Robby Engelmann1, Ni Wang2, Christian Kneitz3, Brigitte Müller-Hilke3. 1. Institute of Immunology, Rostock University Medical Center, Rostock, Germany, Institute of Blood Research, Dalian Blood Center, Liaoning Province, China and Klinik für Innere Medizin II, Klinikum Südstadt Rostock, Rostock, Germany. robby.engelmann@med.uni-rostock.de. 2. Institute of Immunology, Rostock University Medical Center, Rostock, Germany, Institute of Blood Research, Dalian Blood Center, Liaoning Province, China and Klinik für Innere Medizin II, Klinikum Südstadt Rostock, Rostock, Germany. Institute of Immunology, Rostock University Medical Center, Rostock, Germany, Institute of Blood Research, Dalian Blood Center, Liaoning Province, China and Klinik für Innere Medizin II, Klinikum Südstadt Rostock, Rostock, Germany. 3. Institute of Immunology, Rostock University Medical Center, Rostock, Germany, Institute of Blood Research, Dalian Blood Center, Liaoning Province, China and Klinik für Innere Medizin II, Klinikum Südstadt Rostock, Rostock, Germany.
Abstract
OBJECTIVE: The prevention of bone resorption and subsequent joint destruction is one of the main challenges in the treatment of patients suffering from RA. Various mechanisms have previously been described that contribute to bone resorption in tightly defined cohorts. Here we analysed a cross-sectional cohort of RA patients and searched for humoral and cellular markers in the peripheral blood associated with bone resorption. METHODS: We enrolled 61 consecutive RA patients positive for ACPA. Blood was analysed by flow cytometry to determine the percentages of regulatory T cells and B cell subpopulations. Cytokine (TNF-α, IL-6, IL-10) and ACPA levels as well as the bone resorption marker CTX-1 were determined from the patients' sera. Standard clinical disease parameters were included. RESULTS: Multivariate analyses showed that the percentages of CD5(+) B cells were positively correlated with CTX-1 serum levels. However, neither low-avidity ACPA nor serum IL-6 levels, both known to be produced by CD5(+) cells, were associated with CTX-1 in patients' sera. There was no correlation between CTX-1 levels and clinical parameters or ACPA levels. CONCLUSION: In summary, we found that the CD5(+) B cell population is associated with bone resorption as measured via serum CTX-1 levels in a cross-sectional cohort of RA patients. However, a possible functional link between CD5(+) B cells and bone resorption still needs to be defined.
OBJECTIVE: The prevention of bone resorption and subsequent joint destruction is one of the main challenges in the treatment of patients suffering from RA. Various mechanisms have previously been described that contribute to bone resorption in tightly defined cohorts. Here we analysed a cross-sectional cohort of RApatients and searched for humoral and cellular markers in the peripheral blood associated with bone resorption. METHODS: We enrolled 61 consecutive RApatients positive for ACPA. Blood was analysed by flow cytometry to determine the percentages of regulatory T cells and B cell subpopulations. Cytokine (TNF-α, IL-6, IL-10) and ACPA levels as well as the bone resorption marker CTX-1 were determined from the patients' sera. Standard clinical disease parameters were included. RESULTS: Multivariate analyses showed that the percentages of CD5(+) B cells were positively correlated with CTX-1 serum levels. However, neither low-avidity ACPA nor serum IL-6 levels, both known to be produced by CD5(+) cells, were associated with CTX-1 in patients' sera. There was no correlation between CTX-1 levels and clinical parameters or ACPA levels. CONCLUSION: In summary, we found that the CD5(+) B cell population is associated with bone resorption as measured via serum CTX-1 levels in a cross-sectional cohort of RApatients. However, a possible functional link between CD5(+) B cells and bone resorption still needs to be defined.
Authors: Alina A Alshevskaya; Julia A Lopatnikova; Nadezhda S Shkaruba; Oksana A Chumasova; Aleksey E Sizikov; Aleksander V Karaulov; Vladimir A Kozlov; Sergey V Sennikov Journal: Mediators Inflamm Date: 2015-09-10 Impact factor: 4.711
Authors: Rita A Moura; Cláudia Quaresma; Ana R Vieira; Maria J Gonçalves; Joaquim Polido-Pereira; Vasco C Romão; Nádia Martins; Helena Canhão; João E Fonseca Journal: PLoS One Date: 2017-09-08 Impact factor: 3.240