T-cell receptor-specific monoclonal antibodies against a V ? 11-positive mouse T-cell clone

Abstract

Two monoclonal antibodies specific for the mouse T-cell receptor (Tcr) have been established by immunization with a V beta 11+ T-cell clone, clone C6. One is a rat antibody, KT11 (IgG2b, k), specific for the V beta chain of C6, V beta 11. This was demonstrated by the fact that the strain distribution pattern of KT11+ cells was similar to that of V beta 5, 8, 9, 11, 12, and 13 and that the gene that encodes the molecule detected by KT11 was closely linked to V beta 8 in (B10 X SJL)F1 X SJL backcross mice. Furthermore, V beta of C6 has been cloned from a lambda gt10 cDNA library and was demonstrated to be identical to the V beta 11 published sequences. All strains of mice that do not express major histocompatibility complex class II E molecules had higher numbers of KT11+ cells than E+ strains. The KT11+ population in A strain mice and its H-2 congenic strains, however, was not affected by the presence or absence of E molecules. The other is a mouse antibody, KTL2 (IgM), specific for the idiotope of the Tcr expressed on the clone C6. Both antibodies were mitogenic and induced cytotoxicity. Expression of epitopes detected by KT11 or KTL2 was down-modulated by a T3 epsilon-specific antibody 145-2C11.

Mls-1-like superantigen in the MA/MyJ mouse is encoded by a new mammary tumor provirus that is distinct from Mtv-7.

“…These investigators also observed that V/$6 and V~8.1 T cells respond to Mls-1 stimulation in vitro (3,4). Similar results were obtained with other endogenous SAG (5)(6)(7)(8)(9). The genetic mapping of a V~5-tolerizing element close to the murine mammary tumor provirus (MMTV) Mtv-9 provided a hint of the molecular nature of the endogenous SAG (10).…”

Dendritic Cell–Dependent In Vivo Generation of Autoregulatory T Cells by Antidiabetogenic MHC Class II

“…The finding that thymocytes expressing Vb5, Vb11, Vb16, or Vb17a elements undergo central and/or peripheral deletion in I-Ea d or IEa k -transgenic mice suggested that I-E might afford T1D resistance by triggering the deletion of certain key autoreactive T cell specificity/ies via endogenous superantigens (14,(48)(49)(50)(51). Subsequent reports, however, provided evidence that argued against this view (16,17).…”

A nondeletional mechanism of peripheral tolerance in T-cell receptor transgenic mice.

“…The majority of CD3+ lymphocytes reacted with the V11-specific antibody, KT11. In normal mice, <4% oflymph node cells were detected by this antibody (16).…”

“…Purified a and /B constructs were microinjected together into fertilized (CBA x B1O.BR)F2 eggs, as previously described (5). Transgenic mice were identified by Southern hybridization using a V08 probe (13) and by flow cytometry on peripheral blood lymphocytes, using a monoclonal anti-Vp311 antibody, KT11 (16). The transgenic lines, termed F3 after the CTL clone from which the TCR genes were derived, were maintained by repeated crossing to the bml strain.…”

“…Peripheral blood lymphocytes were collected from nontransgenic or F3 transgenic mice of the 131-7 line crossed to bml mice. The cells were allowed to react with monoclonal antibodies to V11 (16) (16) or to CD3 (18), washed, and allowed to react with the fluorochromeconjugated monoclonal antibodies anti-CD8 and anti-CD4 (Becton Dickinson) and with Texas red-conjugated streptavidin (Caltag, South San Francisco, CA). After further washing, the cells were analyzed on a FACStar+ (Becton Dickinson).…”