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Department of Molecular Immunology, Medical Institute of Bioregulation, Kyushu University, Higashi-Ku, Fukuoka, Japan The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
Lyn kinase-deficient (lyn-/-) mice
show several abnormalities such as reduced numbers of circulating B
cells, hyper-IgM, and low proliferative responses induced by CD40
ligand. Lyn-/- mice also develop
splenomegaly, produce autoreactive Abs with age, and finally develop
glomerulonephritis. Another abnormality observed in
lyn-/- mice is that their disability to form
germinal centers (GCs). It has been considered that GCs play an
important role in affinity maturation and differentiation to B cell
memory upon immunization with thymus-dependent Ag. Since Lyn kinase has
been thought to be downstream of the signals from the B cell Ag
receptor as well as CD40, we studied whether or not
lyn-/- mice could exhibit normal Ag-specific
class switching and affinity maturation following somatic
hypermutation. The mice were immunized with
(4-hydroxy-3-nitrophenyl)acetyl-chicken 
-globulin (NP-CG).
Production of NP-specific IgG1 Abs was slightly reduced but clearly
detectable. The affinity of Abs produced was comparable to that in
wild-type mice. Furthermore, somatic hypermutation occurred in the
heavy-chain variable region at the same level as that in wild-type
mice. Therefore, we conclude that isotype switching and affinity
maturation occur normally in lyn-/- mice
without the formation of GCs. The results lead to a speculation that
Lyn may not play a role in induction of isotype switching or affinity
maturation, despite being downstream of the signals from the B cell Ag
receptor complex and CD40, and that GC architecture may not be
absolutely essential for affinity maturation.
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