The role of autoimmunity in the pathogenesis of lung allograft rejection

David S. Wilkes

Research output: Contribution to journalArticle

14 Citations (Scopus)

Abstract

For many patients, lung transplantation is the only definitive treatment modality for different forms of end-stage lung disease. However, the lung is rejected more often than any other type of solid organ allografts, and the 5-year survival rate is less than that of other transplanted organs. While alloimmunity directed against donor transplantation antigens is believed to be the key mechanism that mediates rejection responses, newer immunosuppressive regimens designed to abrogate alloimmune activation have not improved survival. Accordingly, these data suggest that other antigens are involved in rejection. Autoimmune responses, reported to occur during allograft rejection, could participate in graft destruction. This review article discusses the role of autoimmune responses to type V collagen, a minor collagen in the lung, in the pathogenesis of lung allograft rejection. By recognizing that lung transplant rejection involves both alloimmune and autoimmune responses, scientific investigation may uncover novel targets for therapeutic intervention that could prolong the life of the lung transplant recipient.

Original languageEnglish
Pages (from-to)227-230
Number of pages4
JournalArchivum Immunologiae et Therapiae Experimentalis
Volume51
Issue number4
StatePublished - 2003

Fingerprint

Autoimmunity
Allografts
Lung
Collagen Type V
Histocompatibility Antigens
Lung Transplantation
Graft Rejection
Immunosuppressive Agents
Lung Diseases
Collagen
Survival Rate
Transplants
Antigens
Survival
Therapeutics

Keywords

  • Alloimmune response
  • Autoimmune response
  • Lung transplantation
  • Transplant rejection

ASJC Scopus subject areas

  • Immunology

Cite this

The role of autoimmunity in the pathogenesis of lung allograft rejection. / Wilkes, David S.

In: Archivum Immunologiae et Therapiae Experimentalis, Vol. 51, No. 4, 2003, p. 227-230.

Research output: Contribution to journalArticle

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