Table 1.
Number of up and down regulated genes.
Table 2.
Overlapping genes between different treatments.
Table 3.
Antigen expression determined by FACS analysis.
Table 4.
Antigen expression determined by Affymetrix analysis: mean expression values of untreated cells.
Figure 1.
Comparison of genes deregulated by different antibody treatments.
Venn diagrams for numbers of up- (A) or down- (B) regulated genes in SUDHL4 after a 4 h incubation with 10 µg/ml anti-BCR antibody (anti-IgG) and anti-CD20 antibodies (Rituximab, LT20) and Venn diagrams for up- (C) or down- (D) regulated genes in REC1 after treatment with anti-BCR antibodies (anti-IgG and anti-IgM, respectively) and anti-CD20 antibodies (Rituximab, Rx-F(ab')2, LT20).
Figure 2.
Comparison of anti-BCR and anti-CD20.
Venn diagrams of “Union lists” of up- (A) or down- (B) regulated genes after different treatments. Cells were incubated with 10 µg/ml antibody for 4 h. Lists of similar treatments were united to “Union lists” for CD20 or BCR treatment for each cell line R = REC1, S = SUDHL4.
Figure 3.
Comparison of anti-BCR treatments in all cell lines studied.
Venn diagrams of “Union lists” ( = Union of lists for similar treatments) for anti-BCR treatment of up- (A) or down- (B) regulated genes in OciLy18, Z138, SUDHL4 and REC1.
Table 5.
Functional clustering of genes deregulated by anti-BCR antibodies in cell lines OciLy18, Z138, REC1 und SUDHL4.
Table 6.
Functional clustering of genes deregulated by anti-CD20 antibodies in SUDHL4 cells und REC1 cells (KEGG-, Panther- und Biocarta, GO terms).
Table 7.
Genes that are common deregulated in all four cell lines by anti-BCR antibodies and in SUDHL4 and REC1 by anti-CD20 antibodies.
Figure 4.
Interactions between deregulated genes.
IPA generated network of interactions between genes deregulated by anti-CD20 antibodies in SUDHL4 and REC1. The red circle marks genes which are also deregulated by all anti-BCR treatments. Interestingly this unbiased analysis displays deregulations of BCR components and the downstream signaling pathway.
Figure 5.
Repression of chemokine CCL3/4 induction caused by Syk inhibition and silencing.
(A) CCL3 secretion in SUDHL4 induced by anti-IgG antibodies and anti-CD20 antibodies and its inhibition by Syk inhibitors I and IV (Calbiochem) at 1 µM and 0,32 µM respectively. Bars represent mean of three replicates, including standard deviation (<IgG> = anti-IgG antibody, Inh. I = Syk inhibitor I, Inh. IV = Syk inhibitor IV, LT20 = murine anti-CD20 antibody, Rx-Fab'2 = F(ab')2 fragment of rituximab). Inhibition of CCL3 (B) and CCL4 (C) secretion in SUDHL4 induced by anti-IgG antibodies or rituximab after siRNA-mediated Syk silencing. Results represent at least three independent experiments. Students t-test for “Negative controls” vs. “SYK-knockdown”: for CCL3 secretion after anti-IgG treatment p = 6.8*10−7, Rx treatment p = 7.4*10−3. For CCL4 secretion after anti-IgG treatment p = 2.1*10−6, Rx treatment p = 2.5*10−4. (anti-IgG = anti-IgG antibody, Rx = rituximab, Neg. controls = RISCfree and Luciferase-siRNA transfections, respectively; SYK knock down = Syk-siRNA transfections).