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Effect of Passive Administration of Alloantiserum Containing Antibody against Putative Acceptor(s) for T Cell‐Replacing Factor (TRF) in the Neonatal Stage on Development of B Cell Activity Responsive to TRF
Author(s) -
Hashimoto Yasuhiro,
Tsukada Satoshi,
Hamaoka Toshiyuki,
Sano Yoshimi,
Koyama Nobuo,
Takatsu Kiyoshi
Publication year - 1986
Publication title -
microbiology and immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.664
H-Index - 70
eISSN - 1348-0421
pISSN - 0385-5600
DOI - 10.1111/j.1348-0421.1986.tb00920.x
Subject(s) - antiserum , antibody , biology , antigen , microbiology and biotechnology , b cell , balb/c , cell , immunology , medicine , endocrinology , immune system , biochemistry
Previously, we showed that the antiserum raised in male (DBA/2Ha × BALB/c)F 1 (DCF 1 ) mice (T cell‐replacing factor [TRF]‐low response animals) by immunizing them with activated B cells from BALB/c mice (TRF‐high‐responders) contained antibodies against putative TRF‐acceptor site(s). We have now evaluated the hypothesis that neonatal treatment of mice with the above antiserum suppresses the development of B cells responsive to TRF. Male DCF 1 mouse anti‐BALB/c B‐cell antiserum or normal DCF 1 mouse serum as a control was injected into BALB/c mice within 24 hr after birth. In the antiserum‐treated mice, no augmented primary immunoglobulin M (IgM) antibody responses to sheep red blood cells (SRBC) were observed under the conditions in which markedly augmented IgM anti‐SRBC responses were induced in control BALB/c mice, suggesting that development of B cells reacting with male DCFi mouse anti‐BALB/c B‐cell antiserum is suppressed by the neonatal treatment with the antiserum. Furthermore, the development of B cell activity responsible for helper factors derived from T cells, such as TRF, was markedly suppressed in the neonatally antiserum‐treated mice, whereas activity of B cells capable of interacting directly with helper T cells through antigen‐bridges was not significantly affected by the same treatment. Such suppression of the B cell activity could be induced only when the antiserum was administered within 48 hr after birth. Moreover, neonatal treatment of mice with the antiserum induced suppressed responsiveness of B cells to a T‐independent type 2 antigen, TNP‐Ficoll. Neither serum‐borne suppressive serum components nor suppressor cells were detected by the system employed. These results support the hypothesis that TRF responsive B cells constitute a subpopulation distinct from the other B cells capable of cooperating with helper T cells via cognate interaction.