Polyclonal B cell activation in infections: infectious agents’ devilry or defense mechanism of the host?

Abstract

Polyclonal B cell activation is not a peculiar characteristic to a particular infection, as many viruses, bacteria, and parasites induce a strong polyclonal B cell response resulting in hyper-gamma-globulinemia. Here, we discuss the different roles proposed for polyclonal B cell activation, which can be crucial for early host defense against rapidly dividing microorganisms by contributing antibodies specific for a spectrum of conserved structures present in the pathogens. In addition, polyclonal B cell activation can be responsible for maintenance of memory B cell responses because of the continuous, unrestricted stimulation of memory B cells whose antibody production may be sustained in the absence of the antigens binding-specific BCR. Conversely, polyclonal activation can be triggered by microorganisms to avoid the host-specific, immune response by activating B cell clones, which produce nonmicroorganism-specific antibodies. Finally, some reports suggest a deleterious role for polyclonal activation, arguing that it could potentially turn on anti-self-responses and lead to autoimmune manifestations during chronic infections.

Vigorous Response of Human Innate Functioning IgM Memory B Cells upon Infection by Neisseria gonorrhoeae

“…N. gonorrhoeae appears to use an alternative approach to prevent the production of a specific humoral response, suppressing T cell help (12,13) while simultaneously stimulating the IgM memory B cells to produce polyclonal Ig responses; combined, this would effectively lower the relative concentration of gonococcal-specific Ab. However, considering that some of the Ig will bind the bacteria, the relative benefit of a polyspecific Ig response to the infecting pathogen versus the host remains a matter of ongoing debate (71).…”

The Experimental Model of the Autoimmune Glomerulonephritis Induced by the Chronic Graft versus Host Reaction

“…Indeed, the development of chronic GVHD is accompanied by a marked polyclonal activation of B-lymphocytes, which is known to impede an adequate response to new stimulus (Reina-San-Martin et al, 2000;Spera et al, 2006;Montes et al, 2007;Marques et al, 2008). At the same time a decrease of the secondary immune response is less marked especially in the lupus recipients (Fig.…”

Neisseria lactamicaSelectively Induces Mitogenic Proliferation of the Naive B Cell Pool via Cell Surface Ig

“…Induction of polyclonal B cell proliferation by microbial colonizers and the hypergammaglobulinemia that ensues is most often associated with pathology in the host, including immunosuppression (27) and autoimmunity (28). Although the role of this response is still debated, it is widely believed that the induction of polyclonal B cell proliferation can be a strategy used by pathogens to evade specific immune effector mechanisms (29,30).…”