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1 es, including interleukin-17A (also known as interleukin-17).
2 was characterized by its capacity to produce interleukin 17.
3 tory cytokines, such as interferon gamma and interleukin 17.
4 alpha alone or in combination with CD40L or interleukin-17.
5 sease inflammation through the production of interleukin-17.
6 e-colony stimulating factor (G-CSF), but not interleukin-17.
7 iting interleukin-23-dependent production of interleukin-17.
8 peutics, centered on naive T-cell depletion, interleukin-17/21 inhibition, kinase inhibition, regulat
9 ith ex vivo screening, and was essential for interleukin-17 A (IL-17A)-mediated cross-reactivity and
12 milder presentation had increasing levels of interleukin 17 and cytokines in the interferon-gamma/int
13 eased numbers of CD4(+) T cells that secrete interleukin 17 and interferon gamma, and caused CD11b(+)
15 robial defense in intestinal mucosa, through interleukin 17 and interleukin 22 (IL-22) production.
16 Notably, C. parapsilosis induced much less interleukin 17 and interleukin 22 production as compared
17 ID1A, FBXW7, PIGR, ZC3H12A, and genes in the interleukin 17 and Toll-like receptor pathways, under po
18 elated with increased inflammatory cytokines interleukin 17 and tumor necrosis factor-alpha but not g
21 cells was seen with increased expression of interleukin-17 and interleukin-22 by day 5 after injury.
22 expansion of ILC3s in mice and production of interleukin-17 and interleukin-22 were found to be criti
23 n activated naive gammadelta T cells to make interleukin-17 and respond to cytokine signals that perp
27 and efficacy of LY2439821, a humanized anti-interleukin-17 (anti-IL-17) monoclonal antibody, in a fi
28 immunity, specifically T-helper 17 cells and interleukin 17, as well as the lack of protection afford
29 th increased tumor necrosis factor-alpha and interleukin-17, as well as decreased transforming growth
30 ron-gamma), Th-2 (interleukin-4), and Th-17 (interleukin-17)-associated cytokines than wild-type mice
32 of CD4+ Th17 T cells and the interleukin-23/interleukin-17 axis has challenged existing paradigms an
33 esponse and activation of the interleukin-23/interleukin-17 axis have been observed in animal models
34 tion studies suggest that the interleukin-23/interleukin-17 axis plays an important role in spondyloa
35 icate the evolution of both inflammatory and interleukin 17-based immune pathogenesis in GVHD, and pr
36 proteins: Compared with baseline, levels of interleukin-17, basic fibroblast growth factor, granuloc
37 y correlated with a significant reduction in interleukin-17 by in vitro-restimulated splenocytes of T
38 oinflammatory cytokines interferon-gamma and interleukin-17 by lymph node T cells and later with incr
39 ration of responder tumors by CD8+ cells and interleukin-17+ cells, and decreased infiltration of res
41 Plasma transforming growth factor-beta and interleukin-17 concentrations were increased in T-bet(-/
43 gal burden, increased pulmonary Th1-type and interleukin-17 cytokine production, and classical macrop
45 had increased T-cell activation markers and interleukin-17 expression compared to wild-type mice.
50 nd cytokines (interleukin-6, interleukin-10, interleukin-17, granulocyte-macrophage colony-stimulatin
51 cells, characterized by their production of interleukin-17, have emerged as important and broad medi
53 t subsets of gammadelta T cells that produce interleukin 17 (IL-17) (CD27(-) gammadelta T cells) or i
55 llicles was partly dependent on the cytokine interleukin 17 (IL-17) and on the cell surface molecule
57 oward a proinflammatory phenotype, producing interleukin 17 (IL-17) and/or interferon gamma (IFN-gamm
59 utants were associated with higher levels of interleukin 17 (IL-17) expression from lamina propria CD
62 ber of studies have reported the presence of interleukin 17 (IL-17) in patients with Lyme disease, an
67 ned to investigate whether the expression of interleukin 17 (IL-17) is associated with the indetermin
71 rleukin 1beta (IL-1beta) release and reduces interleukin 17 (IL-17) production and bacterial clearanc
72 reflected by heightened interferon gamma and interleukin 17 (IL-17) production as well as by high lev
73 us bacteria (SFB), as well as an increase of interleukin 17 (IL-17) production by intestinal cells.
76 ed to the variable effects of EHS on gastric interleukin 17 (IL-17) responses to H. pylori infection.
77 eron gamma, tumor necrosis factor alpha, and interleukin 17 (IL-17) were all significantly increased
78 tudy examines the ability of MAC to regulate interleukin 17 (IL-17), a proinflammatory cytokine invol
80 make either interferon-gamma (IFN-gamma) or interleukin 17 (IL-17), but the role of the T cell antig
81 nd TH2 cytokines and increased production of interleukin 17 (IL-17), gamma interferon (IFN-gamma), CC
83 ns convincingly show that T-helper 17 (Th17)/interleukin 17 (IL-17)-driven immunity is essential to c
87 rently normal compartments of regulatory and interleukin 17 (IL-17)-producing CD4(+) T cells, as well
88 helper 17 (nTH17) cells are a population of interleukin 17 (IL-17)-producing cells that acquire effe
89 quisition of T helper type 1 (TH1) cell- and interleukin 17 (IL-17)-producing helper T (TH17) cell-li
94 factor BATF controls the differentiation of interleukin 17 (IL-17)-producing helper T cells (T(H)17
96 mouse regulatory T cells (T(reg) cells) and interleukin 17 (IL-17)-producing helper T cells (T(H)17
98 BATF is required for the differentiation of interleukin 17 (IL-17)-producing helper T cells (TH17 ce
99 elitis (EAE) due to autoimmunity mediated by interleukin 17 (IL-17)-producing helper T cells (TH17 ce
101 of segmented filamentous bacteria and fewer interleukin 17 (IL-17)-producing lamina propria T cells.
102 lls resemble the T helper type 1 (T(H)1) and interleukin 17 (IL-17)-producing T helper (T(H)17) subse
107 requencies of T regulatory cells (Tregs) and interleukin 17 (IL-17)/IL-22-producing Th cells (Th17/Th
108 of inflammatory CD4(+) T cells that produce interleukin-17 (IL-17) (termed Th17) has been identified
109 tumor necrosis factor alpha (TNF-alpha), and interleukin-17 (IL-17) after restimulation with LcrV and
110 ve been characterized based on production of interleukin-17 (IL-17) and association with autoimmune d
113 n of murine Th17 cells and the production of interleukin-17 (IL-17) and IL-21, two cytokines associat
116 controlling the production and functions of interleukin-17 (IL-17) and IL-22, cytokines that direct
117 inally reported to produce cytokines such as interleukin-17 (IL-17) and IL-22, we demonstrate here th
119 jor sources of the proinflammatory cytokines interleukin-17 (IL-17) and interferon-gamma (IFNgamma) i
120 ssion of the pro-inflammatory cytokine genes interleukin-17 (IL-17) and macrophage migration inhibito
124 Several groups have recently reported that interleukin-17 (IL-17) confers protection against the li
128 olleagues demonstrate that the production of interleukin-17 (IL-17) during inflammation promotes soci
129 us macaques, we show that the suppression of interleukin-17 (IL-17) expression correlated with upregu
130 roduction, which is accompanied by sustained interleukin-17 (IL-17) expression that persists even aft
131 otype of pathologic IVD specimens, including interleukin-17 (IL-17) expression, from surgically obtai
136 Th17-like immune responses mediated by the interleukin-17 (IL-17) family of cytokines and neutrophi
143 emergence of Th17 cells and higher levels of interleukin-17 (IL-17) in lung tissue, which were reduce
144 the role of T helper type 17 responses, and interleukin-17 (IL-17) in particular, has been controver
145 has been reported that ectopically expressed interleukin-17 (IL-17) in tumor cells suppresses tumor p
146 ltrating T helper type 17 (T(H)17) cells and interleukin-17 (IL-17) induced the expression of granulo
155 d produced a "closed" chromatin structure at interleukin-17 (IL-17) locus to inhibit Th17 cell functi
156 pro-inflammatory roles, the ancient cytokine interleukin-17 (IL-17) modulates neural circuit function
157 f patients with select gene disruptions, the interleukin-17 (IL-17) pathway has emerged as a critical
159 n gamma (IFN-gamma) and Th17 cells producing interleukin-17 (IL-17) play key roles in host protection
161 present study was to analyze the density of interleukin-17 (IL-17) producing T cells and IL-17 mRNA
163 cell assays showed reduced proliferation and interleukin-17 (IL-17) production by lymph node cells fr
165 ollowing experimental challenge and impaired interleukin-17 (IL-17) production by vaccine antigen-sti
166 the DCs that were generated induced enhanced interleukin-17 (IL-17) production from naive CD4+ T cell
167 CD4+ T cells, enhanced interferon-gamma and interleukin-17 (IL-17) production, and elevated levels o
171 neither CXC chemokine receptor 2 (CXCR2) nor interleukin-17 (IL-17) receptor (IL-17R) deficiency chan
172 functional CD4(+) T cells, signaling via the interleukin-17 (IL-17) receptor, and IL-22 production.
173 emonstrated an enhanced innate expression of interleukin-17 (IL-17) relative to wild-type (WT) mice.
178 show that growth factor FGF2 synergized with interleukin-17 (IL-17) to induce genes for repairing of
181 ndothelium and epithelium, and overexpressed interleukin-17 (IL-17) with massive neutrophilic inflamm
183 high levels of the proinflammatory cytokine interleukin-17 (IL-17), accompanied by an induction of I
184 cate that Tregs have the capacity to produce interleukin-17 (IL-17), although the ability of these ce
185 nhibited CD154 expression, interferon-gamma, interleukin-17 (IL-17), and IL-6 production, and T cell-
186 with significant decreases in the levels of interleukin-17 (IL-17), gamma interferon, tumor necrosis
187 opulations, interferon-gamma (IFN-gamma) and interleukin-17 (IL-17), have been shown to play a critic
188 ssociated with decreased local production of interleukin-17 (IL-17), IL-18, and tumor necrosis factor
189 isease, and immunoablated T cells expressing interleukin-17 (IL-17), interferon-gamma and tumor necro
190 Gammadelta T cells are an innate source of interleukin-17 (IL-17), preceding the development of the
192 to control infection, including the role of interleukin-17 (IL-17), which is important in controllin
194 e in T helper 17 (Th17) cells and heightened interleukin-17 (IL-17)-dependent inflammation in experim
195 own that cells and cytokines associated with interleukin-17 (IL-17)-driven inflammation are involved
197 terized by the early and sustained influx of interleukin-17 (IL-17)-positive neutrophils and macropha
198 reg cells are converted into proinflammatory interleukin-17 (IL-17)-producing cells by inflammatory m
199 iotic exposure of dams reduced the number of interleukin-17 (IL-17)-producing cells in the intestine
203 l (ILC2) subpopulation that can convert into interleukin-17 (IL-17)-producing NKp44(-) ILC3-like cell
204 alance between regulatory T (Treg) cells and interleukin-17 (IL-17)-producing T helper (TH17) cells;
205 For example, HIV preferentially depletes interleukin-17 (IL-17)-producing T helper 17 (Th17) cell
212 XCL1 and CCL2) and proinflammatory cytokine (interleukin 17 [IL-17]) expression in tissues surroundin
213 lature, and increased inflammation in brain (interleukin-17 [IL-17] and IL-6) and liver (gamma interf
214 aarticular cytokine expression (P < 0.01 for interleukin-17 [IL-17] and P < 0.001 for IL-23), and dec
215 on [IFN-gamma], tumor necrosis factor [TNF], interleukin-17 [IL-17], and IL-1beta) or chemokine (CXCL
219 oduction of interferon gamma (IFN-gamma) and interleukin 17 in patients with an active retinochoroida
220 roles of the cytokines interferon-gamma and interleukin-17 in determining the localization of inflam
222 scin-C-null mice displayed ablated levels of interleukin-17 in the joint during experimental arthriti
223 this issue of Immunity, Lin et al. implicate interleukin-17 in the regulation of T helper 1 (Th1) cel
224 rleukin 1beta, interleukin 6, interleukin 8, interleukin 17, interferon gamma, and tumor necrosis fac
225 at MCAM(+) CD8(+) T lymphocytes express more interleukin 17, interferon gamma, granulocyte-macrophage
226 tokines released from these cells, including interleukin-17, interferon-gamma, tumor necrosis factora
227 d unique approximately 200-fold expansion of interleukin 17+/interleukin 22+ T effectors with profoun
228 leukin-12/interleukin-23p40, interleukin-13, interleukin-17, interleukin-18, interferongamma, transfo
230 nterleukin-5, interleukin-7, interleukin-13, interleukin-17, macrophage inflammatory protein 1alpha a
231 nterleukin-3, interleukin-6, interleukin-13, interleukin-17, macrophage inflammatory proteins-1alpha,
233 of ixekizumab (LY2439821), a humanized anti-interleukin-17 monoclonal antibody, for psoriasis treatm
236 In particular, the interferon gamma and interleukin 17 pathways are strongly induced in previous
237 egulatory T cells (Tregs) and demonstrate an interleukin-17 phenotype that enhances OC activation.
239 e case in a study of the recently discovered interleukin-17 producing helper T cells (Th17), which ar
242 n of T helper type 2 cells (T(H)2 cells) and interleukin 17-producing helper T cells (T(H)17 cells) b
244 mechanisms underlying the differentiation of interleukin 17-producing T helper cells (T(H)-17 cells)
248 cking the differentiation and/or function of interleukin-17-producing CD4(+) T cells on human autoimm
252 Here we demonstrate the critical role of interleukin-17-producing marrow infiltrating lymphocytes
253 n (MOG(35-55))-specific interferon-gamma and interleukin-17-producing T cells in experimental autoimm
254 ntibody levels increased, and IFN-gamma- and interleukin-17-producing T cells, including cells specif
256 isms that prevent inappropriate or excessive interleukin-17-producing T helper (Th17) cell responses
257 le of STAT3 in regulating differentiation of interleukin-17-producing Th17 cells, but its function in
258 e staining demonstrated interferon gamma and interleukin 17 production and lack of interleukin 10 pro
261 esulted in increases in gamma interferon and interleukin-17 production and decreases in interleukin-1
262 -linked immunospot assay as well as in vitro interleukin-17 production as predictors of vaccination s
263 i-NKG2D treatment significantly reduced both interleukin-17 production from CD4+ T cells in arthritic
264 ome expression, immunoglobulin G deposition, interleukin-17 production in heart tissue, and TnI-direc
265 inflammatory and chemotactic cytokines, less interleukin-17 production, and reduced fibrosis formatio
267 dalumab, a human monoclonal antibody against interleukin-17 receptor A (IL17RA), in a phase 2, random
268 rly clinical studies suggested that the anti-interleukin-17 receptor A monoclonal antibody brodalumab
269 Here, we showed that amplified signaling of interleukin-17 receptor B (IL-17RB) and its ligand IL-17
271 , we describe a role for the orphan receptor interleukin-17 receptor D (IL-17RD) in negatively regula
273 safety of brodalumab (AMG 827), a human anti-interleukin-17-receptor monoclonal antibody, for the tre
274 this organism elicited a commensal-specific interleukin-17 response from gammadelta T cells in the o
275 ere necessary for the propagation of de novo interleukin-17 responses, and activated T cells from MS
276 ie, interleukin 1beta, interferon gamma, and interleukin 17) responses when medium was devoid of glut
277 g both T-bet and Eomes differentiate into an interleukin-17-secreting lineage, reminiscent of the hel
278 reover, the DB fusion in LDAO induced higher interleukin-17 secretion and provided a higher protectiv
281 impaired inflammatory responses and reduced interleukin-17 signalling during oropharyngeal candidias
282 d previously found a dominant interleukin-23-interleukin-17 signature at inflamed sites in humans wit
283 antibody titers, higher interferon gamma and interleukin 17 splenic responses, and more multifunction
286 CD4(+) T helper lymphocytes that express interleukin-17 (T(H)17 cells) have critical roles in mou
288 ed for induction of T-helper cells producing interleukin-17 (Th17 cells) and important in antifungal
290 lpha, interleukin 1beta, interleukin 12, and interleukin 17; the chemokines CCL2, CCL4, and CXCL10; a
291 d in the pretreated probiotic group, whereas interleukin 17 transcription was suppressed with probiot
292 ed less interferon gamma, interleukin 4, and interleukin 17 upon coculture with B cells from schistos
294 sessed by production of interferon gamma and interleukin 17, was preserved in the mucosa of patients
297 oduce cytokines such as interferon gamma and interleukin 17, which facilitate macrophage activation a
298 tial to produce the proinflammatory cytokine interleukin-17, which has been linked to transplant reje
299 ed to as LDb mice) exhibited increased serum interleukin-17, which was associated with increased numb
300 CL9, CXCL10, and CXCL11), interleukin-6, and interleukin-17 with significantly higher levels of Th17