Self‐Reactivity and the Expression of Memory MarkersVary Independently in MRL‐Mp+/+ and MRL‐Mp‐lpr/lprMice

Abstract

exhibit an SLE-like autoimmune disease in which autoantibodies are a prominent feature. We analyzed the phenotype and T-cell receptor V]/ expression pattern in CD4 T cells of this mutant mouse strain to detect abnormalities that could explain the autoimmunity. The CD4 T cells contain two distinct abnormal populations. One of these expresses B220 and HSA, and in these and other respects closely resembles the accumulating CD4-CD8-population. The other expresses a high level of CD44 (Pgp-1), and a high level of the 16A epitope of CD45, and so resembles post-activation T cells. Both of these cell types are exclusive to MRL-Mp-lpr/lpr. We also identified V]/5-and V]/11-positive CD4+ T cells, in both MRL-Mp-lpr/lpr and MRL-Mp-+/+ mice. We conclude that autoimmune T cells can be detected in these mice, but that they are not the cause of the accumulation of abnormal CD4 and CD4-CD8-cells.

In vivo persistence of expanded clones specific for bacterial antigens within the human T cell receptor alpha/beta CD4-8- subset.

“…Indeed, when isolated from the blood, the expanded clones express high levels of ol4/31 integrins and low levels of t-selectin and CD31, a phenotype that has been attributed to memory T ceils (37,38). This phenotype resembles that of cx/3 DN cells in autoimmune MRL-Mplpr/Ipr mice (45) or in transgenic mice, where od3 DN ceils expand and persist in the presence of a self-antigen (9).…”

From T to B and back again: positive feedback in systemic autoimmune disease

“…However, it is now clear that in many situations central lymphocyte selection is similar in normal mice and in mouse strains that develop spontaneous autoimmunity [10][11][12][13][14][15] . Although this issue is still controversialcentral-tolerance defects could have a role in some situations 16 , particularly Fas (CD95) deficiency 17,18 -we emphasize here the loss of tolerance in the periphery, which we believe is the more crucial step.…”

The Roles of B Cells in MRL/lpr Murine Lupus

“…The mechanism behind the phenomenon remains to be determined, as does the Ag specificity of the activated T cells. As these cells were previously shown to be polyclonal and not particularly skewed in terms of Vβ family expression, 38,43,44 it seems unlikely that superantigens, as are known to be expressed on B cells, are responsible. It is also unclear why this phenomenon is Fas‐dependent.…”