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T and B cells participate in bone repair by infiltrating the fracture callus in a two-wave fashion.

Authors
  • Könnecke, Ireen1
  • Serra, Alessandro2
  • El Khassawna, Thaqif3
  • Schlundt, Claudia4
  • Schell, Hanna5
  • Hauser, Anja6
  • Ellinghaus, Agnes7
  • Volk, Hans-Dieter8
  • Radbruch, Andreas9
  • Duda, Georg N10
  • Schmidt-Bleek, Katharina11
  • 1 Julius Wolff Institut and Center for Musculoskeletal Surgery, Charité - Universitätsmedizin Berlin, Augustenburger Platz 1, 13353 Berlin, Germany; Berlin - Brandenburg Center for Regenerative Therapies, Charité - Universitätsmedizin Berlin, Augustenburger Platz 1, 13353 Berlin, Germany. Electronic address: [email protected] , (Germany)
  • 2 German Arthritis Research Center (DRFZ), Charitéplatz 1, 10117 Berlin, Germany. Electronic address: [email protected] , (Germany)
  • 3 Laboratory of Experimental Trauma Surgery, Justus-Liebig University, Kerkraderstr. 9, 35394 Giessen, Germany. Electronic address: [email protected] , (Germany)
  • 4 Julius Wolff Institut and Center for Musculoskeletal Surgery, Charité - Universitätsmedizin Berlin, Augustenburger Platz 1, 13353 Berlin, Germany; Berlin - Brandenburg Center for Regenerative Therapies, Charité - Universitätsmedizin Berlin, Augustenburger Platz 1, 13353 Berlin, Germany. Electronic address: [email protected] , (Germany)
  • 5 Julius Wolff Institut and Center for Musculoskeletal Surgery, Charité - Universitätsmedizin Berlin, Augustenburger Platz 1, 13353 Berlin, Germany; Berlin - Brandenburg Center for Regenerative Therapies, Charité - Universitätsmedizin Berlin, Augustenburger Platz 1, 13353 Berlin, Germany. Electronic address: [email protected] , (Germany)
  • 6 German Arthritis Research Center (DRFZ), Charitéplatz 1, 10117 Berlin, Germany. Electronic address: [email protected] , (Germany)
  • 7 Julius Wolff Institut and Center for Musculoskeletal Surgery, Charité - Universitätsmedizin Berlin, Augustenburger Platz 1, 13353 Berlin, Germany. Electronic address: [email protected] , (Germany)
  • 8 Berlin - Brandenburg Center for Regenerative Therapies, Charité - Universitätsmedizin Berlin, Augustenburger Platz 1, 13353 Berlin, Germany; Institute of Medical Immunology, Charité - Universitätsmedizin Berlin, Augustenburger Platz 1, 13353 Berlin, Germany. Electronic address: [email protected] , (Germany)
  • 9 Berlin - Brandenburg Center for Regenerative Therapies, Charité - Universitätsmedizin Berlin, Augustenburger Platz 1, 13353 Berlin, Germany; German Arthritis Research Center (DRFZ), Charitéplatz 1, 10117 Berlin, Germany. Electronic address: [email protected] , (Germany)
  • 10 Julius Wolff Institut and Center for Musculoskeletal Surgery, Charité - Universitätsmedizin Berlin, Augustenburger Platz 1, 13353 Berlin, Germany; Berlin - Brandenburg Center for Regenerative Therapies, Charité - Universitätsmedizin Berlin, Augustenburger Platz 1, 13353 Berlin, Germany. Electronic address: [email protected] , (Germany)
  • 11 Julius Wolff Institut and Center for Musculoskeletal Surgery, Charité - Universitätsmedizin Berlin, Augustenburger Platz 1, 13353 Berlin, Germany; Berlin - Brandenburg Center for Regenerative Therapies, Charité - Universitätsmedizin Berlin, Augustenburger Platz 1, 13353 Berlin, Germany. Electronic address: [email protected] , (Germany)
Type
Published Article
Journal
Bone
Publication Date
Jul 01, 2014
Volume
64
Pages
155–165
Identifiers
DOI: 10.1016/j.bone.2014.03.052
PMID: 24721700
Source
Medline
Keywords
License
Unknown

Abstract

Fracture healing is a regenerative process in which bone is restored without scar tissue formation. The healing cascade initiates with a cycle of inflammation, cell migration, proliferation and differentiation. Immune cells invade the fracture site immediately upon bone damage and contribute to the initial phase of the healing process by recruiting accessory cells to the injury site. However, little is known about the role of the immune system in the later stages of fracture repair, in particular, whether lymphocytes participate in soft and hard callus formation. In order to answer this question, we analyzed femoral fracture healing in mice by confocal microscopy. Surprisingly, after the initial inflammatory phase, when soft callus developed, T and B cells withdrew from the fracture site and were detectable predominantly at the femoral neck and knee. Thereafter lymphocytes massively infiltrated the callus region (around day 14 after injury), during callus mineralization. Interestingly, lymphocytes were not found within cartilaginous areas of the callus but only nearby the newly forming bone. During healing B cell numbers seemed to exceed those of T cells and B cells progressively underwent effector maturation. Both, osteoblasts and osteoclasts were found to have direct cell-cell contact with lymphocytes, strongly suggesting a regulatory role of the immune cells specifically in the later stages of fracture healing.

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