TY - JOUR
T1 - Concomitant enhancement of the response to Mls-1a antigens and the induction of post-thymectomy autoimmune gastritis in BALB/c mice
AU - Murakami, K.
AU - Hosono, M.
AU - Murayama, H.
AU - Mori, Y.
AU - Nishio, A.
AU - Fukumoto, M.
AU - Watanabe, Y.
AU - Inaba, M.
AU - Kuribayashi, K.
AU - Sakai, M.
AU - Masuda, T.
PY - 1993
Y1 - 1993
N2 - We examined the role of Mls antigens in the induction of autoimmune gastritis (AIG) in BALB/c and DBA/2 mice subjected to thymectomy. The prevalence of AIG in Mls-1b mice which underwent thymectomy on day 3 after birth (3d-Tx) was 78% (mean), while in Mls-1a DBA/2 mice it was < 6%. Whereas AIG-negative 3d-Tx DBA/2 mice produced 2-mercaptoethanol (2-ME)-sensitive antiparietal cell autoantibody, AIG-positive BALB/c mice made 2-ME-resistant anti-parietal cell autoantibody. In addition, the prevalence of AIG in 3d-Tx BALB/c mice which were rendered tolerant to Mls-1a antigens by injection of bone marrow cells from (BALB/c x DBA/2)F1 mice within 24 h after birth was decreased compared with the non-tolerant control mice; the prevalence being 80% in the controls and 30% in the tolerant animals. Thus, the activation of helper T cells, including T cells responding to Mls-1a antigens and including immunoglobulin class switch, appeared to be closely associated with the induction of AIG. Flow cytometric analysis confirmed that CD4-Vβ6 T cells had increased in the regional lymph nodes of the stomach in AIG mice. However, an increase in the number of Vβ11 T cells, which are known to increase in 3d-Tx mice, occurred in the CD8, but not in the CD4 T cell population. Injection of MoAb to L3T4, but not Lyt2, Vβ6- or Vβ8-TCR, into 3d-Tx BALB/c and syngeneic nude mice which had received spleen cells of 3d-Tx BALB/c mice bearing AIG completely abrogated the development of AIG, despite there being remarkable decreases in T cells expressing relevant markers to the injected antibodies in all the mice. These findings suggest that the increase of Vβ6+ L3T4+ T cells in AIG mice was concomitant with the activation of AIG-inducing Vβ6- L3T4+ T cells.
AB - We examined the role of Mls antigens in the induction of autoimmune gastritis (AIG) in BALB/c and DBA/2 mice subjected to thymectomy. The prevalence of AIG in Mls-1b mice which underwent thymectomy on day 3 after birth (3d-Tx) was 78% (mean), while in Mls-1a DBA/2 mice it was < 6%. Whereas AIG-negative 3d-Tx DBA/2 mice produced 2-mercaptoethanol (2-ME)-sensitive antiparietal cell autoantibody, AIG-positive BALB/c mice made 2-ME-resistant anti-parietal cell autoantibody. In addition, the prevalence of AIG in 3d-Tx BALB/c mice which were rendered tolerant to Mls-1a antigens by injection of bone marrow cells from (BALB/c x DBA/2)F1 mice within 24 h after birth was decreased compared with the non-tolerant control mice; the prevalence being 80% in the controls and 30% in the tolerant animals. Thus, the activation of helper T cells, including T cells responding to Mls-1a antigens and including immunoglobulin class switch, appeared to be closely associated with the induction of AIG. Flow cytometric analysis confirmed that CD4-Vβ6 T cells had increased in the regional lymph nodes of the stomach in AIG mice. However, an increase in the number of Vβ11 T cells, which are known to increase in 3d-Tx mice, occurred in the CD8, but not in the CD4 T cell population. Injection of MoAb to L3T4, but not Lyt2, Vβ6- or Vβ8-TCR, into 3d-Tx BALB/c and syngeneic nude mice which had received spleen cells of 3d-Tx BALB/c mice bearing AIG completely abrogated the development of AIG, despite there being remarkable decreases in T cells expressing relevant markers to the injected antibodies in all the mice. These findings suggest that the increase of Vβ6+ L3T4+ T cells in AIG mice was concomitant with the activation of AIG-inducing Vβ6- L3T4+ T cells.
KW - Mls antigen
KW - autoantibody
KW - autoimmune disease
KW - gastritis
KW - thymectomy
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U2 - 10.1111/j.1365-2249.1993.tb03428.x
DO - 10.1111/j.1365-2249.1993.tb03428.x
M3 - Article
C2 - 8513582
AN - SCOPUS:0027266874
VL - 92
SP - 500
EP - 505
JO - Clinical and Experimental Immunology
JF - Clinical and Experimental Immunology
SN - 0009-9104
IS - 3
ER -