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Loss of B cell regulatory function is associated with delayed healing in patients with tibia fracture
Author(s) -
Yang Shufeng,
Ding Wei,
Feng Dapeng,
Gong Haiyang,
Zhu Dongmei,
Chen Bin,
Chen Jianmin
Publication year - 2015
Publication title -
apmis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.909
H-Index - 88
eISSN - 1600-0463
pISSN - 0903-4641
DOI - 10.1111/apm.12439
Subject(s) - bone healing , regulatory b cells , medicine , cytokine , downregulation and upregulation , interleukin 10 , bone fracture , immune system , b cell , immunology , biology , surgery , antibody , biochemistry , radiology , gene
The process of bone regeneration after fracture is a complex and well‐orchestrated process usually requiring 3–12 weeks. A subset of patients, however, exhibit delayed healing time and even incomplete restoration of the normal bone structure. Although the precise mechanism is unknown, studies have shown that smurf1 may play a role during the process. Here, we sought to determine the involvement of the immune system in impaired bone healing. We found that immediately after fracture, the B‐cell composition was shifted toward increased frequency of plasmablasts and decreased frequency of naïve B cells, reflecting higher inflammatory status. The percentage of CD 19 + CD 24 + CD 38 + regulatory B cells was also upregulated in response to bone fracture. The production of IL ‐10, a pivotal cytokine in regulatory B‐cell function, was upregulated in all patients. Interestingly, the increase in IL ‐10 production was only sustained throughout the healing course in normal healing patients but not in delayed healing patients. Rather, delayed healing patients downregulated B‐cell IL ‐10 secretion early and had reduced level of regulatory B‐cell activity. Together, these data revealed a role of regulatory B cells in the endogenous bone regeneration process and an alternation in B‐cell‐mediated regulation in delayed healing patients.