OX-40 antibody enhances for autoantigen specific Vβ8.2+ T cells within the spinal cord of lewis rats with autoimmune encephalomyelitis

✍ Scribed by A. D. Weinberg; M. Lemon; A. J. Jones; M. Vainiene; B. Celnik; A. C. Buenafe; N. Culbertson; A. Bakke; A. A. Vandenbark; H. Offner

• Book ID: 102911624
• Publisher: John Wiley and Sons
• Year: 1996
• Tongue: English
• Weight: 836 KB
• Volume: 43
• Category: Article
• ISSN: 0360-4012
• DOI: 10.1002/jnr.490430105

✦ Synopsis

Abstract

The Vβ8.2 T cell receptor (TCR) component is the predominant Vβ gene product associated with antigen specific CD4^+^ T cell response to the major encephalitogenic epitope of myelin basic protein (MBP) in Lewis rats. Lewis rats were actively immunized with MBP in complete Freund's adjuvant and the Vβ8.2 positive and negative cells were analyzed for IFN‐γ mRNA production and OX‐40 cell surface expression during the onset of EAE. The Vβ8.2^+^ T cells isolated from the spinal cord produced the majority of mRNA for IFN‐γ and also showed a marked enhancement for OX‐40 expression compared to Vβ8.2^+^ T cells isolated from the lymph nodes. Only a fraction of IL‐2 receptor positive T cells examined ex vivo from the inflammatory compartments co‐expressed the OX‐40 antigen. These results suggested that OX‐40 cell surface expression could be used to identify and isolate the most recently activated T cells ex vivo. OX‐40^+^ T cells isolated from the spinal cord were highly enriched for the Vβ8.2 T cell receptor component compared to OX‐40^−^ or unsorted spinal cord lymphocytes. OX‐40^+^ T cells isolated from the spinal cord had an enhanced response to MBP, whereas OX‐40^+^ cells isolated from the lymph nodes responded to both MBP and purified protein derivative. These data suggest that activated T cells can be isolated and characterized with the OX‐40 antibody which only respond to the antigens present at the local site. The data also imply that isolation of OX‐40^+^ T cells will be useful in identifying Vβ biases and autoantigen specific cells within inflamed tissues even when the antigen specificity is unknown. © 1996 Wiley‐Liss, Inc. This article is a US Government work and, as such, is in the public domain in the United States of America