INT153260
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
Because dysregulated expression of CD22 could lead to excessive activation of B cells and autoantibody production [17], targeting this coreceptor in systemic autoimmunity appears to be a potentially new therapeutic pathway. | |||||||||||||||
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CD22 is expressed at low levels on immature B cells, expressed at higher levels on mature IgM+, IgD+ B cells, and absent on differentiated plasma cells. | |||||||||||||||
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Considering the low scattering of CD22 expression on normal B-lymphocytes, we determined a range of normal values and the median CD22 fluorescence on 33 blood samples from normal healthy volunteers. | |||||||||||||||
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These new therapies are: (1) "B lymphocyte (BL)" inhibitors such as anti-CD20 monoclonal antibody, anti-CD22 monoclonal antibody, BlyS antagonists, tolerogens of pathogenic-antibody secreting LB (LJP 394) and edratide; (2) "Inhibitors of the costimulation" between antigen-presenting cells and T lymphocyte (TL) like monoclonal anti-CD40 ligand antibody or CTLA-4-Ig (abatacept); (3) "Cytokine antagonists" inhibiting key cytokines of SLE: interleukin-10, interferon-alpha, interleukin-6 and TNF. | |||||||||||||||
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CD22 is first expressed in the cytoplasm of pro-B and pre-B cells, and then on the surface of B cells as they mature, with expression ceasing with B cell differentiation into plasma cells [23]. | |||||||||||||||
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CD22 is expressed at low levels on immature B cells, expressed at higher levels on mature IgM+, IgD+ B cells, and absent on differentiated plasma cells. | |||||||||||||||
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Monoclonal antibodies used in this study were CD19 allophycocyanin (APC) (clone SJ25C1) and CD22 phycoerythrin (PE) (clone S-HCL-1). | |||||||||||||||
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Therefore, CD22 is an attractive molecular target for therapy because of its restricted expression; it is not exposed on embryonic stem or pre-B cells, nor is it normally shed from the surface of antigen-bearing cells. | |||||||||||||||
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The expression of CD22 is specific to B-cells and is developmentally regulated so that it is expressed at low levels in the cytoplasm of pro-B and pre-B-cells, and its localization shifts to the cell surface and higher expression on mature IgM+, IgD+ B-cells (Dörken et al 1986). | |||||||||||||||
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CD22 is strongly expressed on follicular, mantle, and marginal-zone B-cells, but is weakly present in germinal B-cells (reviewed in (Nitschke 2005; Tedder et al 2005b)). | |||||||||||||||
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In addition, we report here, for the first time, that patients with pSS have a CD22 over-expression in their peripheral B cells, which was downregulated by epratuzumab for at least 12 weeks after the therapy. | |||||||||||||||
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This is consistent with the finding that patients with Sjögren's syndrome have an over-expression of CD22. | |||||||||||||||
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At the final evaluation, all the patients recovered to the same increased CD22 expression compared with normal, as observed in patients with untreated pSS.
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Further, we determined that pSS patients have a CD22 over-expression in their peripheral B cells, which was downregulated by epratuzumab for at least 12 weeks after the therapy. | |||||||||||||||
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In addition, we report here, for the first time, that patients with pSS have a CD22 over-expression in their peripheral B cells, which was downregulated by epratuzumab for at least 12 weeks after the therapy. | |||||||||||||||
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In addition, we report here, for the first time, that patients with pSS have a CD22 over-expression in their peripheral B cells, which was downregulated by epratuzumab for at least 12 weeks after the therapy. | |||||||||||||||
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CD22 is expressed on the surface of normal mature and malignant B lymphocytes. | |||||||||||||||
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In contrast to HS, diffuse large B-cell lymphoma constantly express various pan-B markers such as CD19, CD20, CD22, and CD79a, while anaplastic large cell lymphomas are positive for CD30, and ALK [1]. | |||||||||||||||
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This might explain why most progress has been made so far in the clinical development of antibody toxins that target cell surface molecules such as CD22 and CD25 expressed on certain malignancies of hematologic origin [34,35], where tumor cells are usually more accessible. | |||||||||||||||
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This might explain why most progress has been made so far in the clinical development of antibody toxins that target cell surface molecules such as CD22 and CD25 expressed on certain malignancies of hematologic origin [34,35], where tumor cells are usually more accessible. | |||||||||||||||
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General Comments
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