Purinergic signalling in B cells

Abstract

Adenosine and adenosine triphosphate are involved in purinergic signalling which plays important role in control of immune system. Much data have been obtained regarding impact of purinergic signalling on dendritic cells, macrophages, monocytes and T lymphocytes, however less attention has been paid to purinergic regulation of B cells. This review summarizes present knowledge about ATP- and Ado-dependant signalling in B lymphocytes. Human B cells have been shown to express A2A­-R and A­3-R and each subtype of P2 receptors. Surface of B cells exhibits two antagonistic ectoenzymatic pathways, one relays on constitutive secretion and resynthesis of ATP while the second one depends on degradation of adenosine nucleotides to nucleosides and their subsequent degradation. Inactivated B cells remain under suppressive impact of autocrine and paracrine Ado however activated B lymphocytes increase ATP release and production. ATP protects B cells from suppressive impact of Ado and exerts pro-inflammatory impact on target tissues, it is also involved in IgM release. Ado synthesis however is related with optimal development, implantation and maintenance of plasmocyte population in bone marrow during primary immune response. Moreover Ado plays important role in immunoglobulin class switching which is a key mechanism of humoral immune response. Disruption of purinergic signalling is related with severe clinical implications. Impairment of Ado production in environment of B cells is one of the factors responsible for common variable immunodeficiency. List of evidence suggests also that dysfunction of immune system observed during diabetes may in part depend on disrupted ATP and Ado metabolism in B cells.