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1 +) cells) into and around pancreatic islets (insulitis).
2 with older female counterparts with advanced insulitis.
3 revent diabetes and block the progression of insulitis.
4 oportion of anti-inflammatory macrophages in insulitis.
5 ability of immunomodulatory agents to clear insulitis.
6 es development even at a time of significant insulitis.
7 a recurrence and revealed beta-cell loss and insulitis.
8 ype 1 diabetes (T1D) is preceded by invasive insulitis.
9 onset, increased its incidence, and worsened insulitis.
10 e target organ level in patients with active insulitis.
11 1D when administered late after the onset of insulitis.
12 of nondiabetic animals exhibited pancreatic insulitis.
13 ibited diabetes in NOD mice with established insulitis.
14 phase, the ablation of DC led to accelerated insulitis.
15 ocalized loss of IDO and the acceleration of insulitis.
16 circulation and lead to development of peri-insulitis.
17 x15(null) mice, preceding the development of insulitis.
18 notably inflammatory bowel disease (IBD) and insulitis.
19 Rag-1-/-pfn-/- mice also resulted in IBD and insulitis.
20 e LTbetaR-Ig-treated mice were devoid of any insulitis.
21 s with insulitis compared with those without insulitis.
22 wed donor-specific tolerance and reversal of insulitis.
23 d65 DRlyp/lyp animals possessed eosinophilic insulitis.
24 rexpressed in human T1D islets affected with insulitis.
25 4- plus pIL10-treated recipients was free of insulitis.
26 infiltration into the pancreatic islets, or insulitis.
27 BALB/c mice (but with neither alone) induced insulitis.
28 tochemical evidence of increased destructive insulitis.
29 nearly complete protection from diabetes and insulitis.
30 argeted allele had no insulitis or only peri-insulitis.
31 nts from the latter to the former suppressed insulitis.
32 tomically associated with the development of insulitis.
33 gression to diabetes even after the onset of insulitis.
34 ession of inflammatory genes and exacerbated insulitis.
35 ling compared with NOD mice that do not have insulitis.
36 ions yielded significantly greater levels of insulitis.
37 ally decreased the incidence of diabetes and insulitis.
38 ominent surrounding immune cells in areas of insulitis.
39 ine tissue without the presence of prominent insulitis.
40 ed in diabetic islets and regions exhibiting insulitis.
41 onversion from peri-insulitis to destructive insulitis.
42 ontaneous T1D and a significant reduction in insulitis.
43 HOT-100% (P < 0.005) and paralleled by lower insulitis.
44 s of their antigen specificity and to induce insulitis.
49 tected their NOD offspring from diabetes and insulitis, an effect that was dependent on the intestina
50 und that DORmO.RAG2(-/-) mice do not develop insulitis and are completely protected from diabetes, de
51 utoimmune diabetes in NOD mice by inhibiting insulitis and augmenting regulatory T cells (Tregs) with
52 and lower affinity TCRs could mediate potent insulitis and autoimmune diabetes, suggesting that TCR a
53 major role in pathogenesis characterized by insulitis and beta cell destruction leading to clinical
55 D-B7-1B-transgenic mice) resulted in reduced insulitis and completely protected NOD mice from develop
56 ssion is a phenotype that is associated with insulitis and correlates with overall disease progressio
57 nduction the mice display similar degrees of insulitis and decrements in the beta cell mass, only tra
58 se diabetic (NOD) mice spontaneously develop insulitis and destruction of pancreatic islet beta cells
60 ith genes that contribute to protection from insulitis and diabetes (Idd3, Idd5, Idd10, and Idd18), t
61 n the nonobese diabetic (NOD) model of TIDM, insulitis and diabetes are dependent on the presence of
64 eficiency in the NOD mouse completely blocks insulitis and diabetes due to defects both in the initia
65 ayed diabetes in heterozygous females and no insulitis and diabetes in most homozygous female mice.
66 transfer, BDC T cells rapidly induced severe insulitis and diabetes in NOD.scid mice, whereas those f
69 OVA in pancreatic islet cells induces acute insulitis and diabetes only if endogenous lymphocytes, i
72 ed diabetes is lacking, we sought to produce insulitis and diabetes with either PolyIC and/or B:9-23
73 to partially protect congenic NOD mice from insulitis and diabetes, and to partially tolerize islet-
74 nction would alter the onset or magnitude of insulitis and diabetes, we used transgenic mice expressi
89 n, c-Rel deficiency dramatically accelerated insulitis and hyperglycemia in NOD mice along with a sub
91 maintained on acidic pH water (AW) developed insulitis and hyperglycemia rapidly compared with those
93 Early treatment with LTbetaR-Ig prevented insulitis and IDDM, suggesting that LT plays a critical
94 as well as significantly reduced severity of insulitis and improved beta-cell mass, when compared wit
95 d in islets from nonobese diabetic mice with insulitis and in rodent or human beta cells exposed in v
96 s those from BDC-Idd9 mice mediated a milder insulitis and induced diabetes with a significantly dela
97 se prevention correlated with suppression of insulitis and induction of GAD65-specific regulatory Th2
101 he transgene-dependent induction of profound insulitis and lethal diabetes following multiple low dos
102 of CXCR1/2 was associated with inhibition of insulitis and modification of leukocytes distribution in
103 T cells into the pancreatic islets, reduced insulitis and mononuclear cell infiltration, and promote
106 stration of AAV vIL-10 significantly reduced insulitis and prevented diabetes development in NOD mice
108 ice with Flt3-ligand significantly decreased insulitis and progression to diabetes and was associated
109 e JNK2 protein kinase) decreased destructive insulitis and reduced disease progression to diabetes.
110 ti-CD137-treated mice are not protected from insulitis and still harbor pathogenic T-cells, as demons
111 male recipients prevented the progression of insulitis and subsequent development of overt IDDM.
112 lts implicate chemokines as key mediators of insulitis and suggest that their blockade may represent
113 fecal transfer significantly suppressed the insulitis and T1D incidence in mice that were on AW but
114 nto 10-wk-old NOD mice prevented spontaneous insulitis and T1D, and the inhibitory effect was further
115 ells (nTregs) induce tolerance that inhibits insulitis and T1D, the in vivo cellular mechanisms under
117 se, as assessed by the absence of histologic insulitis and the absence of T-cell reactivity to islet
119 he expression of the mIg transgene increased insulitis and the incidence of diabetes compared with tr
121 es reveal a correlation between incidence of insulitis and the number of islets showing loss of peri-
123 nic (Tg) littermates, SOCS-1-Tg mice develop insulitis and their splenocytes transfer disease to NODs
125 d in the BBDR rat, which develops pancreatic insulitis and type 1A-like diabetes after infection with
126 -wk-old NOD mice before the typical onset of insulitis and was detected in B10 mice congenic for the
128 e expression profiling at day (d) 40 (before insulitis) and d65 (before disease onset) was conducted
129 function and mass, islet inflammation (i.e., insulitis), and autoantibodies specific for beta-cell an
130 cy of Foxp3+ and IL-10+ T cells, less severe insulitis, and a significant delay in the onset of hyper
131 rk activated in pancreatic beta cells during insulitis, and Arl6ip5, Tnfrsf10b, Traf2, and Ubc are ke
132 -producing cells, significant suppression of insulitis, and delay of the onset of hyperglycemia.
133 (+) DC led to the loss of T cell activation, insulitis, and diabetes mediated by CD4(+) T cells.
134 d the onset of T1D, attenuated the degree of insulitis, and improved pancreatic beta cell mass in a d
135 nstrained effector T cells to nondestructive insulitis, and increased numbers of intraislet FOXP3+ Tr
136 s by approximately 95%, decreased subsequent insulitis, and prevented diabetes in >60% of littermates
137 inhibit T cell activation, ablates invasive insulitis, and restores euglycemia, immune tolerance to
139 gulating autoimmunity in the early stages of insulitis, and the loss of IL-13Ralpha1 on islet-reactiv
141 stages of type 1 diabetes phenotype, before insulitis appears, we measured insulin autoantibodies (I
144 absolute prerequisite for the development of insulitis, as shown by studies in perforin-deficient tra
147 CD137 was dispensable for the development of insulitis but played a role to promote progression to ov
148 process was remarkable for not only showing insulitis, but also inflammatory destruction of the exoc
149 ABT-induced IL-4 and humoral responses, and insulitis, but enhanced IL-10 and Treg responses and pro
150 mory-phenotype lymphocytes trafficked to the insulitis, but Foxp3(+) regulatory T cells circulated le
152 f the nonobese diabetic (NOD) strain develop insulitis, but there is considerable variation in their
155 he pancreatic islets by autoimmune cells, or insulitis, can persist for long periods of time before t
156 AhR activation prevented the development of insulitis caused by the depletion of Foxp3(+) cells, dem
159 of lymphocyte infiltration in islet and less insulitis compared with that of the control groups.
162 )(/)(-) mice exhibited accelerated, invasive insulitis, corresponding to increased CD4(+) and CD8(+)
163 The rAAV-IL-10 therapy attenuated pancreatic insulitis, decreased MHC II expression on CD11b+ cells,
164 high prevalence of IAAs and a high degree of insulitis, despite a nearly complete resistance to diabe
165 lopment of insulin autoantibodies (IAAs) and insulitis, despite the recipients' pancreatic islets lac
166 r (GM-CSF) and interleukin-3 (IL-3) manifest insulitis, destruction of insulin-producing beta cells,
168 vivo, immunization with the EXO accelerates insulitis development in nonobese diabetes-resistant mic
169 When islets were examined in treated mice, insulitis development was blocked at early (3 wk) but no
177 nTreg depletion led to accelerated invasive insulitis dominated by CD11c(+) dendritic cells (ISL-DCs
180 e involved in the series of events provoking insulitis; for example, it may play a role in the physio
181 a diabetes-inducing agent, was injected into insulitis-free NOD. lpr/lpr mice, none of these mice dev
183 significant correlation was observed between insulitis frequency and CD45(+), CD3(+), CD4(+), CD8(+),
185 inst diabetes, whereas Tregs expanded during insulitis had minimal mTGF-beta and could not protect ag
187 at 12 weeks of age, mATG reversed pancreatic insulitis, improved metabolic responses to glucose chall
188 eptor (TCR) transgenic mice with spontaneous insulitis in F1 mice (FVB x NOD) and spontaneous diabete
191 detect vascular leakage in association with insulitis in murine models of type 1 diabetes, permittin
193 es, RAE1 expression was sufficient to induce insulitis in older, unmanipulated transgenic mice that w
194 uronan (HA) are characteristic of autoimmune insulitis in patients with type 1 diabetes (T1D), but th
195 and spleen and delayed onset of diabetes and insulitis in the NODrag1(-/-) lymphocyte adoptive transf
196 was higher, during the onset of destructive insulitis in the PLNs of nonobese diabetic (NOD) mice.
197 ialitis did not correlate with the degree of insulitis in the same animal and was less sensitive to a
199 We could detect the onset and evolution of insulitis in vivo and in real time, permitting us to stu
200 e BBDR strain, we observed a time-dependent, insulitis-independent pancreatic upregulation of Ccl11 i
201 olute and were monitored for diabetes onset, insulitis, infiltrating cells, immune cell function, and
203 othesis that inflammatory mechanisms trigger insulitis, insulin resistance, faulty insulin signaling,
204 gal-1 therapy shifted the composition of the insulitis into an infiltrate that did not invade the isl
211 mice with zymosan resulted in suppression of insulitis, leading to a significant delay in hyperglycem
213 amined T cells in pancreas, the diabetogenic insulitis lesion, and lymphoid tissues have revealed a b
216 ion with a spherical indenter and found that insulitis made islets mechanically soft compared with co
217 ntibodies, quantitatively reduced pancreatic insulitis, maintained islet insulin content, and altered
218 y, we reported that two distinct patterns of insulitis occur in patients with recent-onset T1D from t
221 iabetes either at the level of initiation of insulitis or at the level of progression from insulitis
223 ulin did not develop insulin autoantibodies, insulitis or autoimmune diabetes, in contrast with mice
224 limination of IL-4 did not alter the rate of insulitis or diabetes development in NOD mice, while the
225 islet Ag presentation or on the induction of insulitis or diabetes in either transfer or spontaneous
230 hen NOD mice were allowed to progress to the insulitis phase, the ablation of DC led to accelerated i
231 unable to suppress the disease in 10-wk-old insulitis-positive animals whose diabetogenic T cells ha
233 g-GAD expanded Tregs in both young and older insulitis-positive, nonobese diabetic (NOD) mice, but de
234 low-dose anti-CD3, this treatment stabilized insulitis, preserved functional beta-cell mass, and rest
237 21R expression renders NOD mice resistant to insulitis, production of insulin autoantibodies, and ons
238 Blockade of HMGB1 significantly inhibited insulitis progression and diabetes development in both 8
243 CD8(+), and CD20(+) cell numbers within the insulitis (r = 0.53-0.73, P = 0.004-0.04), but not CD68(
244 icant suppression of the late progression of insulitis, reduced infiltration of islets by autoreactiv
245 tes incidence in association with 1) reduced insulitis, reflected by reductions in CD4(+) T cells and
246 nset diabetic NOD mice led to elimination of insulitis, regeneration of host beta cells, and reversal
250 iabetic mice receiving HOT-100% showed lower insulitis scores, reduced T-cell proliferation upon stim
253 linical diabetes, age of diabetes onset, and insulitis severity was performed using subphenotype char
255 nonobese diabetic (NOD) mouse starts with an insulitis stage, wherein a mixed population of leukocyte
257 umbers and percentage during T cell-mediated insulitis, suggesting that this subset might be involved
260 ological and immunohistochemical analyses of insulitis, the identification of autoreactive CD8(+) T c
261 lectively, these results suggest that at the insulitis threshold at which CVB4 infection can first ac
264 ents and murine models, the progression from insulitis to diabetes is neither immediate nor inevitabl
265 Blockade of ICOS rapidly converts early insulitis to diabetes, which disrupts the balance of Tef
266 further analysis of the T cells involved in insulitis to elucidate their role in the etiology of T1D
267 govern the transition from clinically silent insulitis to frank diabetes by cross-presenting autoanti
272 frequency (the percent of islets displaying insulitis to total islets), infiltrating leukocyte subty
273 might be a possible autoimmune target and/or insulitis trigger in NOD or congenic mouse strains.
274 distinct stages of islet inflammation, peri-insulitis versus invasive insulitis, were harvested to e
277 type 1 diabetes, we asked whether autoimmune insulitis was associated with changes in the stiffness o
281 The role of M3 in chemokine blockade during insulitis was further supported by in vitro experiments
290 Foxp3(+) cells in AhR-induced suppression of insulitis was tested using NOD.Foxp3(DTR) mice, which sh
292 ures such as HLA class I hyperexpression and insulitis were specific for T1D and persisted in a small
293 inflammation, peri-insulitis versus invasive insulitis, were harvested to establish the expression pa
295 ted the development of effector function and insulitis whereas Bim-/- clone 4 cells were not autoaggr
296 observed in all type 1 diabetes donors with insulitis, while beta-cell area and mass were significan
297 lymphocytes that manifested as a pancreatic insulitis with beta-islet cell destruction and systemic
299 cific Rg T-cells produced variable levels of insulitis, with one TCR producing delayed diabetes.
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