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Role of T Cells in the Mitogen‐Induced Proliferation and Polyclonal Antibody Response of Murine B Cells
Author(s) -
Ishikawa Hiromichi,
Saito Kazuhisa
Publication year - 1981
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.1348-0421.1981.tb00123.x
Subject(s) - biology , colcemid , microbiology and biotechnology , lipopolysaccharide , b 1 cell , polyclonal antibodies , naive b cell , bone marrow , antibody , b cell , immunology , t cell , immune system , antigen presenting cell , mitosis
The effect of thymus‐derived lymphocytes (T cells) on the responsiveness of bone marrow‐derived lymphocytes (B cells) to bacterial lipopolysaccharide (LPS) was determined in in vitro experiments. Radiation resistant splenic T cells obtained from euthymic nu/+ mice increased the number of proliferating cells in the cultures of splenic B cells from athymic nu/nu mice even in a nonstimulated state. The radiation resistant T cells augmented significantly the responsiveness of B cells to LPS, as determined by an increase in proliferating cells and polyclonally induced anti‐sheep erythrocyte (SRBC) IgM hemolysin plaque‐forming cells (PFC). Addition of the T cells to B cell cultures not only augmented the responsiveness of B cells to suboptimal doses of LPS but also enabled B cells to respond to supraoptimal doses of LPS. As is well documented, the radiation resistant T cells were unable to induce the generation of anti‐SRBC PFC in B cell cultures, unless the cultures were simultaneously stimulated with SRBC. Colcemid, a specific inhibitor of cell mitosis, blocked almost completely the exponential generation of anti‐SRBC PFC in B cell cultures responding to SRBC with the aid of radiation resistant T cells. In contrast, colcemid did not affect the exponential generation of anti‐SRBC PFC of a polyclonal nature in B cell cultures responding to LPS, either in the presence or absence of radiation resistant T cells.