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A more recent version of this article appeared on December 6, 2002
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M200305200v1
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Papers In Press, published online ahead of print September 28, 2002
J. Biol. Chem, 10.1074/jbc.M200305200
Submitted on January 10, 2002
Revised on September 27, 2002
Accepted on September 28, 2002

Transitional type 1 and 2 B lymphocyte subsets are differentially responsive to antigen receptor signaling

James B. Petro, Rachel M. Gerstein, John Lowe, Robert S. Carter, Nicholas Shinners, and Wasif N. Khan

Microbiology and Immunology, Vanderbilt University School of Medicine, Nashville, TN 37232

Corresponding Author: wasif.khan{at}mcmail.vanderbilt.edu

Mature B-lymphocytes develop sequentially from transitional type 1 (T1) and type 2 (T2) precursors in the spleen. To elucidate the mechanisms that regulate the developmental fate of these distinct B cell subsets, we investigated their biochemical and biological responses following stimulation through the B-cell antigen receptor (BCR). As compared with the T1 subset, T2 cells are more responsive to BCR engagement as evidenced by their robust induction of activation markers, expression of the pro-survival protein Bcl-xL, and enhanced proliferation. BCR stimulation of T2 cells leads to the appearance of B cells with mature phenotypic characteristics, whereas T1 cells die. All of these T2 responses are dependent on the BCR signal transducer Bruton’s Tyrosine Kinase (BTK), which is dispensable for the T1 to T2 transition. Furthermore, the serine/threonine kinases extracellular signal-regulated kinase (ERK), p38 MAPK and Akt are predominantly activated in T2 compared to T1 B cells following BCR cross-linking. We conclude that T1 and T2 B cells respond differentially to BCR engagement via the induction of stage-specific signaling pathways. In turn, these signaling pathways likely govern the development and selection processes that are critical for the formation of the mature B cell compartment.


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