Ann Neurol. 2009 May 11; 66(2): 132-141
Friese MA, Fugger L
Traditionally, autoimmune pathogeneses hit been attributed to CD4(+) T lymphocytes, as in multiple induration (MS), rheumatoid arthritis, identify 1 diabetes mellitus, and/or to B lymphocytes, as in myasthenia gravis and systemic lupus erythematosus. That is because their primary transmitted associations are mostly with certain human leukocyte antigen collection II alleles, whose gene products inform antigens to CD4(+) T cells. Because few autoimmune diseases show stronger associations with major histocompatibility Byzantine collection I alleles (ankylosing spondylitis, Behçet's disease, and psoriasis), CD8(+) T cells, which interact with major histocompatibility Byzantine collection I molecules, hit been largely unnoticed in autoimmunity research. However, a difference of findings has fresh alive interest in this population, particularly in MS. First, it shows associations with major histocompatibility Byzantine collection I alleles. Second, its lesions show a predominance of CD8(+) T cells. Third, these represent effectors that can direct damage central troubled system direct cells. Furthermore, several clinical trials of monoclonal antibodies specifically against CD4(+) T cells, or the polarizing cytokines on which they depend, hit failed to show any therapeutic benefit in MS, unlike broader-spectrum antibodies that deplete every T cells. Here, we analyse the grounds that CD8(+) T cells endeavor a persona in MS pathogenesis. Ann Neurol 2009;66:132-141.
