Influence of FCRN expression on lung decline and intravenous immunoglobulin catabolism in common variable immunodeficiency patients
| Authors | |
|---|---|
| Year of publication | 2014 |
| Type | Article in Periodical |
| Magazine / Source | Clinical & Experimental Immunology |
| MU Faculty or unit | |
| Citation | |
| Doi | http://dx.doi.org/10.1111/cei.12529 |
| Field | Immunology |
| Keywords | FCRN; intravenous immunoglobulin catabolism |
| Description | The neonatal Fc receptor (FcRn) was first described as a receptor-mediating transplacental immunoglobulin (Ig)G transfer from mother to fetus, but it has other significant biological functions. It plays a key role in IgG and albumin homeostasis by efficient protection from catabolism [1]. It binds endocytosed IgG at acidic pH (< 6·5) within endosomes, diverts it from degradation in lysosomes and instead transports the IgG–FcRn complexes back to the cell surface where, at neutral pH (> 7·0), IgG is released [1]. This process is highly efficient; FcRn recycles an equivalent amount of albumin and even four times as much IgG as can be produced in a given time [2,3]. |