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1 a-cell destruction during the development of autoimmune diabetes.
2 tolerance, allowing reversal of established autoimmune diabetes.
3 NKG2D is implicated in autoimmune diabetes.
4 play a critical role in the pathogenesis of autoimmune diabetes.
5 marily characterized, in the pathogenesis of autoimmune diabetes.
6 e of Tregs and autoreactive cells regulating autoimmune diabetes.
7 ted the potential of this subset to initiate autoimmune diabetes.
8 least in large part, in the pathogenesis of autoimmune diabetes.
9 nhanced susceptibility to the development of autoimmune diabetes.
10 olerance represents a therapeutic option for autoimmune diabetes.
11 ion treatment of NOD mice effectively treats autoimmune diabetes.
12 IGRP(206-214)) during the earliest stages of autoimmune diabetes.
13 ing this strain with NOD develop spontaneous autoimmune diabetes.
14 eage, which is destroyed in individuals with autoimmune diabetes.
15 G6pc2 is not essential for the emergence of autoimmune diabetes.
16 f the islets of Langerhans and their role in autoimmune diabetes.
17 ted the onset of disease in a mouse model of autoimmune diabetes.
18 ne was not sufficient to prevent spontaneous autoimmune diabetes.
19 as to ascertain the role of complement C3 in autoimmune diabetes.
20 ord blood transfusion to treat patients with autoimmune diabetes.
21 p3(+) cells in the BCD2.5/NOD mouse model of autoimmune diabetes.
22 cytokines, does not reduce the incidence of autoimmune diabetes.
23 genic upon adoptive transfer in the model of autoimmune diabetes.
24 in pancreatic beta-cells and do not develop autoimmune diabetes.
25 lity, enhanced T cell-DC contacts and caused autoimmune diabetes.
26 bout 2% of LEW.1WR1 rats develop spontaneous autoimmune diabetes.
27 cell tolerance, and prevent T cell-mediated autoimmune diabetes.
28 les in allograft rejection and recurrence of autoimmune diabetes.
29 and reprogram B-cells to effectively reverse autoimmune diabetes.
30 These mice develop a low incidence of autoimmune diabetes.
31 ive RIP-OVA mice is also sufficient to cause autoimmune diabetes.
32 t for development of novel therapies to cure autoimmune diabetes.
33 d effective means to treat disorders such as autoimmune diabetes.
34 that has to be placed in the perspective of autoimmune diabetes.
35 tope and T-cell autoreactivity in a model of autoimmune diabetes.
36 utoreactivity for the PI-1(47-64) epitope in autoimmune diabetes.
37 vo BLyS neutralization for the prevention of autoimmune diabetes.
38 iated inflammation using a transfer model of autoimmune diabetes.
39 OD strain of mice that spontaneously develop autoimmune diabetes.
40 4 T-cell system, a critical step to initiate autoimmune diabetes.
41 ouse is an invaluable model for the study of autoimmune diabetes.
42 strategy for immunotherapy in patients with autoimmune diabetes.
43 al value of rituximab as a novel therapy for autoimmune diabetes.
44 ys nonredundant roles in the pathogenesis of autoimmune diabetes.
45 (NOD) mouse, a spontaneous, chronic model of autoimmune diabetes.
46 CD25- also participates in the regulation of autoimmune diabetes.
47 y T cells, and the animals rapidly developed autoimmune diabetes.
48 +) regulatory T-cell expansion, and prevents autoimmune diabetes.
49 o local inflammation, islet destruction, and autoimmune diabetes.
50 fer suppressor function in a murine model of autoimmune diabetes.
51 ransplantation in humans and is effective in autoimmune diabetes.
52 agonist protected NOD mice from spontaneous autoimmune diabetes.
53 iabetic (NOD) mice, an experimental model of autoimmune diabetes.
54 with autoantigens might alter the course of autoimmune diabetes.
55 lin may indeed be the target antigen causing autoimmune diabetes.
56 autoreactive CD4 T cells and relevant Ags to autoimmune diabetes.
57 represents a mechanism of protection against autoimmune diabetes.
58 icient than polyclonal T(reg) in suppressing autoimmune diabetes.
59 , respectively, is completely protected from autoimmune diabetes.
60 cells that will attack beta cells leading to autoimmune diabetes.
61 the relationship between viral infection and autoimmune diabetes.
62 play an important pathophysiological role in autoimmune diabetes.
63 e previously been implicated as a trigger of autoimmune diabetes.
64 ice spontaneously developed T cell-dependent autoimmune diabetes.
65 nzyme A deficiency in the NOD mouse model of autoimmune diabetes.
66 D (GAD65), serve as determinants of risk for autoimmune diabetes.
67 lished NOD and transgenic RIP-LCMV models of autoimmune diabetes.
68 on beta cells accelerates the development of autoimmune diabetes.
69 IL-21, is a key factor in susceptibility to autoimmune diabetes.
70 nst multiple low-dose streptozotocin-induced autoimmune diabetes.
71 l infections and retards effector T cells in autoimmune diabetes.
72 to block the JAK-STAT pathway would prevent autoimmune diabetes.
73 driving disease progress in animal models of autoimmune diabetes.
74 pancreas and contributed to protection from autoimmune diabetes.
75 1J) mice remained resistant to virus-induced autoimmune diabetes.
76 eactive T cells that promotes development of autoimmune diabetes.
77 e of c-Rel in the development of spontaneous autoimmune diabetes.
78 in-induced diabetes, a drug-induced model of autoimmune diabetes.
79 K(b)/A12-21-monospecific CD8(+) T cells and autoimmune diabetes.
80 e in the progeny, influencing development of autoimmune diabetes.
81 o enhanced susceptibility to virus-triggered autoimmune diabetes.
82 a-cell damage, leading to the development of autoimmune diabetes.
83 that HA is critical for the pathogenesis of autoimmune diabetes.
84 yte deletion, BIM, in the NOD mouse model of autoimmune diabetes.
85 Th17 cells contributes to the development of autoimmune diabetes.
86 ainst beta-cells via nitric oxide and induce autoimmune diabetes.
87 The NOD mouse strain spontaneously develops autoimmune diabetes.
88 which to study the development and onset of autoimmune diabetes.
89 er may be sufficient to confer resistance to autoimmune diabetes.
90 the highest risk of developing experimental autoimmune diabetes.
91 proposed to play a role in the initiation of autoimmune diabetes.
92 ancreatic islets and a slower progression to autoimmune diabetes.
93 1D and is dispensable for the development of autoimmune diabetes.
94 the therapeutic potential of these cells in autoimmune diabetes.
95 ansactivator Tbx21/Tbet, and amelioration of autoimmune diabetes.
96 the peripheral blood of humans with type 1 (autoimmune) diabetes.
98 s I molecule is required to induce recurrent autoimmune diabetes after pancreas transplantation in mi
100 uppressed immunopathology in mouse models of autoimmune diabetes and airway inflammation, and increas
101 ve identified a novel endogenous trigger for autoimmune diabetes and an in vivo role for granzyme A i
102 cells (T regs) are important for preventing autoimmune diabetes and are either thymic-derived (natur
103 nts improves identification of patients with autoimmune diabetes and delineates those who have a more
104 mmatory condition, we examined patients with autoimmune diabetes and demonstrated that these subjects
107 epistatic mechanisms in the manifestation of autoimmune diabetes and further indicate the utility of
108 red with measuring Abs improves detection of autoimmune diabetes and how beta-cell function correlate
109 DC expansion is sufficient to prevent type 1 autoimmune diabetes and IBD, which suggests that interfe
110 IL-35 could be used as a potent inhibitor of autoimmune diabetes and implicate its potential therapeu
111 l in preventing the onset and progression of autoimmune diabetes and in promoting islet graft surviva
114 ole genome analyses and verified by Q-PCR in autoimmune diabetes and performed a hierarchical cluster
115 er than hematopoietic cells protects against autoimmune diabetes and point to a novel role for PD-1-P
116 T cells within the intestinal mucosa and to autoimmune diabetes and provide a strong rationale to de
117 a single-cell atlas defining the staging of autoimmune diabetes and reveals that diabetic autoimmuni
118 se findings identify a Tfh cell signature in autoimmune diabetes and suggest that this population cou
119 s in innate immunity influence the course of autoimmune diabetes and support the use of targeted stra
120 tolerance alone can protect NOD8.3 mice from autoimmune diabetes and that profound changes in T-cell
121 ve role for central memory CD8(+) T cells in autoimmune diabetes and that this protection is enhanced
122 ther the role of FasL in the pathogenesis of autoimmune diabetes and to determine whether gld-induced
123 iling Treg activity, Flicr markedly promotes autoimmune diabetes and, conversely, restrains antiviral
124 es in nonobese diabetic (NOD) mice prevented autoimmune diabetes and, importantly, reversed disease i
125 ice treated with AZD1480 were protected from autoimmune diabetes, and diabetes was reversed in newly
126 ing CD4(+) and CD8(+) T cell function during autoimmune diabetes, and thus may contribute to limiting
127 ic (NOD) mice, which are used to model human autoimmune diabetes, are resistant to costimulation bloc
128 ymph node is critical to the pathogenesis of autoimmune diabetes, as it constitutes the initial site
130 letion of T cell CD98 prevented experimental autoimmune diabetes associated with dramatically reduced
131 e diabetic mice, which spontaneously develop autoimmune diabetes based on the I-A(g7) variant of MHC-
132 pletely protects nonobese diabetic mice from autoimmune diabetes but also causes massive double-negat
133 le B7-2 (NOD-B7-2KO mice) are protected from autoimmune diabetes but develop a spontaneous autoimmune
134 critical K(b)/A12-21 epitope) did not induce autoimmune diabetes but elicited a systemic Foxp3(+) CD2
135 tpn22 knockdown did not increase the risk of autoimmune diabetes but, rather, conferred protection fr
136 bout 2% of LEW*1WR1 rats develop spontaneous autoimmune diabetes, but disease penetrance is much high
137 -CD3 treatment to be a promising therapy for autoimmune diabetes, but its mechanism of action remains
138 -CD3 is a promising therapeutic approach for autoimmune diabetes, but its mechanism of action remains
139 perplasia occurs following immune therapy of autoimmune diabetes, but the clinical remission soon aft
140 lls) are known to control the progression of autoimmune diabetes, but when, where, and how they exert
141 t that PTM contributes to the progression of autoimmune diabetes by eliciting T-cell responses to new
142 that IL-7 contributes to the pathogenesis of autoimmune diabetes by enabling T(E/M) cells to remain i
144 ating lymphoid organogenesis, Bcl-3 prevents autoimmune diabetes by inhibiting inflammatory chemokine
147 A(g7), in the NOD mouse model of spontaneous autoimmune diabetes, confers diabetes risk by modulating
148 ration of the immunotoxin to mouse models of autoimmune diabetes delays disease onset, and its admini
149 to substantial, long-term protection against autoimmune diabetes, despite limited intraislet IL-35 se
150 hance encephalomyelitis, but did inhibit the autoimmune diabetes developing spontaneously in nonobese
151 ts gradually lose their VTCN1 protein during autoimmune diabetes development despite upregulation of
152 ffects of hyperbaric oxygen therapy (HOT) on autoimmune diabetes development in nonobese diabetic (NO
153 lymphocytic choriomeningitis virus or during autoimmune diabetes development in the CD8-driven lympho
154 autologous transfer of DN T cells can impede autoimmune diabetes development, at least in the 3A9 TCR
156 a critical self-antigen in animal models of autoimmune diabetes, due to extremely limited access to
157 d is sufficient to prevent the recurrence of autoimmune diabetes following islet transplantation.
158 s, studies have described the progression of autoimmune diabetes, from the first appearance of autoan
159 unotherapy, an approach to selectively block autoimmune diabetes, generally declines in nonobese diab
162 es (Idd) intervals that confer resistance to autoimmune diabetes have been identified in mice and hum
164 ine if these patients, like animal models of autoimmune diabetes, have an early and severe loss of is
166 itis is an important pathological feature of autoimmune diabetes; however, mechanisms governing the r
167 cells are functionally capable of promoting autoimmune diabetes if they have a critical autoimmune s
169 etiopathological relationship between latent autoimmune diabetes in adults (LADA) and classical type
172 (16p13.13) were convincingly associated with autoimmune diabetes in adults (P </= 0.002), with consis
173 ent with the hypothesis that the genetics of autoimmune diabetes in adults and children are different
174 dhood-onset type 1 diabetes, the genetics of autoimmune diabetes in adults are not well understood.
177 vitiligo, autoimmune thyroid disease, latent autoimmune diabetes in adults, rheumatoid arthritis, pso
178 ct of oral anti-CD3 mAb on the prevention of autoimmune diabetes in AKR mice in which the low-dose st
179 the intestinal microbiota as a regulator of autoimmune diabetes in animal models is well-established
182 ats and reduce the incidence of experimental autoimmune diabetes in diabetes-prone (DP-BB/W) rats.
183 lls is deficient before onset of spontaneous autoimmune diabetes in diabetes-prone BB (BBDP) rats.
185 sure to viruses can affect the penetrance of autoimmune diabetes in genetically susceptible animals.
186 betes, we used a model of viral induction of autoimmune diabetes in genetically susceptible biobreedi
187 ow transplantation has been shown to prevent autoimmune diabetes in heavily irradiated nonobese diabe
190 AS605240 effectively prevented and reversed autoimmune diabetes in NOD mice and suppressed T-cell ac
191 ed tissues, delayed the onset of spontaneous autoimmune diabetes in NOD mice by inhibiting insulitis
192 hat Pep overexpression in T cells attenuates autoimmune diabetes in NOD mice by preferentially modula
193 for 12/15-LO in conferring susceptibility to autoimmune diabetes in NOD mice through its effects on m
194 of the costimulatory molecule B7-2 prevents autoimmune diabetes in NOD mice, but leads to the develo
195 a-galactosylceramide (alpha-GalCer) inhibits autoimmune diabetes in NOD mice, in part by inducing rec
196 ve recently shown that during progression to autoimmune diabetes in NOD mice, memory autoreactive reg
203 oreactive CD4 T cells are key for initiating autoimmune diabetes in NOD mice; however, little is know
205 ells obtained from diabetic NOD mice induced autoimmune diabetes in NOD/scid and NOD/CIIT mice, but t
206 similar regimen prevented the recurrence of autoimmune diabetes in NOD/severe combined immunodeficie
210 ) or FasL (called the gld mutation) prevents autoimmune diabetes in nonobese diabetic (NOD) mice, the
211 the conclusion that LADA is a milder form of autoimmune diabetes in patients of an advanced age.
212 R-Vbeta13, is required for susceptibility to autoimmune diabetes in rats, and selective depletion of
214 onistic Ab against PD-1 provoked destructive autoimmune diabetes in RIP-mOVA mice expressing chicken
216 eases and is involved in the pathogenesis of autoimmune diabetes in the BB/Wor animal model of the di
218 atory T (T reg) cells control progression to autoimmune diabetes in the BDC2.5/NOD mouse model by rei
221 ia genetically engineered B cells to prevent autoimmune diabetes in the NOD mouse (see the related ar
222 iabetes (Idd) loci modify the progression of autoimmune diabetes in the NOD mouse, an animal model of
224 n of diverse islet-infiltrating cells during autoimmune diabetes in the nonobese diabetic mouse.
225 ents an Ag-specific immunotherapy to resolve autoimmune diabetes in the presence of residual endogeno
226 provide insight into the polygenic nature of autoimmune diabetes in the rat and the interplay of gene
227 or antigen specificity during progression of autoimmune diabetes in the unmanipulated NOD mouse.
229 T cell clones closely resembles spontaneous autoimmune diabetes in which both CD4 and CD8 T cells ar
230 analyzed HLA class II genotypes, markers of autoimmune diabetes, in 187 children with permanent diab
231 develop insulin autoantibodies, insulitis or autoimmune diabetes, in contrast with mice containing at
232 amplification loop during the progression of autoimmune diabetes, in which initial T cell infiltratio
234 be involved in leukocyte recruitment during autoimmune diabetes, including members of the leukocyte
235 of Toso(-/-) dendritic cells did not induce autoimmune diabetes, indicating their tolerogenic potent
242 hypothesized that enhanced susceptibility to autoimmune diabetes is the result of targeting of insuli
245 estion about the pathogenesis of spontaneous autoimmune diabetes is whether there are primary autoant
248 deficiency in type 1 diabetes and in rodent autoimmune diabetes models is caused by beta-cell-specif
249 ll-destructive process using two independent autoimmune diabetes models, an inducible autoantigen-spe
250 ons were observed in induced and spontaneous autoimmune diabetes models, became apparent at diabetes
253 = 12), type 2 diabetes (T2D, n = 31), latent autoimmune diabetes of adults (LADA, n = 6) and type 1 d
254 ted GAD65 to patients classified with latent autoimmune diabetes of the adult (LADA) is safe and sugg
256 highly active in antigen presentation in the autoimmune diabetes of the NOD mouse: they do this by pr
257 lity complex (MHC) class II molecules in the autoimmune diabetes of the nonobese diabetic (NOD) mouse
259 of diabetes-resistant BB rats, which develop autoimmune diabetes only after perturbation of the immun
260 c) allele) for susceptibility to spontaneous autoimmune diabetes, or to diabetes elicited by reciproc
261 udy provides a novel natural system to study autoimmune diabetes pathogenesis and reveals a previousl
262 mmary, ADMSC therapy efficiently ameliorates autoimmune diabetes pathogenesis in diabetic NOD mice by
267 a-cell line were implanted subcutaneously in autoimmune diabetes-prone NOD mice, beta-cell-reactive T
268 a genetically disrupted CD38 allele into the autoimmune diabetes-prone NOD/Lt background accelerated
269 estigated the potential of LSF in preventing autoimmune diabetes recurrence after islet transplantati
273 esolution maps of pancreatic inflammation in autoimmune diabetes should prove invaluable in assessing
274 th R3 insulin-IA(g7) complexes would inhibit autoimmune diabetes specifically without interfering wit
275 nity TCRs could mediate potent insulitis and autoimmune diabetes, suggesting that TCR affinity does n
279 depletes and reprograms B-cells and reverses autoimmune diabetes, thereby providing a blueprint for d
280 of Itgb2 or ItgaL confers protection against autoimmune diabetes through distinctly different mechani
281 role for CD137 acting in the early phase of autoimmune diabetes to enhance regulatory cell productio
282 ffective in T cell-mediated diseases such as autoimmune diabetes to generate Ag-specific immunosuppre
283 for development of CD8 lymphocyte-dependent autoimmune diabetes (type 1 diabetes [T1D]) in the rat i
284 n the nonobese diabetic (NOD) mouse model of autoimmune diabetes using nonablative, combinatorial reg
285 he parvovirus Kilham rat virus (KRV) develop autoimmune diabetes via a mechanism that does not involv
290 of proinsulin, which plays a pivotal role in autoimmune diabetes, we found that targeting to the ER h
291 tudy the role of RAGE/ligand interactions in autoimmune diabetes, we tested the ability of soluble RA
292 munomodulatory candidate because it prevents autoimmune diabetes when expressed in beta cells or subc
293 OVA in pancreatic beta cells, develop severe autoimmune diabetes when given OT-I cells (OVA-specific
294 that mature DC (mDC) prevented the onset of autoimmune diabetes, whereas immature DC (iDC) were ther
295 reveals a unique protective role of c-Rel in autoimmune diabetes, which is distinct from other T-cell
296 mouse strain is that it develops spontaneous autoimmune diabetes, which shares many similarities to a
297 significantly lower incidence of spontaneous autoimmune diabetes, which was accompanied by fewer IFN-
298 ole of citrullination in the pathogenesis of autoimmune diabetes, with PAD inhibition leading to dise
299 ly, partial disruption of FasL protects from autoimmune diabetes without causing T-cell lymphoprolife
300 ets facilitates beta-cell destruction during autoimmune diabetes, yet specific mechanisms governing t