Effects of allotype specific anti-IgD on the immune responses of homozygous mice.
Effects of allotype specific anti-IgD on the immune responses of homozygous mice.
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同种异型特异性抗 IgD 对纯合小鼠免疫反应的影响。
DOI:
10.1111/j.1749-6632.1982.tb25683.x
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发表时间:
1982
影响因子:
5.2
通讯作者:
Jacobson,EB
中科院分区:
文献类型:
--
作者:
Thorbecke,GJ;Baine,Y;Xue,B;Chen,YW;Pernis,B;Siskind,GW;Jacobson,EB
In previous studies' on mice treated with anti-IgD from birth we found no suppression of primary or secondary responses to trinitrophenylated B. abortus (TNP-BA) injected intravenously (iv 1. This was considered surprising in view of the low numbers of Ig-bearing cells present in the spleens of such anti-IgD treated mice. Primary responses to other antigens including TNP-hernocyanin (TNP-KLH] or TNP-ficoll were also found to be, if anything, enhanced rather than suppressed in spite of the virtual absence of IgD+ B-cells (TABLE 1). The presence of normal immune responses to TNP-ficoll, a response usually attributed to Lyb5+ cells? prompted us to determine, in collaboration with R. Skelly and A. Ahmed (Merck Institute, Rahway, NJ], whether Lyb5+ cells were present among the approximately 2-10% Ig+ cells found in the spleen of anti-IgD treated mice. A relatively high percentage of Lyb5+ cells was found? In addition, histological observations of the lymphoid tissues of the anti-IgD treated mice showed the presence of germinal centers which had a normal mitotic rate, blast cell content, and affinity for peanut even though the dense lymphocyte coronas, normally present next to each germinal center, were lacking. IgD+ cells could be detected in the coronas of normal mice by immunoperoxidase (PAP) staining,'.'~~ but were absent in the suppressed mice. Similar findings have been reported by others.'-'It was concluded that the deficiency in recirculating IgD+ B-cells did not affect responses to intravenously injected antigens, and that the difference in B-cell maturation and/or proliferation between normal and anti-IgD suppressed mice was primarily quantitative, possibly because the deficiency in IgD+ B-cells, at least in the spleen, was compensated for by enhanced representation of IgM+ IgD-B-cells.