In contrast, B1 cells are considered as specialized B cells of in

In contrast, B1 cells are considered as specialized B cells of innate immunity [12]. The murine B1 and human B1-like cells secrete mainly natural IgM antibodies that are often polyreactive and low affinity in nature. These natural antibodies, while autoreactive, mediate protective immune surveillance

and maintenance of tissue homeostasis by facilitating clearance of dead cell bodies LY2835219 [12, 13]. Conversely, antibodies produced by murine and human B2 cells are less likely to be autoreactive but are high in specificity and affinity due to their ability to undergo affinity maturation, somatic hypermutations and clonal selection via B cell receptor (BCR) activation [15]. Mature murine and human B2 cells can also undergo class-switch DNA recombination (CSR) to give rise to the production of IgA, IgE and IgG antibody subclasses [11,

15]. Murine B1 cells are also generally more sensitive to BCR activation-induced apoptosis when subjected to affinity maturation [12]. Thus, they are often prevented from differentiating into autoreactive memory B cells or plasma cells capable of secreting high-affinity autoantibodies. However, murine B1 cells can migrate to spleen, where they differentiate Poziotinib research buy into splenic marginal zone (MZ) B cell precursors that can undergo somatic hypermutation and isotype switching to give rise to antibody-secreting memory B cells and plasma cells [16]. In addition, B1 cells have the capacity to respond and migrate to distal sites of inflammation,

where they act as phagocytic cells or as immune regulators through the secretion of cytokines [17-19]. B cell subsets during pregnancy are poorly studied. B cell-deficient mice are not embryonic lethal and have normal litter sizes, suggesting that B cells are dispensable for normal murine pregnancy [20]. The treatment of mice and non-human primates with B cell-depleting agents also does not affect normal pregnancy [21-23]. During murine pregnancy, the formation of B cell precursors is suppressed selectively in the bone marrow [24]. This suppression occurs at the early stage of B lymphopoiesis and is driven by the pregnancy hormone oestrogen [24]. Maternal B cells that express autoantibodies specific for fetal antigens are also depleted Farnesyltransferase during murine pregnancy, suggesting a mechanism of maternal–fetal immune tolerance [25-27]. However, oestrogen also has a positive effect on the survival of mature murine B cells [28], suggesting a compensatory effect of oestrogen at different stage of development to maintain a balance within the B cell compartment. Similar changes in B cell compartment have been reported in a number of human pregnancy studies [29-36]. The absolute numbers and frequencies of circulating CD5+ B cells are decreased in normal human pregnancy (Table 1), and can persist for up to 1 month postpartum [29, 33, 37, 38].

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