Oral Presentations - Federation of Clinical Immunology Societies

S34 Abstracts
University, Maidashi, Japan, Tadashi Matsuda, Professor,
Department of Immunology, Graduate School of Pharmaceutical
Sciences Hokkaido University, Sapporo, Japan
Signal transducing adaptor protein-2 (STAP-2) is a recently
identified adaptor protein, which contains pleckstrin homology
(PH) and Src homology 2 (SH2)-like domains as well as a prolinerich
domain in its C-terminal region. Our previous studies have
demonstrated that STAP-2 binds to MyD88 and IKK-α/β, and
modulates NF-kappaB signaling in macrophages. In this study,
STAP-2 was induced by expression of the Epstein–Barr virus LMP1
in B cells, while overexpression of STAP-2 inhibited LMP1mediated
NF-kappaB signaling. Furthermore, STAP-2 associated
with LMP1 in EBV-positive B cells. These results strongly suggest
that STAP-2 acts as an endogenous negative inhibitor of the EBV
LMP1-mediated signaling, which is critical for the EBV persistent
infection and EBV-associated pathogenesis.
doi:10.1016/j.clim.2007.03.273
F.61 Defensins Block Bacterial Toxin-induced
Interleukin-1β Production
Jishu Shi, Assistant Professor, Anatomy, Physiology and
Pharmacology, Auburn, AL, Shelly Ao, Research Assistant,
APP, Auburn, AL, Charalabos Pathoulakis, Professor,
Gasterenterology, Boston, MA
This study was designed to test the hypothesis that
defensins can block the release of IL-1β induced by
Clostridium difficile toxin A (TxA) and Staphylococcus
aureus α-toxin (a-Tox). LPS-activated (20 ng/ml, 2 h)
human monocytes were treated with 3 nM TxA in the
presence or absence of human neutrophil defensin HNP-1
(25–50 μg/ml) or human Paneth cell defensin HD-5 (25–50
μg/ml) for 6 h. In the absence of defensins, TxAstimulated
monocytes released a large amount of mature
IL-1β (17 kDa) into the extracellular milieu. The release
of mature IL-1β from TxA-stimulated monocytes was
blocked by HNP-1 and HD-5 in a dose-dependent manner.
Different from ATP, TxA-induced IL-1β release was not
inhibited by KN-62, a P2X7 receptor antagonist. In
contrast to TxA, a-Tox (250 ng/ml) induced the release
of both proIL-1β (31 kDa) and mature IL-1β from LPSactivated
monocytes. In the presence of 20 μg/ml of
HNP-1 or HD-5, the amount of mature IL-1β released from
a-Tox-treated monocytes was reduced by 70%, while a-
Tox-induced release of proIL-1β was completely blocked.
Similar to TxA, a-Tox-induced IL-1β release was not
inhibited by KN-62. Furthermore, the release of mature
IL-1β was caspase-1-dependent for both toxins. These
data suggest that TxA- and a-Tox-induced IL-1β release is
independent of the ATP/P2X7 receptor pathway, and that
defensins can block bacterial toxin-induced posttranslational
processing and release of IL-1β. In addition to their
antimicrobial activity, defensins may play an important
role in host inflammatory response to bacterial infection
by controlling the production of IL-1β.
doi:10.1016/j.clim.2007.03.274
F.62 Lack of Association of Interleukin-8 Gene
Polymorphism with Helicobacter Pylori-induced
Gastritis in Iranian Patients
Ayda Hosseinkhani, Pharmacist, Clinical Microbiology
Research Center, Shiraz University of Medical Sciences,
Shiraz, Iran, Farshad Shohreh, Microbiologist, Clinical
Microbiology Research Center, Shiraz University of Medical
Sciences, Shiraz, Iran, Akram Jamshidzadeh, PhD, Faculty of
Pharmacy-Shiraz University of Medical Sciences, Shiraz,
Iran, Manoochehr Rasouli, PhD, Clinical Microbiology
Research Center, Shiraz University of Medical Sciences,
Shiraz, Iran, Simin Kiany, MSc, Clinical Microbiology
Research Center, Shiraz University of Medical Sciences,
Shiraz, Iran
Background: Helicobacter pylori is a major cause of
neoplastic and inflammatory gastroduodenal diseases of the
stomach. H. pylori infection and associated gastric diseases are
common in developing countries. Cytokine gene polymorphisms
and H. pylori have been linked to gastric disease. We determined
the role of host interleukin-8 (−251 A/T) gene polymorphism in
the development of gastritis in south Iranian population.
Methods: We genotyped IL-8 (−251 A/T) gene polymorphism in
54 H. pylori infected individuals with gastritis and 337 infected
individuals with normal mucosa using polymerase chain reaction-restriction
fragment length polymorphism (PCR-RFLP). The
diagnosis of gastritis was established on the basis of endoscopic
findings.
Results: We did not find any significant differences in
allele and genotype frequencies of IL-8 (−251A/T) among our
study groups. Discussion: Our analysis did not reveal a
significant difference between the frequencies of IL-8
(−251) genotypes and alleles which might be the result of
our limited number of patient population. We suggest this
study be continued on larger population of the patients. Also,
analysis of polymorphism in other positions of IL-8 gene is
recommended.
doi:10.1016/j.clim.2007.03.275
F.63 The Impact of HLA Polymorphisms on
Measles Virus-specific T-Cell Memory Responses
in Vaccinated Subjects
Inna Ovsyannikova, Senior Research Associate, Mayo Clinic,
Mayo Vaccine Research Group, Rochester, MN, Jenna Ryan,
Senior Research Technologist, Mayo Clinic, Mayo Vaccine
Research Group, Rochester, MN, Norman Pinsky, Senior
Research Technologist, Mayo Clinic, Mayo Vaccine Research
Group, Rochester, MN, Robert Jacobson, Professor of
Pediatrics, Mayo Clinic, Department of Pediatric and
Adolescent Medicine, Rochester, MN, Robert Vierkant,
Senior Statistician, Mayo Clinic, Division of Biostatistics,
Rochester, MN, Gregory Poland, Professor of Medicine, Mayo
Clinic, Department of Internal Medicine, Rochester, MN
The humoral and cellular immune responses to measles virus
(MV) are genetically influenced. We hypothesized that the
antigen-presenting function of HLA molecules could play a role
in the variability in measles-specific T cell memory responses in