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B cell development in mice with a defective λ 5 gene
Author(s) -
Rolink Antonius,
Karasuyama Hajime,
Grawunder Ulf,
Haasner Dirk,
Kudo Akira,
MeLchers Fritz
Publication year - 1993
Publication title -
european journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.272
H-Index - 201
eISSN - 1521-4141
pISSN - 0014-2980
DOI - 10.1002/eji.1830230614
Subject(s) - biology , b cell , cd5 , microbiology and biotechnology , bone marrow , stromal cell , cd43 , immunoglobulin light chain , immunology , antibody , cancer research , cd20
Abstract The surrogate light chain encoded by the two pre‐B cell‐specific genes V preB and λ 5 plays a critical role in B cell development of the mouse. It has been shown that targeted disruption of the λ 5 gene results in a depletion of B220 + CD43 − IgM − pre‐B cells in bone marrow, and in a delayed appearance both of CD5 + as well as CD5 − surface immunoglobulin (slg) + B cells in the periphery. In this report we show that D H J H ‐rearranged B220 − and B220 + , CD43 + , c‐kit + , sIgM − pro‐ and pre‐B‐I cells with long‐term capacity to proliferate in vitro on stromal cells in the presence of interleukin‐7 are present in normal numbers in the bone marrow of λ 5 T/λ. 5 T mice at various ages. They express normal levels of V preB mRNA but, in contrast to normal pre‐B‐I cells, do not express surrogate light chain on their surface. Pre‐B‐I cells from fetal liver and bone marrow of λ 5 T/λ 5 T mice differentiate with normal kinetics and in normal numbers to sIg + , mitogen‐reactive B cells. These results suggest that the delayed generation of sIg + B cells in the peripheral, mature compartments of CD5 + and CD5 − cells could be accounted for by the daily production of approximately 5 × 10 5 sIg + B cells from the pre‐B‐I cell pool in the absence of a normal pool of pre‐B‐II cells.