Table 1.

Major miRNAs playing a role in B cells.

miRNA	Targets	Biological effects	Associated disorders
miR-17-92 Cluster	Bim (3, 4)	Participate in B-cell proliferation and cell-death control (3, 4)
	Pten (4)
miR-24	Bim and Caspase 9 (5)	Inhibit B-cell development, under the control of PU.1 (5, 6)
miR-29a	TCL1, MCL10, and CDK6 (7)		Up-regulated in indolent B-cell chronic lymphocytic leukemia (CLL) compared to normal B cells (8).
miR-34a	Foxp1 (9)	Induces block of B-cell development whereas its deletion induces high number of mature B cells (9)
miR-146a	Irak1 and Traf6 (10)	Participate in B-cell development, over-expression causes spontaneous autoimmune disorders in mice (10, 11)	Over-expressed in patients suffering from rheumatoid arthritis and psoriasis (12–14)
	Fas (11).		Over-expressed in kidney biopsy and urine from patients with IgA nephropathy (15)
			Induced by EBV and inhibits the expression of interferon related genes (16)
miR-150	c-Myb (17).	Its over-expression in B-cell progenitors results in a partial block of B-cell development and a reduction in B1-cell numbers (17).	Under-expressed in peripheral B cells from SLE patients (18)
miR-155	Pu.1 (Sfpi1 gene) (19)	Reduced generation of high-affinity antibodies against a T-cell-dependent antigen (19, 20)	Over-expressed in peripheral B cells from SLE patients (18)
	Shp1 (21)		Is induced by EBV, through LMP1 and:
	Aid (20, 22)		-targets BMP signaling cascade suggesting an inhibition of the antitumor effects of BMP signaling (23)
			-contributes to the resistance toward Rituximab in inducing cell survival signal (24)
miR-181a	Bim (25)	Its over-expression inhibits the pro-apoptotic protein BIM (25) and increases number of B-lineage cells (26)
miR-181b	Aid (27)	Impairs the class-switch recombination (27)
miR-210		Control of immunoglobin class-switch and under the control of Oct-2 (28)
miR-221		Implicated in the retention of early B-lineage cells in bone marrow and under the control of PAX5 (29).