Emerging role of the mannose-binding lectin-dependent pathway of complement activation in clinical organ transplantation

Stefan P Berger, Mohamed R Daha

Research output: Contribution to journalReview article

15 Citations (Scopus)


PURPOSE OF REVIEW: Over the past decade, the role of the complement system in solid organ transplantation has received increased attention. A number of experimental and epidemiological studies have suggested that the lectin pathway plays a role in infectious complications, rejection and long-term outcome after transplantation. This review discusses recent data on the role of the lectin pathway in solid organ transplantation.

RECENT FINDINGS: Studies on the role of mannose-binding lectin (MBL) in organ transplantation have shown an association of MBL-deficient states with an increased risk of infection after liver and simultaneous pancreas-kidney transplantation. On the contrary, a high MBL status in the recipient has been associated with poorer organ survival and increased rejection associated damage in various transplant settings. Experimental data points towards a role for MBL in ischemia-reperfusion damage in various organs. Several lines of evidence suggest that MBL may contribute to immunoglobulin-mediated complement activation in both ischemia-reperfusion and rejection. The interaction of MBL with IgM may be of particular importance in this setting.

SUMMARY: We review recent epidemiological data on the role of MBL in solid organ transplantation. We relate these findings to the emerging experimental data and attempt to explain some of the conflicting results on beneficial and harmful effects of the lectin pathway.

Original languageEnglish
Pages (from-to)28-33
Number of pages6
JournalCurrent opinion in organ transplantation
Issue number1
Publication statusPublished - Feb-2011
Externally publishedYes


  • Animals
  • Complement Activation
  • Humans
  • Mannose-Binding Lectin
  • Mannose-Binding Lectins
  • Organ Transplantation
  • Transplantation Immunology
  • Journal Article
  • Review

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