Disease relevance of Cd72

• Genetic dissection of vasculitis in MRL/lpr lupus mice: a novel susceptibility locus involving the CD72c allele [1].
• A 4-day culture system is described in which bone marrow lymphocytes from neonatal mice acquire in sequence the ability to express Lyb-2, IgM, Ia and IgD in response to a 3-h induction with E. coli lipopoly-saccharide (LPS) [2].
• Coexpression of Lyb-2 and Mac-1 by murine lymphomas and subpopulations of normal spleen and bone marrow cells [3].
• NOD and lupus prone strains share the CD72c allele and its functions may contribute to overlapping features of organ specific and systemic autoimmune disorders [4].
• To understand how the fate and function of B lymphocytes may be regulated in the context of an organ specific autoimmune disease, the B cell co-receptor CD72 (Lyb-2) was examined in NOD mice [4].

High impact information on Cd72

• On the function of Ly-5 in the regulation of antigen-driven B cell differentiation. Comparison and contrast with Lyb-2 [5].
• A critical distinction of Ly-5 from Lyb-2 is that Ly-5 antibody reduces PFC generation to trinitrophenylated Ficoll, a thymus-independent type 2 antigen requiring T cells and M phi for maximal PFC generation in vitro [5].
• Monoclonal Lyb-2 antibody, added to Mishell-Dutton cultures within the first 2 d, but not later, greatly reduces the generation of alpha-sheep erythrocyte (SRBC) PFC from T-depleted spleen cells whether help is provided in the form of intact T cells or as soluble factors contained in mixed lymphocyte culture (MLC) supernatants [6].
• Reduction of PFC generation by Lyb-2 antibody is antigen dependent in the sense that reduction of the PFC response to one antigen (SRBC) does not affect subsequent generation of PFC to a second antigen (horse erythrocytes) from the same cell population [6].
• Lyb-2 has been shown to play a role in B-cell activation and differentiation and may be a receptor for a B-cell growth factor or lymphokine [7].

Biological context of Cd72

• The serologically defined Ly-19.2 and Ly-32.2 lymphocyte alloantigens have mouse strain distribution patterns similar to that of the Lyb-2/CD72 alleles and map to the same region on chromosome 4 as Lyb-2/CD72 [8].
• In this study, we investigated the surface phenotype of three types of effector T cells: helper cells, nonspecific suppressor cells, and cytotoxic T cells, using four recently discovered alloantigen systems of T cells: Ly-m10, Ly-m18, Ly-m19, and Ly-m22 [9].
• These findings may provide insight into the complexities and functional roles of Lyb-2 gene-cluster products [10].
• 2. This strain distribution pattern distinguishes Ly-m19 from any known murine lymphocyte alloantigen, but it parallels the Lyb-2c haplotype [11].
• Differential regulation of surface Ig- and Lyb2-mediated B cell activation by cyclic AMP. I. Evidence for alternative regulation of signaling through two different receptors linked to phosphatidylinositol hydrolysis in murine B cells [12].

Anatomical context of Cd72

• Biochemical identity of the mouse Ly-19.2 and Ly-32.2 alloantigens with the B cell differentiation antigen Lyb-2/CD72 [8].
• Lyb-2 mRNA is expressed only in B-lineage cells and is absent from antibody-secreting cell lines [7].
• NK cells did not express significant amounts of Qa-1, Qa-3, Lyt-2, and Lyb-2 antigens [13].
• Expression of Lyb-2 is restricted to B lineage cells and turned off in antibody-secreting plasma cells in both mice and humans [14].
• 1. One established hybridoma cell line (clone K10.6) continuously secreted antibody that recognized a new antigenic specificity tentatively named Ly-m19 [11].

Associations of Cd72 with chemical compounds

• Failure of forskolin or N6,2'-O-dibutyryl cyclic AMP to inhibit Lyb2-mediated responses did not appear to be due to induction of cAMP-specific phosphodiesterase activity [12].
• To gain further insight into the function of these two molecules, we examined the effect of monoclonal Lyb-2 and Ly-5 antibodies on lipopolysaccharide (LPS)-induced B cell growth and maturation [15].
• Pretreatment of resting B cells with cholera toxin as well as other agents that raise the intracellular cAMP [(cAMP)i] such as forskolin, N6,2'-O-dibutyryl cyclic AMP, and 3-isobutyl-1 methyl xanthine inhibited the Ag receptor but not Lyb2-mediated DNA synthesis [12].
• These findings suggest that distinct PLC-coupled receptors, such as sIgM and Lyb2 molecules in B cells, may use either alternative mechanisms for phosphatidylinositol 4,5-bisphosphate hydrolysis or may use different intermediary transducer molecules that differ in their sensitivity to increased (cAMP)i levels [12].
• They possessed Lyb 2 surface antigens, were dependent on mercaptoethanol for growth, and contained only low levels of terminal deoxynucleotidyl transferase [16].

Physical interactions of Cd72

• Lyb-2/CD72 is a 45-kDa mouse B cell surface protein that binds CD5 (Ly-1) and has been shown to induce B cell proliferation upon mAb binding [8].

Regulatory relationships of Cd72

• It is shown that interaction of monoclonal anti (alpha)-Lyb-2 antibody with Lyb-2 on the B cell surface induces B cell proliferation by synergistic action with B cell growth factor II-containing factor or interleukin 1 [17].
• The present study was conducted to examine this possibility by elucidating the molecular mechanisms whereby CD45 and Lyb-2 control IgG synthesis in B cells activated by LPS and IL-4 [18].

Other interactions of Cd72

• This interpretation was tested in the present report by positive selection for cells expressing B220, Lyb-2, or AA4.1, surface markers known to be present on cell lines of the B lineage [19].
• Regulation of lipopolysaccharide- and IL-4-induced immunoglobulin heavy chain gene activation: differential roles for CD45 and Lyb-2 [18].

Analytical, diagnostic and therapeutic context of Cd72

• The Lyb-2/CD72 PCR products from mRNA of mice expressing Lyb-2a and Lyb-2c contain a DNA fragment that corresponds in size to the transmembraneless form, suggesting that these mouse strains also express this mRNA [20].

References