In homozygous mice for autosomal recessive gene,
lpr or gld, i.e., MRL/Mp-
lpr/
lpr (MRL/
lpr) or C3H/HeJ-gld/gld (C3H/
gld) mice, generalized lymphoproliferation of the aberrant L3 T4
- /Ly2
- T cells associated with systemic lupus erythematosus (SLE) -like autoimmune disease develop. To investigate the relationship between this lymphoproliferative disease and the pathogenesis of SLE, the cell surface phenotypes of the proliferating cells were analyzed with two newly established monoclonal antibodies ALP-1, ALP-2, raised against
lpr cells, using two-color flow cytometry analysis.
The Lp 1 antigen, recognized by ALP-1, was expressed exclusively on about one-half of the proliferating cells obtained from MRL/
lpr and C3H/
gld mice. The Lp 2 antigen, defined by ALP-2, was expressed on approximately 80-90% of proliferating lymph node cells, all the B cells and a population (25 %) of Ly 2
+ T cells from normal mice. Based on the distribution of Lp 1 and Lp 2 antigens, the lymph node cells from MRL/
lpr or C 3 H/
gld mice were classified into three subsets, Lp 1
+/Lp 2
+, Lp 1
-/Lp 2
+ and Lp 1 -/Lp 2 All the aberrant 1pr and
gld cells with a phenotype of L 3 T 4
-/Ly 2
- belonged to either Lp 1
+ /Lp 2
+ or Lp 1- /Lp 2 +. Since in vitro stimulation with mitogens induced either Lp 1 or Lp 2 antigen on a small population of T lymphocytes from normal mice, these antigens are related to the event of lymphocytic activation. It is possible that the phenotypically unique
lpr and
gld cells are activated and generated from a very small undefined population of normal lymphocytes.
The proliferating
lpr and
gld lymph node cells contained a significant proportion of L 3 T 4
++/Lp 2
+ T cells which were rarely found in non-
lpr/
lpr or non-
gld/
gld mice. It is important to determine whether these cells are activated normal helper T cells or originated from aberrant L 3 T 4
-/Ly 2
- cells. In addition, studies are now under way to ascertain if these cells are related to autoimmunity.
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