Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

Patients with autoantibodies which target neuronal proteins can have pain as an under-recognised clinical manifestation.

Clinical characterization of leucine-rich glioma-inactivated 1 antibody (LGI1-Ab+) and contactin-associated protein-like 2 antibody (CASPR2-Ab+) patients with pain. (A) Representative example of live cell-based assay demonstrating HEK293T cells transfected with LGI1 or CASPR2 (green; tagged with enhanced green fluorescent protein [EGFP]) and colocalized humanimmunoglobulin G (IgG) binding (red) in patients with LGI1 antibodies, patients with CASPR2 antibodies, and a healthy control.(B) Representative example of sera from patients with LGI1 or CASPR2 antibodies, but not from healthy controls, binding to rodent hippocampal sections.

In a new study, four research groups within the Department combine their strengths in autoimmunity (Irani), pain (Bennett and Dawes) and peripheral nerve diseases (Rinaldi).

Their collective findings reveal that patients with antibodies to LGI1 and CASPR2 show different clinical, immunological and neurobiological characteristics which may relate to the antibodies differentially targeting neurons which can mediate pain.

The findings have implications for improving the long-term outcomes of these patients and for our understanding of the basic biology of these antigenic targets.

Read the paper