Characterization of antigen-specific T cells in multiple sclerosis twins with elevated proliferative responses to measles virus

• Published in: The Journal of immunology (1950) Vol. 137; no. 2; pp. 546 - 550
• Main Authors: Greenstein, JI, McFarland, HF, Richert, JR
• Format: Journal Article
• Language: English
• Published: Bethesda, MD Am Assoc Immnol 15-07-1986; American Association of Immunologists
• Subjects: Antigen-Presenting Cells - immunology; Autoimmunity (experimental aspects and models); Biological and medical sciences; Dose-Response Relationship, Immunologic; Epitopes; Fundamental and applied biological sciences. Psychology; Fundamental immunology; HLA Antigens - analysis; Humans; Interleukin-2 - biosynthesis; Lymphocyte Activation; measles virus; Measles virus - immunology; Multiple Sclerosis - genetics; Multiple Sclerosis - immunology; Phenotype; T-Lymphocytes - classification; T-Lymphocytes - immunology; T-Lymphocytes - metabolism; Twins; Autoimmunity; Human; Cell proliferation; Multiple sclerosis; Immune regulation; Mechanism; Paramyxoviridae; Infection; Virus; Antigen; Characterization; Specificity; Viral disease; Measles; T-Lymphocyte; Morbillivirus; Mumps; Mumps paramyxovirus; Paramyxovirus; Measles virus
• ISSN: 0022-1767; 1550-6606
• DOI: 10.4049/jimmunol.137.2.546

The proliferative response to measles virus in normal individuals is low compared with the response to mumps virus. This is probably due to a low precursor frequency of OKT4+, IL 2-secreting helper cells. The presence of a measles high-responder state has previously been identified in some twin individuals with multiple sclerosis. Further characterization of the measles response in these high-responder individuals has demonstrated that the enhanced measles responses are due to a greater response by OKT4+ cells, which secrete higher levels of IL 2; this contrasting with the low levels of IL 2 secretion and OKT4+ cell proliferation seen in the unaffected twins. No evidence for suppression by either accessory or T cells, which would account for the quantitative differences between the high responders with multiple sclerosis and their unaffected low-responder twin siblings, was detected. The results indicate that a clonally expanded population of measles-specific responder cells is responsible for the high-responder state in these twins with multiple sclerosis. The mechanism producing this state may have relevance to possible immunoregulatory abnormalities producing autoimmunity in multiple sclerosis.