Guillain–Barré Syndrome in Northern China: A Retrospective Analysis of 294 Patients from 2015 to 2020

Objectives: Acute motor axonal neuropathy (AMAN) was first reported to be the main subtype of Guillain–Barré syndrome (GBS) in northern China in the 1990s. About 30 years has passed, and it is unknown whether the disease spectrum has changed over time in northern China. We aimed to study the epidemiological, clinical, and electrophysiological features of GBS in northern China in recent years. Methods: We retrospectively analyzed the medical records of GBS patients admitted to the Second Hospital of Hebei Medical University in northern China from 2015 to 2020. Results: A total of 294 patients with GBS were enrolled, with median age 53 years and 60.5% of participants being male, and a high incidence in summer and autumn. AMAN was still the predominant subtype in northern China (40.1%). The AMAN patients had shorter time to nadir, longer hospitalization time, and a more severe HFGS score at discharge than acute inflammatory demyelinating polyneuropathies (AIDP) (p p < 0.05). In comparison with other regions, the proportion of AMAN in northern China (40.1%) was higher than in eastern (35%) and southern (19%) China. Conclusions: AMAN is still the predominant subtype in northern China after 30 years, but there have been changes over time in the GBS spectrum since the 1990s. There are regional differences in GBS in China

Development of LAG-3/FGL1 blocking peptide and combination with radiotherapy for cancer immunotherapy

Aside from antibodies, peptides show great potential as immune checkpoint inhibitors (ICIs) due to several advantages, such as better tumor penetration and lower cost. Lymphocyte-activation gene 3 (LAG-3) is an immune checkpoint which can induce T cell dysfunction through interaction with its soluble ligand fibrinogen like protein-1 (FGL1). Here, we found that LAG-3 expression was higher than programmed cell death protein 1 (PD-1) in multiple human cancers by TCGA databases, and successfully identified a LAG-3 binding peptide LFP-6 by phage display bio-panning, which specifically blocks the interaction of LAG-3/FGL1 but not LAG-3/MHC-II. Subsequently, d-amino acids were introduced to substitute the N- and C-terminus of LFP-6 to obtain the proteolysis-resistant peptide LFP-D1, which restores T cell function in vitro and inhibits tumor growth in vivo. Further, a bispecific peptide LFOP targeting both PD-1/PD-L1 and LAG-3/FGL1 was designed by conjugating LFP-D1 with PD-1/PD-L1 blocking peptide OPBP-1(8–12), which activates T cell with enhanced proliferation and IFN-γ production. More importantly, LFOP combined with radiotherapy significantly improve the T cell infiltration in tumor and elevate systemic antitumor immune response. In conclusion, we developed a novel peptide blocking LAG-3/FGL1 which can restore T cell function, and the bispecific peptide synergizes with radiotherapy to further enhance the antitumor immune response