Download Deadline: August 31, 2006

Deadline: August 31, 2006.
ABSTRACT FROM FOR INVITED SPEAKERS
Instruction for Abstract Preparation
An abstract is requested no later than August 31, 2004.
Each abstract should include title, authors’ names and affiliations. State in the abstaract
for the purpose of the work, the materials and methods, and summarizes the results and
conclusions.
For the purpose of informing audiences a precious presentation of the Invited speaker
with more an accurate outline, we would like you to prepare the long abstract with your
cooperation. Guidelines of abstract are as follows:
•Abstract should be typed on a single-A4 paper (21x29.7 cm) with 2.5 cm (each side) x
3.5 cm (top and bottom) margins.
•Font should be “Times”.
•Abstract title should be bold, 14 point in size.
•Speaker’s name should be bold, 12 point in size with blank line below the title.
•Affiliations, city, and country are required.
•Abstract should be a Word document. Figures and Tables are expected by Jpeg, Gif or
Power Point.
•Fill in the registration form below and send it with abstract to the office by e-mail as
attached files. Send to :
More information is available on our website.
(Sample abstract)
Molecular mechanism of affinity maturation of the antigen specific
germinal center B cells during T cell-dependent antigen response
Nobuo Sakaguchi
Department of Immunology, Graduate School of Medical and Pharmaceutical Sciences,
Kumamoto University, 1-1-1 Honjo, Kumamoto 860-8556, Japan
Acquired immunity is dependent on the specificity, the isotype, and the affinity of the
antibodies against the exogenous antigens introduced into the body. Antigen-specific B
cells proliferate and differentiate in the germinal centers and express high-affinity BCR.
A 210-kDa nuclear protein GANP is inducibly expressed in germinal center B cells and
the lack of this molecule caused an impairment of generation of high-affinity BCR+ B
cells after immunization with T cell-dependent antigen, NP-chicken g-globulin. The
GANP-/- B cells showed the decreased level of DNA double strand breaks of the
corresponding V-region gene and increased transcripts of molecules involved in DNA
repair of both Rad51 (homologous recombination) and Ku80 (non-homologous
endjoining). In contrast, B cells with augmented GANP expression showed the
generation of higher antibodies in the GANP-gene transgenic (GANPTg) mouse. The
affinity increase was caused not only by the enrichment of high affinity antibody
producing cells expressing canonical VH186.2 region but also by the drastic alteration of
the V-region usage with much increased somatic hypermutations in the noncanonical
VH7183-region. Affinity measurement using BIAcore sensorgram demonstrated that of
the monoclonal antibodies established with GANPTg mice showed 10~100 fold increase
of the affinity against model antigens as NP-hapten and the peptide epitope of the V3
region of HIV.
GANP has three major domains with N-terminal RNA-primase, yeast Sac3 homology
region, and C-terminal MCM3-binding/acethylating activities, all of which suggested the
function of GANP involved in either DNA replication and RNA transcription during rapid
proliferation and differentiation of antigen-driven B cells in germinal centers. Our results
suggest the role of GANP after the DNA injury of the V-region gene, which is presumably
important in generation of high-affinity antibody.