The potential of GM-CSF to improve resistance against infections in organ transplantation

Jian Xu, Rudolf Lucas, Albrecht Wendel

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

Immunosuppressed patients retain transplants but become more susceptible to opportunistic infections, which is a major complication in organ transplantation. Life-long immunosuppression for such patients could be reduced by creating immune tolerance, although this might be associated with an increased risk for infections and malignancies. An alternative therapeutic concept could consist of boosting the innate immune response against infections while continuing to suppress the adaptive immune response to prevent graft rejection. We propose granulocyte-macrophage colony-stimulating factor (GM-CSF) as a novel candidate to achieve this goal, based on recent studies in which beneficial effects were demonstrated in immunosuppressed mice with skin allografts and in dexamethasone-suppressed blood from healthy volunteers and blood from liver transplant recipients undergoing immunosuppressive therapy. Such data suggest that GM-CSF or other endogenous factors with similar properties should be examined in clinical trials.

Original languageEnglish (US)
Pages (from-to)254-258
Number of pages5
JournalTrends in Pharmacological Sciences
Volume25
Issue number5
DOIs
StatePublished - Jan 1 2004
Externally publishedYes

Fingerprint

Transplantation (surgical)
Transplants
Organ Transplantation
Granulocyte-Macrophage Colony-Stimulating Factor
Blood
Immune Tolerance
Opportunistic Infections
Graft Rejection
Adaptive Immunity
Immunosuppressive Agents
Infection
Innate Immunity
Grafts
Liver
Immunosuppression
Dexamethasone
Allografts
Skin
Healthy Volunteers
Clinical Trials

ASJC Scopus subject areas

  • Toxicology
  • Pharmacology

Cite this

The potential of GM-CSF to improve resistance against infections in organ transplantation. / Xu, Jian; Lucas, Rudolf; Wendel, Albrecht.

In: Trends in Pharmacological Sciences, Vol. 25, No. 5, 01.01.2004, p. 254-258.

Research output: Contribution to journalArticle

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