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CD200RLa / CD200R1L Antibody, Rabbit PAb, Antigen Affinity Purified

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    Human CD200RLa Antibody Product Information
    Immunogen:Recombinant Human CD200RLa / CD200R1L protein (Catalog#11620-H08H)
    Clone ID:
    Ig Type:Rabbit IgG
    Concentration:
    Formulation:0.2 μm filtered solution in PBS with 5% trehalose
    Preparation:Produced in rabbits immunized with purified, recombinant Human CD200RLa / CD200R1L (rh CD200RLa / CD200R1L; Catalog#11620-H08H; AAT00538.1; Met1-Leu239). CD200RLa / CD200R1L specific IgG was purified by Human CD200RLa / CD200R1L affinity chromatography.
    Other CD200RLa Antibody Products
    CD200RLa Background

    Cell surface glycoprotein CD200 receptor 2, also known as Cell surface glycoprotein CD200 receptor 1-like, Cell surface glycoprotein OX2 receptor 2, CD200 receptor-like 2, CD200Rla, CD200R1L and CD200R2, is a single-pass type I  membrane protein which belongs to the CD200R family. CD200R1L / CD200R2. It contains one Ig-like C2-type (immunoglobulin-like) domain and one Ig-like V-type (immunoglobulin-like) domain. CD200 is a transmembrane protein delivering immunoregulatory signals after engagement of CD200R. A family of CD200Rs exist ( CD200R1, CD200R2, CD200R3, CD200R4 ) with different tissue expression and functional activity. In the presence of anti-CD200R2 / CD200R3 monoclonal antibodies (mAbs), bone-marrow cells cultured in the presence of (interleukin [IL]-4+granulocyte-macrophage colony-stimulating factor) differentiate into dendritic cells (DCs), which induce CD4+CD25+ Treg. Interaction between the relatively ubiquitously expressed molecule CD200 and one of its receptors, CD200R1, resulted in direct suppression of alloreactivity, engagement of alternate receptors led instead to altered differentiation of dendritic cells (DCs) from marrow precursors, which could in turn foster development of Foxp3(+) regulatory T cells. Unlike anti-CD200R1, anti-CD200R2 both promotes development of DCs with capacity to induce Treg and directly augments thymocyte production of Treg.

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