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On the basis of a multidimensional and concomitant profiling of circulating T follicular helper (T\n                      <jats:sub>FH<\/jats:sub>\n                      ) cells and B cells, the authors identified highly coordinated responses of circulating T\n                      <jats:sub>FH<\/jats:sub>\n                      cells and activated B cells at phenotypic, functional, and transcriptional levels in patients with antibody-mediated rejection. The levels of circulating T\n                      <jats:sub>FH<\/jats:sub>\n                      cell and B cell activation were predictive of DSA pathogenicity, histologic severity, and allograft loss. This study provides novel mechanistic insights into the cellular and molecular processes underlying antibody-mediated rejection and a rationale for monitoring and therapeutic targeting of circulating T\n                      <jats:sub>FH<\/jats:sub>\n                      cell\u2013B cell interaction during antibody-mediated rejection.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Although antibody-mediated rejection (ABMR) has been long recognized as a leading cause of allograft failure after kidney transplantation, the cellular and molecular processes underlying the induction of deleterious donor-specific antibody (DSA) responses remain poorly understood.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Using high-dimensional flow cytometry,\n                      <jats:italic toggle=\"yes\">in vitro<\/jats:italic>\n                      assays, and RNA sequencing, we concomitantly investigated the role of T follicular helper (T\n                      <jats:sub>FH<\/jats:sub>\n                      ) cells and B cells during ABMR in 105 kidney transplant recipients.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      There were 54 patients without DSAs; of those with DSAs, ABMR emerged in 20 patients, but not in 31 patients. We identified proliferating populations of circulating T\n                      <jats:sub>FH<\/jats:sub>\n                      cells and activated B cells emerging in blood of patients undergoing ABMR. Although these circulating T\n                      <jats:sub>FH<\/jats:sub>\n                      cells comprised heterogeneous phenotypes, they were dominated by activated (ICOS\n                      <jats:sup>+<\/jats:sup>\n                      PD-1\n                      <jats:sup>+<\/jats:sup>\n                      ) and early memory precursor (CCR7\n                      <jats:sup>+<\/jats:sup>\n                      CD127\n                      <jats:sup>+<\/jats:sup>\n                      ) subsets, and were enriched for the transcription factors IRF4 and c-Maf. These circulating T\n                      <jats:sub>FH<\/jats:sub>\n                      cells produced large amounts of IL-21 upon stimulation with donor antigen and induced B cells to differentiate into antibody-secreting cells that produced DSAs. Combined analysis of the matched circulating T\n                      <jats:sub>FH<\/jats:sub>\n                      cell and activated B cell RNA-sequencing profiles identified highly coordinated transcriptional programs in circulating T\n                      <jats:sub>FH<\/jats:sub>\n                      cells and B cells among patients with ABMR, which markedly differed from those of patients who did not develop DSAs or ABMR. The timing of expansion of the distinctive circulating T\n                      <jats:sub>FH<\/jats:sub>\n                      cells and activated B cells paralleled emergence of DSAs in blood, and their magnitude was predictive of IgG3 DSA generation, more severe allograft injury, and higher rate of allograft loss.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      Patients undergoing ABMR may benefit from monitoring and therapeutic targeting of T\n                      <jats:sub>FH<\/jats:sub>\n                      cell\u2013B cell interactions.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1681\/asn.2020030320","type":"journal-article","created":{"date-parts":[[2020,7,28]],"date-time":"2020-07-28T19:05:50Z","timestamp":1595963150000},"page":"2457-2474","source":"Crossref","is-referenced-by-count":51,"title":["Coordinated Circulating T Follicular Helper and Activated B Cell Responses Underlie the Onset of Antibody-Mediated Rejection in Kidney Transplantation"],"prefix":"10.1681","volume":"31","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1766-2548","authenticated-orcid":false,"given":"Kevin","family":"Louis","sequence":"first","affiliation":[{"name":"Department of Surgery, Thomas E. 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Starzl Transplantation Institute, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania"},{"name":"Human Immunology and Immunopathology, Institut National de la Sant\u00e9 et de la Recherche M\u00e9dicale, Unit\u00e9 Mixte de Recherche 976, Universit\u00e9 de Paris, Paris, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Louis","family":"Lau","sequence":"additional","affiliation":[{"name":"Center for Systems Immunology, Department of Immunology, University of Pittsburgh, Pittsburgh, Pennsylvania"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0402-526X","authenticated-orcid":false,"given":"Bala","family":"Ramaswami","sequence":"additional","affiliation":[{"name":"Department of Surgery, Thomas E. 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