814 / 827
844
cytometry was determined the number of CD3, CD19, CD4, CD8,
CD16/56 cells; the level of expression of activation markers on the
monocytes and lymphocytes (HLA- DR/CD14, CD71/CD14, CD25/
CD4, CD95/CD3); adhesion receptor (CD11b). All premature babies
with leukopenia in the background found an increase in the relative
number of lymphocytes and decreased ability to absorb opsonized
bacteria by granulocytes. Defined a reduction in the percentage
of HLA-DR+/CD14+-cells, increasing the number of CD3+CD95+-
population in group of children with a GA 25-28 weeks. Decrease at
the level of NK-cells in group infants less than 32 weeks of GA was
observed. It was determined a reduced percentage of CD3+CD11b+
cells in the 29-32; 33-36 weeks of GA. At the 33-36 weeks of the GA
found a reduction in the number CD3+CD95+ lymphocytes and
increasedexpressionof theCD25+CD4+ lymphocytes.
Overall, the findings suggest about the features of the immune
system, specific to a particular GA preterm infants. A number of
the investigated parameters give the opportunity to talk about the
partial achievement of the immunological response preparedness
for a potential antigen that dictates the need for further research
aimed at understanding the functional activity of immune cells.
The importance of serum visfatin levels in Behcet’s disease
patients
Ozbalkan,Z.
1
,Enecik,M.E.
1
,Keskin,G.
2
,Karaaslan,Y.
1
1
AnkaraNumuneEducationandResearchHospital,Rheumatology
Department,Ankara,Turkey,
2
AnkaraUniversitySchoolof Medicine,
ImmunologyDepartmet,Ankara,Turkey
Objectives:
Addipose tissue is an active endocrine organ and
releases adipositokines. Visfatine is one of them. Visfatin is related to
TNF-α and IL-6, IL-1 beta, co-stimulators like CD40, CD54 ,CD 80 and
endothelial ICAM-1 and ICAM-2. We aimed to search the relation
among levels of serumvisfatin in BD activity.
Materials andmethods:
60BD patients (30 in active state and 30 in
remission) diagnosed according to criteria of WGIBD and 20 healthy
subjects as controls were involeved in to the study. Serum visfatin
levels were compared in between three groups.
Results:
Visfatin levels were significantly higher in both group of
patients compared to the healthy control group (both p< 0,001).
Serum visfatin levels in active state patients were higher than those
in inactive state (p < 0.001). The same way in all cases statistically
significant correlation between visfatin and CRP (p < 0.001) and
visfatin and ESR (p< 0.01). According to the symptoms of the
patients in the active state, patients with genital aphtous ulcers had
higher serum visfatin levels than the active patients without genital
aphthous ulcers (p<0,001).
Conclusion:
Serum visfatin levels in BD patients with active and
inactive states are higher than the healthy control group. That could
be concluded as visfatin as a proinflammatory cytokines have a
role in chronic inflammatory reactions and sustains the cellular
expressionof the inflammatory cytokines inBD.
Kinetic analysis of type 2 innate lymphoid cells in tissues from
IL-25- and IL-33-induced murine models of asthma
Li, Y.
1
, Lv, Z.
2
,Wang, J.
3
, Chi, Y.
3
, Huang, P.
2
, Corrigan, C.J.
4
, Huang, K.
1
,
Wang,W.
2
, Ying, S.
2
1
Beijing Chao-Yang Hospital, Capital Medical University & Beijing
Institute of Respiratory Medicine, Department of Respiratory and
Critical Care Medicine, Beijing, China,
2
Capital Medical University,
Department of Immunology, School of Basic Medical Sciences,
Beijing,China,
3
CapitalMedicalUniversity,DepartmentofLaboratory
Animal Sciences, Beijing, China,
4
King’s College London, MRC &
Asthma UK Centre in Allergic Mechanisms of Asthma, Division of
Asthma, Allergy & Lung Biology, London, UnitedKingdom
Background:
Type-2innatelymphoidcells(ILC2)playimportantrole
in the pathogenesis of asthma through producing large amounts of
Th2-type cytokines. The mechanisms of ILC2 chemotaxis into lungs,
however, are still unclear.
Methods:
To answer these, BALB/c mice were intranasally changed
with murine IL-25 or IL-33, while OVA and saline challenged mice
were used as positive and negative controls. Bone marrow, spleen,
thymus, mesenteric lymph nodes, mediastinal lymph nodes, lung
tissue and bronchoalveolar lavage fluid (BALF) were collected from
themice at experimental acute, subacute, chronic and convalescent
phases. Flowcytometry, invitrochemotaxis assayandsmall animal in
vivo imaging were used tomeasure the distribution and abundance
and chemotaxis of ILC2
invitro
and
invivo
.
Results:
Both IL-25 and IL-33 alone induced accumulation of ILC2
into mediastinal lymph nodes, lung tissue and BALF, but with
different kinetics. The peak of IL-25 induced ILC2 accumulation into
lung tissue and BALF was earlier than that of the IL-33- induced
mice. In quantity, the numbers of ILC2 in BALF, lung tissue and
mediastinal lymph nodes were significantly higher in IL- 33-induced
mice compared with IL-25-induced mice.
In vitro
IL-33, but not IL-
25 directly induced ILC2 chemotaxis. Small animal
in vivo
imaging
further confirmed that single intranasally inhalation of IL-33 was
sufficient to induce accumulation of injected ILC2 through tail vein
into the lungs.
Conclusion:
The data suggest that airways epithelium-derived IL-25
or IL-33 can induce accumulation of ILC2 to the lungs and that IL-33
has direct effect on ILC2 chemotaxis.
Immune responses to oral polio vaccine (OPV) in patients with
X-linked agammaglobulinemia (XLA)
Wu, Y.
1
,Mao, H.W.
2
, Chan, S.M.
1
, Lam, K.T.
1
, Tu,W.
1
, Lau, Y.L.
1
1
UniversityofHongKong,PaediatricsandAdolescentMedicine,Hong
Kong,HongKong,
2
HKU-ShenZhenHospital,ShenZhen, China
Background
: XLA is characterized by impaired antibody response
resulting fromBruton´s tyrosine kinase (BTK) mutation. Unlike other
primary immunodeficiency with no predisposition to extraordinary
risk of viral infection, XLA renders a unique susceptibility to
enteroviruses infection including poliovirus. OPV can induce
paralytic poliomyelitis in XLA patients. Of great public concern is
that the attenuated OPV can persist and revert to a virulent form in
these patients, which renders a high risk of reintroducing virulent
poliovirus into general population. It is known that BTK is involved
in toll-like receptor 3 (TLR3) signaling, and TLR3-mediated type I IFN
responses play critical roles in host protection against poliovirus.
However, whether XLA patients have impaired type I IFN responses
toOPV are not clear.
Hypothesis
: BTK mutations in XLA impair TLR3-mediated type I IFN
response, leading to the unique susceptibility to poliovirus in XLA
patients.