The role of donor-derived exosomes in lung allograft rejection

Ranjithkumar Ravichandran, Sandhya Bansal, Mohammad Rahman, Monal Sharma, Wei Liu, Ankit Bharat, Ramsey Hachem, Ashraf Omar, Michael A. Smith, T. Mohanakumar

Research output: Contribution to journalReview articlepeer-review

9 Scopus citations


Lung transplant recipients (LTxRs) with acute or chronic rejection release circulating exosomes that mostly originate from donor lung tissue and express mismatched human leucocyte antigens (HLA) and lung-associated self-antigens (SAgs), Collagen-V and K alpha 1 Tubulin. During lung transplant (LTx), donor lungs often undergo injuries that increase the antigenicity of the transplanted organ. 30% of LTxRs also have pre-transplant antibodies (Abs) to HLA and lung SAgs, which may induce conditions that increase the risk of chronic lung allograft dysfunction (CLAD). Post-transplant, some recipients experience de novo development of Abs to mismatched donor HLA (donor-specific antibody [DSA]) and Abs to lung SAgs, which have been implicated in CLAD pathogenesis. Because most LTxRs who develop DSA also develop Abs to SAgs, some have suggested a synergistic relationship between alloimmunity and autoimmunity in CLAD immunopathogenesis. These processes likely occur from stress-induced exosome release. Exosomes carry allo-antigens, lung SAgs, several micro RNAs, proteasome, co-stimulatory molecules, and pro-inflammatory transcription factors—resulting in efficient antigen presentation by direct, semidirect, and indirect pathways, leading to immune responses to both allo-antigens and lung-associated SAgs. This review summarizes recent findings on the role of exosomes, and processes triggering immune responses to allo-antigens and lung SAgs that ultimately culminate in CLAD.

Original languageEnglish
Pages (from-to)588-594
Number of pages7
JournalHuman Immunology
Issue number8
StatePublished - Aug 2019


  • Autoimmune
  • CLAD
  • Exosomes
  • Self-antigens
  • Transplantation


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