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B Cell Memory in xid Mice is Long‐Lived Despite Reduced Memory B Cell Frequency
Author(s) -
RIDDERSTAD A.,
TARLINTON D. M.
Publication year - 1997
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1046/j.1365-3083.1997.d01-444.x
Subject(s) - bruton's tyrosine kinase , b cell , memory b cell , immune system , memory cell , antibody , immunology , antigen , immunization , naive b cell , cell , biology , t cell , tyrosine kinase , microbiology and biotechnology , genetics , antigen presenting cell , signal transduction , physics , transistor , voltage , quantum mechanics
Brutons tyrosine kinase (Btk) deficient xid mice have a diminished primary T cell dependent immune response, resulting in a reduced memory B cell frequency. Boosting at 35 days post primary immunization, however, generates a normal secondary immune response, indicating a functional memory B cell compartment. The longevity of B cell memory appears to depend on both the presence of antigen and expression of cell survival genes such as bcl‐2 . Since there is a natural decay in the number of memory B cells over time and since xid B cells have been demonstrated to have reduced Bcl‐2 levels, we aimed at determining whether B cell memory of xid mice would be long‐lasting. This report demonstrates that memory B cell precursors are detectable in xid mice more than 100 days after primary immunization. Furthermore, a secondary immune response of normal magnitude and kinetics can be generated in xid mice at 150 days after primary immunization indicating that B cell memory is long‐lived in xid mice. Thus, although survival of B cell memory is presumably dependent on immunoglobulin (Ig)‐mediated interaction with antigen, this interaction does not depend solely on signalling through Btk.