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Differential Distribution of HLA-DQ/DR Epitopes in the Two Forms of Guillain-Barré Syndrome, Acute Motor Axonal Neuropathy and Acute Inflammatory Demyelinating Polyneuropathy (AIDP): Identification of DQ Epitopes Associated with Susceptibility to and Protection from AIDP¹

Eleni E. Magira^*, Miltiadis Papaioakim, Irving Nachamkin, Arthur K. Asbury^¶, Chun Y. Li^||, Tony W. Ho^#, John W. Griffin^#, Guy M. McKhann^#,** and Dimitri S. Monos^2,*,

^* Department of Pediatrics, University of Pennsylvania School of Medicine and Children's Hospital of Philadelphia, Philadelphia, PA 19104; Department of Medicine and Laboratory of Human Biology and Genetics, Democritus University of Thrace School of Medicine, Alexandroupolis, Greece; Departments of Pathology and Laboratory Medicine and ^¶ Neurology, University of Pennsylvania School of Medicine, Philadelphia, PA 19104; ^|| Second Affiliated Teaching Hospital, Hebei Medical School Shijiazhuamg, People's Republic of China; ^# Department of Neurology, The Johns Hopkins University School of Medicine, Baltimore, MD 21287; and ^** Zanvyl Krieger Mind/Brain Institute, Baltimore, MD 21218

Guillain-Barré syndrome (GBS), an acute, immune-mediated paralytic disorder affecting the peripheral nervous system, is the most common cause of acute flaccid paralysis in the postpolio era. GBS is classified into several subtypes based on clinical and pathologic criteria, with acute inflammatory demyelinating polyneuropathy (AIDP) and acute motor axonal neuropathy (AMAN) being the most common forms observed. To better understand the pathogenesis of GBS and host susceptibility to developing the disease, the distribution of HLA class II Ags along with the seroreactivity to Campylobacter jejuni were investigated in a population of GBS patients from northern China. Using DNA-based typing methods, 47 patients with AMAN, 25 patients with AIDP, and 97 healthy controls were studied for the distribution of class II alleles. We found that the DQ RLD^55–57/ED^70–71 and DR E⁹V¹¹H¹³ epitopes were associated with susceptibility to AIDP (p = 0.009 and p = 0.004, respectively), and the DQ RPD^55–57 epitope was associated with protection (p = 0.05) from AIDP. These DQ/DR positional residues are a part of pockets 4 (DQ 70, 71, DR13), 6 (DR11), and 9 (DQ 56, 57, DR9); have been demonstrated to be important in peptide binding and T cell recognition; and are associated with other diseases that have a pathoimmunological basis. Class II HLA associations were not identified with AMAN, suggesting a different immunological mechanism of disease induction in the two forms of GBS. These findings provide immunogenetic evidence for differentiating the two disease entities (AMAN and AIDP) and focuses our attention on particular DR/DQ residues that may be instrumental in understanding the pathophysiology of AIDP.

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