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1 ment was likely due to systemic reduction in interleukin 5.
2 correlated with levels of tryptase, EDN, and interleukin-5.
3 asma eosinophil-derived neurotoxin (EDN) and interleukin-5.
4 roduced interferon-gamma and lower levels of interleukin-5.
5 ing mice with neutralizing antiserum against interleukin-5.
6 umab, a monoclonal antibody directed against interleukin-5.
7 ukin-2, interferon-gamma, interleukin-4, and interleukin-5.
8 ryptase in sputum and lower plasma levels of interleukin-5.
9 duction of granzyme B, interferon-gamma, and interleukin-5.
10 a humanized monoclonal antibody that targets interleukin-5, a cytokine that plays a central role in e
11 a humanised monoclonal antibody that targets interleukin-5, a key cytokine in type 2 inflammation, is
12 erapy, bolstering eosinophils by intravenous interleukin-5 administration promotes the efficacy of ra
13 markers associated with response to the anti-interleukin 5 agent, mepolizumab, and to the anti-immuno
14 e the lack of production of the Th2 cytokine interleukin 5 and the chemokine eotaxin, which are cruci
16 uch as increased expression of IgA-promoting interleukin-5 and anti-inflammatory transforming growth
18 E, IgG, IgG1, and IgG2a levels as well as in interleukin-5 and interferon-gamma levels in BALF and in
19 terized by elevated antibody titers and high interleukin-5 and interleukin-10 cytokine levels; import
20 esize extremely low levels of interleukin-4, interleukin-5 and interleukin-10, but normal amounts of
21 n-gamma in the type-1 response, and enhanced interleukin-5 and interleukin-13 in the type-2 response.
22 ce of adaptive T-cell immunity that involves interleukin-5 and interleukin-13-induced esophageal epit
24 tudy found significantly increased levels of interleukin-5 and interleukin-8, critical cytokines of t
25 s, such as humanised antibodies against IgE, interleukin 5, and interleukin 13, offer hope to improve
26 molecular signaling, physiologic sources of interleukin-5, and interactions between interleukin-5, e
27 Mig, as well as variable induction of B7.1, interleukin-5, and interferon gamma expression was noted
28 vealed induction of IP-10, Mig, B7.1 (CD80), interleukin-5, and interferon gamma in selected patients
29 and in vivo, with more robust interleukin-4, interleukin-5, and interleukin-13 production than their
30 , RSV F(51-66)-specific CD4 T cells secreted interleukin-5, and mice developed pulmonary eosinophilia
31 ntiation and gene expression, independent of interleukin-5, and regardless of inclusion of cytokines
32 -D content, gamma interferon, interleukin-4, interleukin-5, and tumor necrosis factor alpha in BAL fl
33 rferon-gamma-producing) and type 2 T helper (interleukin-5- and -10-producing) peripheral blood lymph
34 ron-gamma, and interleukin-6, with increased interleukin-5] and decreased CNS white matter inflammati
35 ies examining cytokine blockers such as anti-interleukin-5, anti-interleukin-4Ralpha, and anti-interl
36 ministration's recommendation to use an anti-interleukin-5 antibody for the treatment of severe eosin
37 es targeting IgE, interleukin-4 and -13, and interleukin-5 are effective in treating severe type 2 as
38 yte-macrophage colony-stimulating factor and interleukin 5, Bax spontaneously underwent activation an
39 ing biological drug engineered with enhanced interleukin-5 binding affinity, high potency, and an ext
40 tion of interferon-gamma, interleukin-2, and interleukin-5, but up-regulates transforming growth fact
41 eral blood of healthy donors, incubated with interleukin 5, cocultured with fibroblasts, and analyzed
46 hybridization analysis, mT4 is expressed in interleukin-5-dependent mouse eosinophils, as well as in
47 ked down-regulation of the hSP-C promoter is interleukin-5-dependent, implying a critical role for eo
48 s of interleukin-5, and interactions between interleukin-5, eosinophils, and the bone marrow microenv
49 This mRNA was expressed at high levels in interleukin 5-exposed eosinophils, elicited peritoneal m
50 T-helper type 1 (Th1) cells but increases in interleukin 5-expressing Th2 cells and eosinophils in pe
51 T-helper type 1 (Th1) cells but increases in interleukin 5-expressing Th2 cells and eosinophils in pe
53 show that transcriptional repression of the Interleukin-5 gene involves recruitment of GR to a DNA r
55 orm infection, albendazole treatment reduced interleukin-5 (geometric mean ratio 0.50, 95% CI 0.30-0.
57 persistent airway eosinophilia, blockade of interleukin-5 has significant steroid-sparing effects an
58 lonal antibody that binds to and inactivates interleukin-5, has been shown to reduce asthma exacerbat
59 ntibodies targeted to interleukin 4alpha and interleukin 5 have shown substantial benefit in patients
61 with monoclonal antibodies directed against interleukin-5, IgE or CD4 yielded results that were crit
62 inophil survival-promoting cytokines such as interleukin 5 (IL-5) and granulocyte-macrophage colony-s
63 ed DCs were associated with higher levels of interleukin 5 (IL-5) and IL-13 and a lower level of CXCL
64 cells (Th2 cells) are the primary source of interleukin 5 (IL-5) and IL-13 during type 2 (allergic)
65 an enhanced T helper type-2 (Th2) [increased interleukin 5 (IL-5) and interleukin 13 (IL-13)] and T r
66 In vivo studies in mice with eotaxin and/or interleukin 5 (IL-5) deficiency showed that FI-RSV vacci
67 y suggests a potentially protective role for interleukin 5 (IL-5) in sepsis; however, the loss of eos
69 The ligand-binding alpha-chain of the human interleukin 5 (IL-5) receptor was expressed in its solub
71 ex vivo differentiation assay, we found that interleukin 5 (IL-5) supports the generation of Ly6G(+)
72 of single-chain and monomeric forms of human interleukin 5 (IL-5) was performed to investigate mechan
74 ncept, we developed a 5-plex assay measuring interleukin 5 (IL-5), interleukin 6 (IL-6), interleukin
77 d mRNA expression of the TH2-type cytokines, interleukin-5 (IL-5) and granulocyte-macrophage colony-s
78 s (n = 33) had higher levels of constitutive interleukin-5 (IL-5) and IL-10, increased microfilarial
79 t a relatively steroid-insensitive source of interleukin-5 (IL-5) and IL-13 and are considered critic
80 2 ILCs (ILC2s) produce type 2 cytokines like interleukin-5 (IL-5) and IL-13 and require GATA3, and gr
81 xpression of mRNA for the Th2-type cytokines interleukin-5 (IL-5) and IL-13 as well as some increase
82 g epithelial cells inducing the elevation of interleukin-5 (IL-5) and IL-13 from natural helper (NH)
83 increased amounts of inflammatory cytokines interleukin-5 (IL-5) and IL-13 in lung lavage fluid, dec
84 leads to an increase in the Type 2 cytokines interleukin-5 (IL-5) and IL-13; however, the effect of s
85 s of PP CD4(+) T helper (Th) cells secreting interleukin-5 (IL-5) and IL-6 and splenic CD4(+) Th cell
87 ml), and culture supernates were assayed for interleukin-5 (IL-5) and interferon-gamma by enzyme-link
88 in the bronchoalveolar lavage fluid (BALF); interleukin-5 (IL-5) and leukotriene concentrations in B
89 ent killer cell activity, elevated levels of interleukin-5 (IL-5) and percentages of eosinophils in t
91 Observations that monoclonal antibodies to interleukin-5 (IL-5) are well tolerated appear unsurpris
93 ents with severe asthma, treatment with anti-interleukin-5 (IL-5) biologics can lead to a reduction i
98 n of the airways and increased production of interleukin-5 (IL-5) in cultures of peribronchial lymph
101 hil-active cytokines showed unique patterns: interleukin-5 (IL-5) increased in the antigen segment on
103 ition of eosinophil apoptosis by exposure to interleukin-5 (IL-5) is associated with the development
108 netic interactions of a humanized anti-human interleukin-5 (IL-5) monoclonal antibody (SCH 55700) wit
109 p of patients with HES show T-cell-dependent interleukin-5 (IL-5) overexpression, we determined if ex
116 transcript levels rapidly increase following interleukin-5 (IL-5) stimulation of CD34(+) hematopoieti
117 of phagocytizing bacteria, neutralization of interleukin-5 (IL-5) to inhibit eosinophil recruitment l
118 4(+) gamma interferon (IFN-gamma)(+), CD4(+) interleukin-5 (IL-5)(+), and CD4(+) IL-17A(+) phenotypes
119 (GM-CSF) and the single structural domain of interleukin-5 (IL-5), all of which share a common recept
120 suppressed by a new class of drugs targeting Interleukin-5 (IL-5), an eosinophil growth, activation,
121 nts using a humanised monoclonal antibody to interleukin-5 (IL-5), and animal studies involving speci
122 of CII-specific interferon-gamma (IFNgamma), interleukin-5 (IL-5), and IL-10 was determined by enzyme
124 interleukin-2 (IL-2), interleukin-4 (IL-4), interleukin-5 (IL-5), and tumor necrosis factor alpha (T
125 ession of three eosinophil chemoattractants: interleukin-5 (IL-5), eotaxin, and regulated on activato
128 alysis of tumour necrosis factor (TNF) beta, interleukin-5 (IL-5), IL-10, Forkhead box P3 (FOXP3) and
129 increased levels of eosinophils, mast cells, interleukin-5 (IL-5), IL-13, gamma interferon, immunoglo
130 type 2 (anti-helminths) effectors, including interleukin-5 (IL-5), IL-13, immunoglobulin E and eosino
132 at regions of LSA-1 stimulated production of interleukin-5 (IL-5), interleukin-10 (IL-10), gamma inte
134 reatment with the rat anti-mouse antibody to interleukin-5 (IL-5), TRFK-5 (10-300 microg, intraperito
137 nown, but they are accompanied by a dramatic interleukin-5 (IL-5)-dependent increase in eosinophilia
139 s, we analyzed eosinophil differentiation in interleukin-5 (IL-5)-stimulated umbilical cord stem cell
143 gamma [IFN-gamma]) as well as selective Th2 (interleukin-5 [IL-5] and IL-6) cytokine responses than d
144 in T cell cytokine levels (interferon-gamma, interleukin-5 [IL-5], IL-10, IL-17) were detected after
145 , vascular endothelial growth factor (VEGF), interleukin 5 (IL5), CCL17, CCL22, CXCL9 and CXCL10.
146 s, interleukin 3 (Il3), interleukin 4 (Il4), interleukin 5 (Il5), interleukin 13 (Il13), and granuloc
148 previously demonstrated that AF17121 mimics Interleukin-5 (IL5) by binding in a region of IL5Ralpha
149 21 is a library-derived antagonist for human interleukin-5 (IL5) receptor alpha (IL5Ralpha) and inhib
150 sinophils around the airway, lower levels of interleukin 5 in the lung, and reduced serum levels of i
152 IgE in serum, and increased eosinophilia and interleukin-5 in bronchoalveolar lavage (BAL) compared t
154 and -13 in antigen-induced dysmotility, and interleukin-5 in the pathogenesis of mucosal eosinophili
157 ll responsive (as measured by proliferation, interleukin-5, interleukin-10, interferon-gamma, and gra
158 + Cort) levels of two Th-2 cytokines (i.e., interleukin-5, interleukin-13) and one Th-1 cytokine (i.
159 ecreased leukocytes and mediators, including interleukin-5, interleukin-13, eotaxin, prostanoids and
161 ssayed for interleukin-1beta, interleukin-4, interleukin-5, interleukin-6, interleukin-8, interleukin
162 rleukin-1beta, interleukin-2, interleukin-4, interleukin-5, interleukin-6, interleukin-9, interleukin
163 interleukin-2 receptor-alpha, interleukin-4, interleukin-5, interleukin-7, interleukin-13, interleuki
166 th mepolizumab-a monoclonal antibody against interleukin 5-is associated with a reduced risk of exace
168 a significant reduction in interleukin-4 and interleukin-5 levels and a significant increase in inter
170 vels (P<.06) and a tendency toward increased interleukin-5 levels, compared with helminth-free patien
173 controls, levels of the chemotactic factors interleukin-5, macrophage inflammatory protein-1 alpha,
174 ilic syndrome, the therapeutic niche of anti-interleukin-5 (mepolizumab) and anti-CD52 (alemtuzumab)
179 valuating the safety and efficacy of an anti-interleukin-5 monoclonal antibody, mepolizumab, in patie
181 tle phenotypes, whereas other genes, such as interleukin-5 or osteoprotegerin, were initially identif
182 actor beta, gamma interferon, interleukin-4, interleukin-5, or interleukin-6 for all mouse strains.
185 n-atopic donors suppressed proliferation and interleukin 5 production by their own allergen-stimulate
186 HPV antigen--specific interferon--gamma and interleukin-5 production were measured from PBMC culture
188 phils stimulated with IgA immune complex and interleukin 5 promote neurite extension of the PC-12 phe
189 ty also showed significant correlations with interleukin-5 (r = 0.66, p = 0.002), transforming growth
190 in patients who died, with a serum G-CSF to interleukin 5 ratio of >100 at admission being the most
192 efficacy and safety of benralizumab, an anti-interleukin 5 receptor alpha monoclonal antibody that de
194 ls per muL, possibly due to targeting of the interleukin 5 receptor rather than interleukin 5 ligand.
195 BCR) or the mast cell Fcepsilon receptor, or interleukin 5 receptor stimulation each induced rapid ph
196 contrast, introduction and activation of the interleukin-5 receptor (IL-5R) or of the granulocyte-mac
197 lular domain of the alpha chain of the human interleukin-5 receptor (IL-5Ralpha), but share no primar
202 Benralizumab is an anti-eosinophilic, anti-interleukin-5 receptor alpha monoclonal antibody that ha
203 ralizumab is a humanised, afucosylated, anti-interleukin-5 receptor alpha monoclonal antibody that in
206 benralizumab, a monoclonal antibody against interleukin-5 receptor alpha that depletes eosinophils b
207 enralizumab is a monoclonal antibody against interleukin-5 receptor alpha, which is expressed on huma
210 dy directed against the alpha subunit of the interleukin-5 receptor that significantly reduces the in
212 utive and alternative splicing of the murine interleukin-5 receptor-alpha (IL-5Ralpha) chain pre-mRNA
214 production are enhanced by interleukin-4 and interleukin-5, respectively, these findings suggest that
215 nduction of PA-specific gamma interferon and interleukin 5 responses was observed in splenocytes.
218 eatment with TRFK5, a monoclonal antibody to interleukin-5, resulted in a 76% decrease in eosinophil
219 n the presence of 10 pg/ml human recombinant interleukin-5 (rhIL-5) and activated with formyl-met-leu
220 nctional phage display of single chain human interleukin-5 (scIL-5) and its use for receptor-binding
221 Dual asymmetric mutagenesis of single-chain interleukin 5 (scIL5) was used to obtain evidence that t
223 Immunization with antigen and AlOH induced interleukin-5-secreting, antigen-specific T cells, and i
225 daily; four male patients with normal serum interleukin 5 showed complete haematological responses;
227 e sequencing of a cDNA library prepared from interleukin-5-stimulated umbilical cord precursor cells
228 te-macrophage colony-stimulating factor, and interleukin-5, suggesting a role for the beta common (be
229 c therapy with enhanced binding affinity for interleukin-5 that may enable effective 6-month dosing i
230 lonal antibody that binds to and neutralizes interleukin-5, the major cytokine involved in eosinophil
231 tiple other medical treatments for EoE: anti-interleukin-5 therapy, anti-interleukin-13 therapy, anti
232 en-specific gamma interferon (IFN-gamma) and interleukin 5 to levels comparable to those achieved wit
236 evented by anti-very late antigen-4 and anti-interleukin-5 treatments, which blocked airway eosinophi
238 analysis with gene-targeted mice showed that interleukin-5 was required for esophageal eosinophilia a
239 ere not degranulated and increased levels of interleukin-5 were measured in bronchoalveolar lavage an
240 locyte colony-stimulating factor, as well as interleukin 5, which may be responsible for the decrease
241 mab, a humanized monoclonal antibody against interleukin-5, which was administered as either a 75-mg
242 strains of mice produced only low levels of interleukin-5, with no detectable level of interleukin-4
243 ux and shifted cytokine production away from interleukin-5 without reducing the resistance to viral r