REGULATION OF CD72 EXPRESSION ON CD19+CD27+ MEMORY B CELL BY CD40L IN PRIMARY IMMUNE THROMBOCYTOPENIA
(Abstract release date: 05/19/16)
EHA Library. Lyu M. 06/09/16; 132539; E990
Mrs. Mingen Lyu
Contributions
Contributions
Abstract
Abstract: E990
Type: Eposter Presentation
Background
CD72, a co-receptor of B cell receptor, regulates B cell activation and is involved in B cell-related autoimmune diseases. Despite the knowledge that expression of CD72 on peripheral B cell is aberrant in patients with some autoimmune diseases, it is uncertain whether this aberrant expression is restricted to specific B cell subsets in primary immune thrombocytopenia (ITP). Furthermore, the mechanisms that regulate CD72 expression on peripheral B cell in ITP are unknown.
Aims
This study aimed to examine CD72 expression on subsets of B cells and uncover the regulatory mechanisms of CD72 expression on peripheral B cell in ITP.
Methods
Frequencies of B cell subsets and expression of CD72 and CD40L were determined by flow cytometry in patients with active ITP, patients in remission and health controls. To activate B cells, the following reagents were added at the initiation of culture in vitro, anti-IgM, CD40L, LPS. The following cytokines were used to evaluate their effect on CD72 expression: interleukin-4 (IL-4), IL-10, IL-21, B-cell-activating factors (BAFF). The level of CD72 mRNA was assessed by real-time PCR. The concentration of plasma CD40L was measured by ELISA. Specific anti-platelet autoantibodies were measured by the Pak Auto method.
Results
Patients with active ITP had a significantly higher frequency of CD19+B cells, CD19+CD27+ memory B cell and lower frequency of CD19+CD27- naive B cells than did controls and patients in remission. The mean fluorescence intensity of CD72 on circulating B subcells is upregulated in active ITP patients compared to that recorded in controls and patients in remission. In active ITP patients, the expression of CD72 on CD19+ CD27+B cells was inversely correlated with platelet counts, but there is no difference among groups with different age and gender. Patients with anti-platelet autoantibodies had significantly higher expression of CD72 on CD19+CD27+B cells. In vitro, analysis of B cell activation revealed that the CD40L could induce CD72 significant upregulation on B cells and CD19+CD27+ B cells both in patients and controls. The mRNA levels of CD72 in peripheral blood mononuclear cells activated by CD40L were increased. When used in combination with CD40L, IL-10 and BAFF further enhanced the expression of CD72 on CD19+CD27+B cell, whereas IL-21 reduced CD72 upregulation. CD40L expression on CD4 T cells and plasma CD40L levels were significantly higher in active ITP patients compared to controls. Significant increases in plasma CD40L were correlated with CD72 expression on CD19+CD27+ B cell in ITP patients.
Conclusion
These data provide evidence that active ITP patients have higher CD72 expression on increased CD19+CD27+ memory B cells, which is associated with platelet counts and autoantibody. Soluble higher CD40L found in active ITP patients might contribute to the increased levels of CD72 on CD19+CD27+ B cell.
Session topic: E-poster
Keyword(s): B cell, CD40 Ligand (CD40L), Immune thrombocytopenia (ITP)
Type: Eposter Presentation
Background
CD72, a co-receptor of B cell receptor, regulates B cell activation and is involved in B cell-related autoimmune diseases. Despite the knowledge that expression of CD72 on peripheral B cell is aberrant in patients with some autoimmune diseases, it is uncertain whether this aberrant expression is restricted to specific B cell subsets in primary immune thrombocytopenia (ITP). Furthermore, the mechanisms that regulate CD72 expression on peripheral B cell in ITP are unknown.
Aims
This study aimed to examine CD72 expression on subsets of B cells and uncover the regulatory mechanisms of CD72 expression on peripheral B cell in ITP.
Methods
Frequencies of B cell subsets and expression of CD72 and CD40L were determined by flow cytometry in patients with active ITP, patients in remission and health controls. To activate B cells, the following reagents were added at the initiation of culture in vitro, anti-IgM, CD40L, LPS. The following cytokines were used to evaluate their effect on CD72 expression: interleukin-4 (IL-4), IL-10, IL-21, B-cell-activating factors (BAFF). The level of CD72 mRNA was assessed by real-time PCR. The concentration of plasma CD40L was measured by ELISA. Specific anti-platelet autoantibodies were measured by the Pak Auto method.
Results
Patients with active ITP had a significantly higher frequency of CD19+B cells, CD19+CD27+ memory B cell and lower frequency of CD19+CD27- naive B cells than did controls and patients in remission. The mean fluorescence intensity of CD72 on circulating B subcells is upregulated in active ITP patients compared to that recorded in controls and patients in remission. In active ITP patients, the expression of CD72 on CD19+ CD27+B cells was inversely correlated with platelet counts, but there is no difference among groups with different age and gender. Patients with anti-platelet autoantibodies had significantly higher expression of CD72 on CD19+CD27+B cells. In vitro, analysis of B cell activation revealed that the CD40L could induce CD72 significant upregulation on B cells and CD19+CD27+ B cells both in patients and controls. The mRNA levels of CD72 in peripheral blood mononuclear cells activated by CD40L were increased. When used in combination with CD40L, IL-10 and BAFF further enhanced the expression of CD72 on CD19+CD27+B cell, whereas IL-21 reduced CD72 upregulation. CD40L expression on CD4 T cells and plasma CD40L levels were significantly higher in active ITP patients compared to controls. Significant increases in plasma CD40L were correlated with CD72 expression on CD19+CD27+ B cell in ITP patients.
Conclusion
These data provide evidence that active ITP patients have higher CD72 expression on increased CD19+CD27+ memory B cells, which is associated with platelet counts and autoantibody. Soluble higher CD40L found in active ITP patients might contribute to the increased levels of CD72 on CD19+CD27+ B cell.
Session topic: E-poster
Keyword(s): B cell, CD40 Ligand (CD40L), Immune thrombocytopenia (ITP)
Abstract: E990
Type: Eposter Presentation
Background
CD72, a co-receptor of B cell receptor, regulates B cell activation and is involved in B cell-related autoimmune diseases. Despite the knowledge that expression of CD72 on peripheral B cell is aberrant in patients with some autoimmune diseases, it is uncertain whether this aberrant expression is restricted to specific B cell subsets in primary immune thrombocytopenia (ITP). Furthermore, the mechanisms that regulate CD72 expression on peripheral B cell in ITP are unknown.
Aims
This study aimed to examine CD72 expression on subsets of B cells and uncover the regulatory mechanisms of CD72 expression on peripheral B cell in ITP.
Methods
Frequencies of B cell subsets and expression of CD72 and CD40L were determined by flow cytometry in patients with active ITP, patients in remission and health controls. To activate B cells, the following reagents were added at the initiation of culture in vitro, anti-IgM, CD40L, LPS. The following cytokines were used to evaluate their effect on CD72 expression: interleukin-4 (IL-4), IL-10, IL-21, B-cell-activating factors (BAFF). The level of CD72 mRNA was assessed by real-time PCR. The concentration of plasma CD40L was measured by ELISA. Specific anti-platelet autoantibodies were measured by the Pak Auto method.
Results
Patients with active ITP had a significantly higher frequency of CD19+B cells, CD19+CD27+ memory B cell and lower frequency of CD19+CD27- naive B cells than did controls and patients in remission. The mean fluorescence intensity of CD72 on circulating B subcells is upregulated in active ITP patients compared to that recorded in controls and patients in remission. In active ITP patients, the expression of CD72 on CD19+ CD27+B cells was inversely correlated with platelet counts, but there is no difference among groups with different age and gender. Patients with anti-platelet autoantibodies had significantly higher expression of CD72 on CD19+CD27+B cells. In vitro, analysis of B cell activation revealed that the CD40L could induce CD72 significant upregulation on B cells and CD19+CD27+ B cells both in patients and controls. The mRNA levels of CD72 in peripheral blood mononuclear cells activated by CD40L were increased. When used in combination with CD40L, IL-10 and BAFF further enhanced the expression of CD72 on CD19+CD27+B cell, whereas IL-21 reduced CD72 upregulation. CD40L expression on CD4 T cells and plasma CD40L levels were significantly higher in active ITP patients compared to controls. Significant increases in plasma CD40L were correlated with CD72 expression on CD19+CD27+ B cell in ITP patients.
Conclusion
These data provide evidence that active ITP patients have higher CD72 expression on increased CD19+CD27+ memory B cells, which is associated with platelet counts and autoantibody. Soluble higher CD40L found in active ITP patients might contribute to the increased levels of CD72 on CD19+CD27+ B cell.
Session topic: E-poster
Keyword(s): B cell, CD40 Ligand (CD40L), Immune thrombocytopenia (ITP)
Type: Eposter Presentation
Background
CD72, a co-receptor of B cell receptor, regulates B cell activation and is involved in B cell-related autoimmune diseases. Despite the knowledge that expression of CD72 on peripheral B cell is aberrant in patients with some autoimmune diseases, it is uncertain whether this aberrant expression is restricted to specific B cell subsets in primary immune thrombocytopenia (ITP). Furthermore, the mechanisms that regulate CD72 expression on peripheral B cell in ITP are unknown.
Aims
This study aimed to examine CD72 expression on subsets of B cells and uncover the regulatory mechanisms of CD72 expression on peripheral B cell in ITP.
Methods
Frequencies of B cell subsets and expression of CD72 and CD40L were determined by flow cytometry in patients with active ITP, patients in remission and health controls. To activate B cells, the following reagents were added at the initiation of culture in vitro, anti-IgM, CD40L, LPS. The following cytokines were used to evaluate their effect on CD72 expression: interleukin-4 (IL-4), IL-10, IL-21, B-cell-activating factors (BAFF). The level of CD72 mRNA was assessed by real-time PCR. The concentration of plasma CD40L was measured by ELISA. Specific anti-platelet autoantibodies were measured by the Pak Auto method.
Results
Patients with active ITP had a significantly higher frequency of CD19+B cells, CD19+CD27+ memory B cell and lower frequency of CD19+CD27- naive B cells than did controls and patients in remission. The mean fluorescence intensity of CD72 on circulating B subcells is upregulated in active ITP patients compared to that recorded in controls and patients in remission. In active ITP patients, the expression of CD72 on CD19+ CD27+B cells was inversely correlated with platelet counts, but there is no difference among groups with different age and gender. Patients with anti-platelet autoantibodies had significantly higher expression of CD72 on CD19+CD27+B cells. In vitro, analysis of B cell activation revealed that the CD40L could induce CD72 significant upregulation on B cells and CD19+CD27+ B cells both in patients and controls. The mRNA levels of CD72 in peripheral blood mononuclear cells activated by CD40L were increased. When used in combination with CD40L, IL-10 and BAFF further enhanced the expression of CD72 on CD19+CD27+B cell, whereas IL-21 reduced CD72 upregulation. CD40L expression on CD4 T cells and plasma CD40L levels were significantly higher in active ITP patients compared to controls. Significant increases in plasma CD40L were correlated with CD72 expression on CD19+CD27+ B cell in ITP patients.
Conclusion
These data provide evidence that active ITP patients have higher CD72 expression on increased CD19+CD27+ memory B cells, which is associated with platelet counts and autoantibody. Soluble higher CD40L found in active ITP patients might contribute to the increased levels of CD72 on CD19+CD27+ B cell.
Session topic: E-poster
Keyword(s): B cell, CD40 Ligand (CD40L), Immune thrombocytopenia (ITP)
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