Neuritogenic Lewis rat T cells use Tcrb chains that include a new Tcrb-V8 family member.
Publication/Presentation Date
1-1-1994
Abstract
The P2 protein obtained from Schwann cells induces a population of T cells which, upon adoptive transfer, causes the disease experimental allergic neuritis (EAN), an animal model for Guillain-Barre syndrome. In this report, a truncated peptide, FR22, derived from a previously reported neuritogenic T-cell determinant, was used to generate from Lewis rats T cells that were shown to cause EAN. Since our previous studies showed that Tcrb-V8 was used by a majority of T-cell hybridomas specific for the neuritogenic peptide P26, which contains the FR22 sequence, we sequenced the Tcrb-V8+ mRNA from FR22-specific T-cell lines, and compared the sequences obtained with those obtained from similarly generated myelin basic protein (MBP) 68-88-specific Lewis rat T-cell lines. We found that in the EAN lines, several members of the Tcrb-V8 family were used, including a new family member, Tcrb-V8E. This was more diverse than the MBP-68-88-specific response in which only a single Tcrb-V8 family member was used. Also, in the EAN lines, the beta chain sequences did not show the same conserved junctional regions seen in the MBP lines. Thus, T-cell receptor beta chain usage in the response to this dominant neuritogenic peptide appears to be less restricted than the response to the dominant encephalitogenic determinant of MBP both in V region usage and in CDR3 usage.
Volume
40
Issue
4
First Page
266
Last Page
270
ISSN
0093-7711
Published In/Presented At
Zhang, X. M., Esch, T. R., Clark, L., Gregorian, S., Rostami, A., Otvos, L., Jr, & Heber-Katz, E. (1994). Neuritogenic Lewis rat T cells use Tcrb chains that include a new Tcrb-V8 family member. Immunogenetics, 40(4), 266–270. https://doi.org/10.1007/BF00189971
Disciplines
Business Administration, Management, and Operations | Health and Medical Administration | Management Sciences and Quantitative Methods
PubMedID
7521858
Department(s)
Administration and Leadership
Document Type
Article