IADR Abstract Archives
CD180 Expression on B Cells in Primary Sjogren's Syndrome Mice
Objectives:
Primary Sjogren’s syndrome (pSS) is an autoimmune disease. The etiology of pSS is poorly understood and no curative treatments are available. Thus, there is a need to identify the causes of pSS to improve treatments. B cell abnormalities are well documented in pSS, and therapies that target B cells may have therapeutic utility. Mature B cells express a receptor termed CD180 that promotes B cell proliferation and protects against apoptosis. Preliminary work shows CD180-deficient B cells are increased in salivary tissue and peripheral blood of patients with SS. Additionally, ligation of Toll-like receptor 7 (TLR7) reduces CD180 expression in healthy mice, although this has not been studied in the context of pSS. The objective of this study was to evaluate whether B cell CD180 levels differ between pSS mice and controls, and to determine if TLR7 agonism diminishes CD180 expression by B cells in pSS.
Methods: We used a pSS mouse model and age and sex-matched controls. Cells were harvested from females at the pre-disease and clinical disease stages and CD180 expression on B cells derived from splenic follicular and marginal zone subsets, cervical lymph nodes, and peritoneal B1a cells was assessed using flow cytometry. B cells were also cultured in the presence or absence of the TLR7 agonist imiquimod, and flow cytometry was performed to assess CD180 expression.
Results:
CD180 was expressed on all B cell subsets from both pSS and control mice. No differences were observed in B cell CD180 expression between the strains at either time point. TLR7 agonism altered B cell CD180 expression in pSS mice.
Conclusions:
Our preliminary data demonstrate CD180 is expressed in pSS mice at both pre-disease and clinical disease time points and TLR7 agonism alters CD180 expression in distinct B cell subsets. Further studies are needed to determine how CD180 contributes to pSS pathogenesis.
Primary Sjogren’s syndrome (pSS) is an autoimmune disease. The etiology of pSS is poorly understood and no curative treatments are available. Thus, there is a need to identify the causes of pSS to improve treatments. B cell abnormalities are well documented in pSS, and therapies that target B cells may have therapeutic utility. Mature B cells express a receptor termed CD180 that promotes B cell proliferation and protects against apoptosis. Preliminary work shows CD180-deficient B cells are increased in salivary tissue and peripheral blood of patients with SS. Additionally, ligation of Toll-like receptor 7 (TLR7) reduces CD180 expression in healthy mice, although this has not been studied in the context of pSS. The objective of this study was to evaluate whether B cell CD180 levels differ between pSS mice and controls, and to determine if TLR7 agonism diminishes CD180 expression by B cells in pSS.
Methods: We used a pSS mouse model and age and sex-matched controls. Cells were harvested from females at the pre-disease and clinical disease stages and CD180 expression on B cells derived from splenic follicular and marginal zone subsets, cervical lymph nodes, and peritoneal B1a cells was assessed using flow cytometry. B cells were also cultured in the presence or absence of the TLR7 agonist imiquimod, and flow cytometry was performed to assess CD180 expression.
Results:
CD180 was expressed on all B cell subsets from both pSS and control mice. No differences were observed in B cell CD180 expression between the strains at either time point. TLR7 agonism altered B cell CD180 expression in pSS mice.
Conclusions:
Our preliminary data demonstrate CD180 is expressed in pSS mice at both pre-disease and clinical disease time points and TLR7 agonism alters CD180 expression in distinct B cell subsets. Further studies are needed to determine how CD180 contributes to pSS pathogenesis.