo steroid application diminishes all types of immune cells
- ECP does not impair anti-tumor immunity
- ECP treated splenocytes are phagocytosed by macrophages
- ECP treated splenocytes are phagocytosed in highly inflamed tissues
- M2-like macrophages are enriched in inflamed tissues upon ECP treatment
- Arginase-1 is central in ECP-induced immunomodulation
- Conclusions
Topics Covered
- Acute graft-versus-host disease (aGVHD): Clinical presentation
- Intestinal inflammation during aGVHD
- Treatment of aGVHD
- Kinase targets in GVHD
- REACH2 trial
- Colitis and other irAEs after immune checkpoint blockade
- ECP is an effective therapy for inflammatory diseases
- Arginase-1 is central in ECP-induced immunomodulation
Links
Series:
Categories:
Therapeutic Areas:
External Links
Talk Citation
Zeiser, R. (2026, October 29). Targeting the intestinal barrier in GVHD and checkpoint colitis [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved November 2, 2026, from https://doi.org/10.69645/NSDD5840.Export Citation (RIS)
Publication History
- Published on October 29, 2026
Financial Disclosures
- Prof. Robert Zeiser has disclosed that he has received consulting fees from Incyte, Mallinckrodt, and Novartis.
A selection of talks on Metabolism & Nutrition
Transcript
Please wait while the transcript is being prepared...
0:00
Hello. My name is Robert Zeiser.
I'm the Director of
the Division of
Tumor immunology and
Stem Cell Transplantation at
Freiburg University
Medical Center.
Today I will talk about
Therapeutic Targeting of
the Intestinal Barrier in
GVHD and Immune
Checkpoint-induced Colitis.
0:23
These are my disclosures.
0:26
Acute graft-versus-host
disease has
a clinical presentation that
the skin can be affected,
the intestinal tract,
and the liver.
When you look at
these images here,
you can see that
this patient has
a rash indicative of tissue
inflammation in the skin.
Then, the next images
show you here,
endoscopic view into
the intestinal tract
of patients with
early intestinal GVHD or
more advanced acute
intestinal GVHD.
When you biopsy these organs,
you would find in the
skin apoptotic cells
in the basal membrane
of the skin.
In the liver biopsy
you would find
infiltration of the small
bile ducts with lymphocytes,
and in the colon biopsies you
would find apoptotic cells.
1:12
What is the response
to steroids in
patients with acute GVHDs?
Steroids are
effective in only 40%
of patients with acute GVHD and
only 30% of the patients
with acute GVHD
have a long lasting response
to corticosteroids.
1:30
Does GVHD impact survival?
Here you see the mortality
of patients with
intestinal steroid-refractory
acute GVHD,
and as you can see, mortality
is above 50% at three years.
In order to better
treat this disease,