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NEUROLOGY 1998;51:379-384
© 1998 American Academy of Neurology

HLA and T-cell receptor gene polymorphisms in Guillain-Barré syndrome

J. J. Ma, MD, M. Nishimura, MD, H. Mines, BS, S. Kuroki, MD, M. Nukina, DVM, M. Ohta, PhD, H. Saji, PhD, H. Obayashi, PhD, T. Saida, MD, H. Kawakami, MD and T. Uchiyama, MD

From the Department of Neurology and Clinical Research Center (Drs. Ma, Nishimura, Ohta, Saida), Utano National Hospital, Kyoto; Kyoto Red Cross Blood Center (Drs. Mine and Saji); Kyoto Microbiological Institute (Dr. Obayashi); Department of Pediatrics (Dr. Kuroki), Kobe City General Hospital, Public Health Research Institute of Kobe City (Dr. Nukina); Third Department of Internal Medicine (Dr. Kawakami), Hiroshima University School of Medicine, Hiroshima; and Virus Research Institute (Dr. Uchiyama), Kyoto University, Kyoto, Japan.

Address correspondence and reprint requests to Dr. M. Nishimura, Department of Neurology and Clinical Research Center, Utano National Hospital, Ukyo-ku, Kyoto 616, Japan.

Objective: We examined a possible involvement of genetic factors influencing the development of Guillain-Barré syndrome (GBS).

Methods: We studied T-cell receptor (TCR), alpha-chain constant (AC), and beta-chain variable (BV) gene polymorphisms using microsatellite markers and serologic HLA class I antigens, HLA-DRB1, and HLA-DQB1 alleles in 81 Japanese patients with GBS and 87 controls.

Results: There were no significant differences in these genetic markers between GBS patients and controls. Subgrouping of GBS patients according to recent Campylobacter jejuni infection, the presence of anti-GM1 antibody in the sera, or their combinations also failed to reveal significant associations with these genetic markers. There was, however, a tendency for an increased frequency of HLA-DRB1*0803 in the C. jejuni + GM1 + GBS group, when compared with controls.

Conclusions: The data suggest that the roles of TCRAC, T-cell receptor beta-chain variable (TCRBV), HLA class I or class II in the development of GBS are not critical, and further research is necessary to clarify other genes encoded within the HLA region for genetic susceptibility to GBS.

Received December 15, 1997. Accepted in final form March 17, 1998.




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