IgG4-Related Fibrotic Diseases from an Immunological Perspective: Regulators out of Control?
Figure 1
Proposed model of B-cell infiltration into affected tissue. (a) B cells from the circulation enter the inflamed tissue. (b) Differential glycosylation of IgG4-switched B cells allows retention and activation of this cell type via an as-yet-unidentified lectin on the stellate cell. (c) In this model, the local environment of the affected tissue will further promote survival/proliferation of IgG4-switched B cells due to a tolerogenic environment that may in part be created via signals from the IgG4 B cells themselves.
