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The Role of B7‐2 in the Regulation of T cell Activation in Multiple Sclerosis
Author(s) -
Herrera Carolina,
Rios Lillian A.,
Johnson Carol L.,
Conrad Ashley,
Dittel Bonnie N.
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.lb317
Subject(s) - multiple sclerosis , t cell , cd28 , immune system , antigen , myelin basic protein , major histocompatibility complex , microbiology and biotechnology , myelin , immunology , cytotoxic t cell , antigen presenting cell , central nervous system , biology , neuroscience , chemistry , genetics , in vitro
Multiple Sclerosis (MS) is a disease of the central nervous system that affects individuals 20 ‐ 40 years old. MS is thought to be an autoimmune disease in which T cells attack and destroy the myelin sheath surrounding neurons. Demyelinated neurons have a reduced capacity to transmit electrical impulses, causing symptoms from loss of muscle control to memory loss. One protein thought to play a role in MS is B7‐2, a member of a family of proteins that regulate T cell functions expressed by antigen presenting cells (APC). Generation of an immune response by T cells requires two signals: binding of the T‐cell receptor to the antigen/MHC complex on APC and binding of B7‐1 to CD28 on the T cells. B7‐2 is thought to be involved in suppression of the T cell response through binding to CTLA‐4. Research using the mouse model of MS, EAE, demonstrated that injection of B7‐2 specific antibodies resulted in a more severe disease course. These data suggest that B7‐2 plays a role in negative regulation of the immune response during EAE, possibly by binding CTLA‐4. To investigate how B7‐2 interacts with CTLA‐4, we developed a physical model of B7‐2 based on its crystal structure (1ncn.pdb) using 3D printing technology that highlights the protein's β sheet structure and amino acids thought to be important in CTLA‐4 binding. This model was built as a part of the SMART team program at Milwaukee School of Engineering. Supported by a grant from NIH‐NCRR‐SEPA.