Supplementary Materials

Supplementary Material for:

Zbtb7a induction in alveolar macrophages is implicated in anti-HLA–mediated lung allograft rejection

Deepak K. Nayak,* Fangyu Zhou, Min Xu, Jing Huang, Moriya Tsuji, Jinsheng Yu, Ramsey Hachem, Andrew E. Gelman, Ross M. Bremner, Michael A. Smith, Thalachallour Mohanakumar*

*Corresponding author. Email: tm.kumar{at} (T.M.); deepak.nayak{at} (D.K.N.)

Published 12 July 2017, Sci. Transl. Med. 9, eaal1243 (2017)
DOI: 10.1126/scitranslmed.aal1243

This PDF file includes:

  • Materials and Methods
  • Fig. S1. Ab ligation of MHC class I increases lung-infiltrating B cells and neutrophils.
  • Fig. S2. Zbtb7a knockdown in lungs reduces anti-MHC–induced pulmonary inflammation.
  • Fig. S3. Zbtb7a knockdown reduces development of anti-MHC–induced iBALT in lungs.
  • Fig. S4. Zbtb7a deficiency does not diminish endocytosis by AMs.
  • Fig. S5. Zbtb7a deficiency in AM alters molecular responses to anti-MHC ligation.
  • Fig. S6. Exogenous alloAb induces Zbtb7a expression in the accepted lung allograft after mouse orthotopic lung transplantation.
  • Fig. S7. Lymphocytes are dispensable in anti-MHC–induced Zbtb7a expression but are required for OAD development.
  • Table S1. Differential gene expression in lungs after Ab ligation of MHC class I.
  • Table S2. Clinical characteristics of the lung transplant recipients.
  • Table S3. ZBTB7A expression in lung transplant recipients.
  • Table S4. Summary of Zbtb7a expression in response to exogenous Abs after mouse orthotopic lung transplantation.
  • Table S5. Summary of the allogeneic AM transfer protocol.
  • Table S6. Summary of the AM-derived alloexosome production.
  • References (71, 72)

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Other Supplementary Material for this manuscript includes the following:

  • Table S7 (Microsoft Excel format). Primary data.