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Xenoantisera directed against the proliferating T-cells of MRL/Mp-lpr/lpr mice
MRL/Mp-lpr/lpr (lpr/lpr) mice develop a generalized lymph node (LN) hypertrophy reflecting the expansion of a T-cell subset that seems to act as an accelerating factor for autoimmunity. In an attempt to produce antisera specific for this T-cell subset, NZW rabbits and Lewis rats were hyperimmunized with cells from hypertrophied lpr/lpr LN. The resulting xenoantisera were extensively absorbed with lymphoid cells from the congenic MRL/Mp +/+ (+/+) strain. As assessed by complement-dependent microcytotoxicity and indirect immunofluorescence using flow cytofluorometry analysis, these xenoantisera reacted with 70-90% of the cells in the enlarged LN of 4-month-old lpr/lpr mice but only with 10-35% of the cells in the normal-sized LN of age-matched +/+ mice or of 2-month-old lpr/lpr mice. These xenoantisera which appear to identify surface antigens associated with the proliferating lpr/lpr T-cells may prove useful to investigate the mechanism by which these cells contribute to the autoimmune disease of lpr/lpr mice.
MRL/Mp-lpr/lpr (lpr/lpr) mice develop a generalized lymph node (LN) hypertrophy reflecting the expansion of a T-cell subset that seems to act as an accelerating factor for autoimmunity. In an attempt to produce antisera specific for this T-cell subset, NZW rabbits and Lewis rats were hyperimmunized with cells from hypertrophied lpr/lpr LN. The resulting xenoantisera were extensively absorbed with lymphoid cells from the congenic MRL/Mp +/+ (+/+) strain. As assessed by complement-dependent microcytotoxicity and indirect immunofluorescence using flow cytofluorometry analysis, these xenoantisera reacted with 70-90% of the cells in the enlarged LN of 4-month-old lpr/lpr mice but only with 10-35% of the cells in the normal-sized LN of age-matched +/+ mice or of 2-month-old lpr/lpr mice. These xenoantisera which appear to identify surface antigens associated with the proliferating lpr/lpr T-cells may prove useful to investigate the mechanism by which these cells contribute to the autoimmune disease of lpr/lpr mice.