Perhaps a more popular theory is that the immunosuppressive effects of immunoglobulin therapy are mediated through IgG's Fc glycosylation. By binding to receptors on antigen presenting cells, IVIG can increase the expression of the inhibitory Fc receptor , FcgRIIB and shorten the half-life of auto-reactive antibodies.    The ability of immunoglobulin therapy to suppress pathogenic immune responses by this mechanism is dependent on the presence of a sialylated glycan at position CH2- of IgG.  Specifically, de-sialylated preparations of immunoglobulin lose their therapeutic activity and the anti-inflammatory effects of IVIG can be recapitulated by administration of recombinant sialylated IgG1 Fc. 
Data from a small prospective study support the use of rituximab (in combination with IV immune globulin) in patients with pemphigus vulgaris that was refractory to multiple lines of therapy, including systemic corticosteroids and with minimal response to IV immune globulin alone [Ahmed 2006] . Clinical experience and data from retrospective studies also suggest the utility of rituximab in the management of refractory pemphigus vulgaris [Cholera 2016] , [El Tal 2006] , [Kasperkiewicz 2011] . Additional data may be necessary to further define the role of rituximab in this condition.