euro-immunology-2017-posters-accepted-abstracts

40 / 50

Page 109
conferenceseries.com
Volume 8, Issue 3 (Suppl) J Clin Cell Immunol, an open access journal
ISSN: 2155-9899 Euro Immunology 2017
June 29-July 01, 2017
June 29-July 01, 2017 Madrid, Spain
8th European
Immunology Conference
J Clin Cell Immunol 2017, 8:3(Suppl)
DOI: 10.4172/2155-9899-C1-037
Validation of Candida colonization associated with anamnestic response of anti-enolase IgG at early
stage of invasive candidosis by memory B-cell ELISPOT
Fang-qiu Li, Xiu-juan Shang, Xiao Chen, Yu-an Hu and Li-ning Shi
Nanjing University, China
Objective: The rapid elevation of IgG antibody against Candida enolase has been observed in the patients at early stage of invasive
candidosis. The aim of the study was to build a comprehension of the rapid increase of specific IgG titers against dominant antigens
(such as enolase) at the early stage of invasive Candida infection resulted from humoral immune anamnestic response associated with
previous Candida colonization.
Methods: The oral Candida colonization mouse model was established, and the immuno-competent and immuno-compromised
Candida colonized mice were challenged by intraperitoneal injection of Candida spore. The numbers of enolase-specific memory
B-cells in the spleen were measured by ELISPOT and compared with the levels of specific IgG, IgM and IgA antibodies in the
peripheral blood.
Results: The burst of enolase-specific memory B cells was detected in both immuno-competent and immuno-compromised mice at
day 7 post-invasive infection; which was followed by a strong increase in specific antibody titre in the Candida colonized mice. The
Eno-IgG antibody was positively correlated with the antigen specific Bm (r=0.737, P<0.01).
Conclusion: It was confirmed that the Candida colonization associated with anamnestic response of IgG against dominant antigen at
early stage of invasive candidosis and the rapid elevation of specific-IgG would suggest a diagnosis of invasive infection.
The quinoline-3-carboxamide paquinimod prevents development of diabetes in the non-obese diabetic
(NOD) mouse
Sahar Tahvili1, Marie Törngren2, Dan Holmberg1, Tomas Leanderson1 and Fredrik Ivars1
1Lund University, Sweden
2Personalmatsalen Active Biotech, Sweden
The NOD mouse spontaneously developed type 1 diabetes (T1D). At the age of 3-4 weeks, there was detectable infiltration of
mononuclear cells in the pancreatic islets of Langerhans of these mice. This process known as insulitis, causes selective cell death
of the insulin producing β-cells in the islets. Female NOD mice displayed severe insulitis at about 15 weeks of age and developed
hyper-glycaemia at around 15-30 weeks of age. We have previously shown that the immunomodulatory compound paquinimod
can reduce the influx of monocytes to sites of inflammation. Since monocyte-derived macrophages are known to be involved in
pathogenesis in NOD pancreas, we have in here investigated the impact of paquinimod treatment on the development of T1D in
the NOD mouse. In cohorts of mice treated between weeks 10 to 20 of age and followed up until 40 weeks of age, we observed dose-
dependent reduction of incidence of disease as well as delayed onset of disease. Further, in mice treated with paquinimod from 15
weeks of age, most of the treated mice had not developed glycosuria at 30 weeks of age and displayed strongly reduced insulitis.
Importantly, in these treated mice there were significantly more non-infiltrated islets than in untreated controls. Collectively, these
data indicate that paquinimod treatment inhibits progression of insulitis to overt diabetes in the NOD mouse.