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1 inting, which is essential for infection and autoimmunity.
2 P3), resulting in impaired Treg function and autoimmunity.
3 L-6 and B cells promotes TH17-mediated neuro-autoimmunity.
4 er effective tumor immunity or contribute to autoimmunity.
5 intestinal barrier, but also contributing to autoimmunity.
6  new therapeutic interventions in cancer and autoimmunity.
7 imit antibody repertoire breadth and prevent autoimmunity.
8 fic T cells capable of mediating destructive autoimmunity.
9 ntaining peripheral tolerance and preventing autoimmunity.
10  determines the choice between tolerance and autoimmunity.
11 r helper (iNKTfh) cells that in turn promote autoimmunity.
12 tential role and therapeutic implications in autoimmunity.
13 y encompass elements of immunodeficiency and autoimmunity.
14  into the biology underlying B cell-mediated autoimmunity.
15 contributes, at least in part, to preventing autoimmunity.
16 glycome have been associated with cancer and autoimmunity.
17 ed in the bronchial mucosa, induces systemic autoimmunity.
18 3Kdelta alone in Treg cells does not lead to autoimmunity.
19  infection, mediate inflammation and prevent autoimmunity.
20 ant implications for vaccine development and autoimmunity.
21 n of NLR SUMM2 for initiating cell death and autoimmunity.
22 Th17 cells act synergistically to worsen CNS autoimmunity.
23  endogenous antigen and initiates lupus-like autoimmunity.
24 es, during both anti-fungal host defense and autoimmunity.
25 o self-antigens and limit the development of autoimmunity.
26 therapeutic target in cancer, infection, and autoimmunity.
27 eg) cells shows limited efficacy or leads to autoimmunity.
28  tools to decipher fundamental mechanisms of autoimmunity.
29 re required for downstream manifestations of autoimmunity.
30 gulates humoral immunity and limits systemic autoimmunity.
31 ammatory microenvironment such as cancer and autoimmunity.
32 ing protected mice from CD4(+) T cell-driven autoimmunity.
33 n females, demonstrating its broad impact on autoimmunity.
34 illance in cancers, infectious diseases, and autoimmunity.
35 response to infections and predisposition to autoimmunity.
36  antigen-specific TR1 cells suppressed liver autoimmunity.
37  for cancer immunotherapy and the control of autoimmunity.
38 icient to confirm a pathogenic link with GAD autoimmunity.
39 s in chronic infection, immunodeficiency, or autoimmunity.
40 ion (LOF) mutations who developed lupus-like autoimmunity.
41 balances that maintain tolerance and prevent autoimmunity.
42 s with serum markers of thyroid function and autoimmunity.
43 and broad implications in cancer, aging, and autoimmunity.
44 of B cell tolerance in this form of systemic autoimmunity.
45 etion exclusively during infection, avoiding autoimmunity.
46 ressive side-effects beyond control of islet autoimmunity.
47  Ikaros in mature B cells developed systemic autoimmunity.
48 s their underlying systemic inflammation and autoimmunity.
49 '-repeat serving as sensors for avoidance of autoimmunity.
50 e endocrine cellular stress as a trigger for autoimmunity.
51 ss was primarily caused by the recurrence of autoimmunity.
52 I3K pathway dysregulation in mouse models of autoimmunity.
53 id not undergo aberrant expansion or mediate autoimmunity.
54 r pool may likely ensure adequate control of autoimmunity.
55 epletion in an established model of systemic autoimmunity.
56 has important implications for virus-induced autoimmunity.
57 tion and preventing the onset of spontaneous autoimmunity.
58 nd highlight a potential role in suppressing autoimmunity.
59 ally, especially in the fields of cancer and autoimmunity.
60 and immune homeostasis, cancer immunity, and autoimmunity.
61 ory effects of exposure to EE, especially in autoimmunity.
62  expanded effector T cells and caused severe autoimmunity.
63  widely studied in contexts of infection and autoimmunity.
64 ll defects during the period of asymptomatic autoimmunity.
65 em contributes to the expression of systemic autoimmunity.
66 associated with humoral immune responses and autoimmunity.
67 tive target for modulating type I IFN-driven autoimmunity.
68 ing proposed as an environmental trigger for autoimmunity.
69 17 cell differentiation and pathogenicity in autoimmunity.
70 sease as well as the mechanisms that lead to autoimmunity.
71 gmented by the provision of soluble CTLA4 in autoimmunity.
72 s with implications for pathogen defense and autoimmunity.
73 druggable pathway to treat antibody-mediated autoimmunity.
74        None had any significant infection or autoimmunity.
75  for interferon production prior to clinical autoimmunity.
76 ted T cells, and can control T-cell-mediated autoimmunity.
77 intracellular C3 as biomarker of severity in autoimmunity.
78 ore and after the onset of preclinical islet autoimmunity.
79 rotein has the potential to drive lupus-like autoimmunity.
80 on could lead to abrogation of recurrence of autoimmunity.
81 ing patients with ICI-related heart-specific autoimmunity.
82 lead to chronic inflammation, or precipitate autoimmunity.
83 nts age-dependent development of spontaneous autoimmunity.
84 on can result in severe immunodeficiency and autoimmunity.
85 epwise fashion from asymptomatic preclinical autoimmunity.
86 cluding solid organ transplant (SOT; 33.8%), autoimmunity (15.9%), and hematologic malignancies (11.7
87 ential for deciphering genetic mechanisms of autoimmunity(4,5).
88               However, the high frequency of autoimmunity (57.4%), lymphoproliferation (52.4%), nonin
89     While genetic factors may predispose for autoimmunity, additional environmental triggers, such as
90  in quintiles and serum thyroid function and autoimmunity, adjusting for age, body mass index (BMI),
91  reverts diabetes and prevents recurrence of autoimmunity after islet transplantation in ~50% of NOD
92               PANDAS may result from induced autoimmunity against brain antigens, although this remai
93 We hypothesized that her syndrome was due to autoimmunity against muscarinic acetylcholine receptors,
94                                              Autoimmunity against pancreatic beta-cell autoantigens i
95       Previous studies indicate that induced autoimmunity against the voltage-gated KCNQ1 K(+) channe
96                                           In autoimmunity, aggressive immune responses are counteract
97 on to chronic GVHD involves the emergence of autoimmunity, although the underlying mechanisms driving
98 ations of mixtures with thyroid function and autoimmunity among potentially susceptible subgroups suc
99 years]), 1216 (18%) developed celiac disease autoimmunity and 447 (7%) developed celiac disease.
100 stem activation is typically associated with autoimmunity and a broad array of autoinflammatory disea
101                     Cycles of fasting reduce autoimmunity and activate lymphocyte-dependent killing o
102 trinsic Tgfb1 gene dose in the prevention of autoimmunity and allergic disease.
103 ral immune repertoire capable of controlling autoimmunity and also providing a new target for therape
104 netic factors impact risk for dermatological autoimmunity and anti-PD-L1 monotherapy in bladder cance
105 , which eliminate tumors without concomitant autoimmunity and are transcriptionally distinct from cla
106                       Repurposing drugs from autoimmunity and cancer immunotherapy has rapidly yielde
107 rrent and often life-threatening infections, autoimmunity and cancer, and it poses major diagnostic a
108 increase or decrease suppressive activity in autoimmunity and cancer, respectively.
109 ss responses and therefore predisposition to autoimmunity and cancer.
110 their roles and potential therapeutic use in autoimmunity and cancer.
111 .Fc protein in murine experimental models of autoimmunity and cancer.
112  The present report addresses the concept of autoimmunity and cardiac arrest.
113 f methylation differences that predate islet autoimmunity and clinical diagnosis may suggest a role f
114      Surprisingly, in mice having both liver autoimmunity and EAE, liver inflammation sequestered the
115 ering requirements for RRS1-R/RPS4-dependent autoimmunity and effector-triggered immunity.
116 hus, we identify a new regulatory pathway in autoimmunity and elucidate upstream signals that adjust
117            Here, we show that in preclinical autoimmunity and established systemic lupus erythematosu
118 is (SSc) is a disease at the intersection of autoimmunity and fibrosis.
119 continuous source of autoantigens to promote autoimmunity and further amplifying humoral responses.
120 ed with OVA-Sp) were protected from anti-MPO autoimmunity and GN, confirming the induction of therape
121           Currently, there are new trials in autoimmunity and heart and kidney transplantation to det
122         Understanding the pathophysiology of autoimmunity and hyperinflammation in these disorders ma
123 ient (Lyn(-/-)) mice are susceptible to both autoimmunity and IBD, we investigated the immunological
124 ether, these data support a role for CLRs in autoimmunity and implicate the MCL/MINCLE pathway as a p
125 und that expression of OVA resulted in fatal autoimmunity and in prevention of peripheral Treg genera
126 naling in B cells is critical for preventing autoimmunity and indicate that loss of alphav promotes e
127 sed or decreased intracellular C3 results in autoimmunity and infections, respectively.
128 ors with an emphasis on clinically validated autoimmunity and inflammatory pathways.
129 ls (Treg cells) are important for preventing autoimmunity and maintaining tissue homeostasis, but whe
130 rant ADAR1 activity has been associated with autoimmunity and malignancies.
131 eleton maintenance, providing a link between autoimmunity and neurodegeneration.
132 hy that is characterized by immunodeficiency autoimmunity and non-immunological symptoms.
133 s, hepatitis B and C, and HIV, as well as in autoimmunity and old age, highlighting the importance of
134 ally involved in the development of systemic autoimmunity and organ inflammation in systemic lupus er
135 ovided newer insights, including evidence of autoimmunity and previously unrecognized genes controlli
136                  After years of asymptomatic autoimmunity and progressive immune system remodeling, t
137  positive correlation with eventual systemic autoimmunity and proteinuria onset.
138 asis and sinopulmonary infection, as well as autoimmunity and squamous cell carcinoma, in addition to
139                                 The risk for autoimmunity and subsequently type 1 diabetes is 10-fold
140 monstrate that miR142-3p is induced in islet autoimmunity and that its inhibition enhances Treg induc
141 interrogating antigenic repertoires in human autoimmunity and the importance of antigen discovery for
142 g) cells play key roles in the prevention of autoimmunity and the maintenance of immune homeostasis a
143  numbers have been observed in patients with autoimmunity and the opposite effects on T(reg) cells oc
144  cells, T(H)17 cells have prominent roles in autoimmunity and tissue inflammation and are characteriz
145                  We showed that in models of autoimmunity and transplant rejection, adoptive transfer
146 n that the success of T(reg) cell therapy in autoimmunity and transplantation will encourage the clin
147 s settings of immune regulation that include autoimmunity and transplantation.
148 f proinflammatory properties(2), can promote autoimmunity and/or facilitate more effective tumour imm
149 nic islets is critical for the regulation of autoimmunity, and although the effect is systemic, the i
150 pathogens but also in inflammatory diseases, autoimmunity, and cancer in inflammasome-dependent and i
151 ding inflammatory diseases, atherosclerosis, autoimmunity, and cancer.
152 herapies for cancer, infectious disease, and autoimmunity, and discuss advances in cellular engineeri
153 immune disorders including immunodepression, autoimmunity, and GVHD might be intensified by injury.
154 ing problems of viral escapes, unpredictable autoimmunity, and heterogeneous responses appearing as a
155  key regulator of immunity during infection, autoimmunity, and inflammatory conditions.
156  cell checkpoint result in immunodeficiency, autoimmunity, and leukemia.
157 hy, hepatosplenomegaly, developmental delay, autoimmunity, and lymphoma of B-cell (n = 2) or T-cell (
158  paradox surrounding IFN-I and TH17 in neuro-autoimmunity, and may have utility in predicting therape
159 the use of low-dose IL-2 in transplantation, autoimmunity, and other inflammatory conditions.
160 aintains immune system homeostasis, prevents autoimmunity, and reduces immunopathology.
161 ers a new approach to monitor organ-specific autoimmunity, and represents a platform to analyze immun
162 e immunity and have relevance for infection, autoimmunity, and tumor immunology.
163 f-target effects include acute organ injury, autoimmunity, and variable effects on the tumor microenv
164 g thymic central tolerance and prevention of autoimmunity are not fully understood.
165 elf-peptide:MHC class II complex might limit autoimmunity arising from checkpoint blockade.
166  a transcriptional repressor that constrains autoimmunity, as an upstream promoter of GATA3 expressio
167  aged Fgl2(-/-) mice spontaneously developed autoimmunity associated with elevated autoantibodies.
168 essive immune phenotype and reduced CD11C(+) autoimmunity-associated B cells in healthy ANA+ European
169                                         Most autoimmunity-associated SNPs in the genome map to noncod
170 tigated the proportion of adults with celiac autoimmunity at a community medical center and their pro
171 -derived TGF-beta1 in regulating allergy and autoimmunity at distinct checkpoints in a Tgfb1 gene dos
172  phenotype, which includes immunodeficiency, autoimmunity, autoinflammation, and cancer.
173 cterized by an increased risk of infections, autoimmunity, autoinflammation, malignancy, and allergic
174 suppressive function that led to spontaneous autoimmunity but protected against tumour growth in mult
175                   Central tolerance prevents autoimmunity, but also limits T cell responses to potent
176  may be involved in the development of islet autoimmunity, but not T1D, in some young children.
177                                 Manipulating autoimmunity by inducing regulatory T cells is potential
178 cule FGIN-1-27 can be re-purposed to relieve autoimmunity by metabolic reprogramming of pathogenic Th
179 ells are eliminated in the thymus to prevent autoimmunity by promiscuous expression of tissue-restric
180 ly, we provide a link between c-Rel gain and autoimmunity by showing that c-Rel overexpression in B c
181 s') in which both beta-cell stress and islet autoimmunity can be harnessed as targets for interventio
182                                              Autoimmunity can occur when a checkpoint of self-toleran
183                                              Autoimmunity can result when cells fail to properly disp
184 on; however, adverse side effects, including autoimmunity, can occur.
185  in other settings as sterile wound healing, autoimmunity, cancer, and homeostasis.
186  diseases such as chronic neuroinflammation, autoimmunity, CNS injury, and more.
187                               Within the CNS autoimmunity control cohort, autoantibodies against aqua
188 resulted in spontaneous, lethal, multisystem autoimmunity, despite preserved numbers of phenotypicall
189 ipheral tolerance may play a greater role in autoimmunity development.
190  pathways involved in progression from islet autoimmunity differ from those pathways identified once
191 is of cancer cells and is also implicated in autoimmunity-driven type-1 diabetes, diabetic nephropath
192 tive strategy for cancer treatment; however, autoimmunity due to systemic impairment of their suppres
193 in metabolically demanding processes such as autoimmunity, graft rejection, cancer and uncontrolled i
194 termination of celiac disease (called celiac autoimmunity) have not been thoroughly evaluated.
195 have suggested possible links between DO and autoimmunity, Hepatitis C (HCV) infection, and cancer, b
196 roteomic biomarkers for development of islet autoimmunity (IA) and progression to type 1 diabetes in
197 me candidate environmental triggers of islet autoimmunity (IA), with potential as vaccine targets for
198 is of genes associated with inflammation and autoimmunity identified the c-Fos proto-oncogene as a me
199  B cell activation to prevent development of autoimmunity in a mouse model.
200  human immune homeostasis and contributes to autoimmunity in a TNFalpha-dependent manner.
201 ht define and prevent transition to clinical autoimmunity in ANA+ healthy individuals.
202 mune responses of the gut mucosa to systemic autoimmunity in lupus.
203 titutive activation typically causes harmful autoimmunity in mice and humans, often including severe
204 ency causes dysregulated IFN-I signaling and autoimmunity in mice.
205  and effector function, and ultimately fatal autoimmunity in mice.
206 mpairs Treg cell activation and causes fatal autoimmunity in mice.
207 to inhibition of autoantibody production and autoimmunity in mouse lupus models.
208 indings indicate that the autoantigen drives autoimmunity in MuSK MG through the accumulation of soma
209 tion and stability, leading to reduced islet autoimmunity in non-obese diabetic mice.
210 ve mechanism by which COPA mutations lead to autoimmunity in patients.
211 ), have shown remarkable effects in limiting autoimmunity in preclinical models.
212 rlying cause of increased polyreactivity and autoimmunity in RA.
213 ombined data indicate a role for anti-BC RNA autoimmunity in SLE and its neuropsychiatric manifestati
214 sponses, linking infection with induction of autoimmunity in the human immune system.
215 sence of AHAs and AIDAs provides evidence of autoimmunity in the majority of familial and in almost h
216  between autoantibodies and organ-restricted autoimmunity, including a link between anti-KHDC3L autoa
217 situ adaptive immunity broadly applicable to autoimmunity, infection, and cancer.
218 ans causes immune dysregulation resulting in autoimmunity, inflammatory bowel disease (IBD), hypogamm
219 r in-depth mechanistic studies on microbiota-autoimmunity interplay in AIDs are urgently needed and u
220 evidence leading to the consensus that islet autoimmunity is an essential component in the pathogenes
221                                      Risk of autoimmunity is associated with multiple genetic variant
222 utoimmune diabetes and reveals that diabetic autoimmunity is driven by transcriptionally distinct cel
223                                   Once islet autoimmunity is initiated, functional mapping identified
224 ns and tissue damage; however, their role in autoimmunity is less clear.
225 allenges in cancer, infectious diseases, and autoimmunity is presented.
226         Although the impact of Th17 cells on autoimmunity is undisputable, their pathogenic effector
227 l link between enteropathy and triggering of autoimmunity is yet to be established.
228 es with hyperactive immune disorders such as autoimmunity, lymphoproliferation, or atopy, but this co
229 uent adaptive immune activity and anti-heart autoimmunity may also contribute to the development of h
230 to convincingly linking RNA viruses to islet autoimmunity may be attributed to rapid viral mutation r
231 offer a mechanistic model where during islet autoimmunity miR142-3p/Tet2-mediated Treg instability co
232 nuate inflammation in murine T cell-mediated autoimmunity models.
233 rkers of PNS cells and a partially conserved autoimmunity module induced in glia cells.
234 tudy provides a rational explanation for the autoimmunity of patients with missense mutations of PRKD
235  autoantibodies indicates the onset of islet autoimmunity, often many years before clinical symptoms
236 t decipher how this process goes awry during autoimmunity or could be exploited for therapy.
237 ever, immune dysregulation, manifesting with autoimmunity or hyperinflammatory disease, has emerged a
238 ing breast, thyroid and other cancers and/or autoimmunity or neurodevelopmental issues including auti
239 rome type 1 (APS1), a rare monogenic form of autoimmunity, presents as widespread autoimmunity with T
240 ivity, Gal1 expression decreased with age in autoimmunity-prone nonobese diabetic (NOD) mice.
241  microbiota modulating susceptibility to CNS autoimmunity, providing insights into microbiome-directe
242 forts have focused on endocrine function and autoimmunity, recent studies identified a series of uniq
243 and natural killer (NK) cells which leads to autoimmunity, recurrent infections, and combined immune
244 and Th1/17 states, and overproduction of the autoimmunity-related cytokines IL-17A and IL-22.
245 t confirmation of a pathogenic link with GAD autoimmunity requires demonstration of intrathecal GAD a
246 omising therapeutic activities in cancer and autoimmunity, respectively.
247 eptor type 22 (PTPN22) is encoded by a major autoimmunity risk gene.
248 ic, with increased early-onset infection and autoimmunity risk that is not seen in most patients who
249 ents a potential candidate for targeting CNS autoimmunity.SIGNIFICANCE STATEMENT Multiple sclerosis i
250 in 1988, but several controversies about GAD autoimmunity still remain.
251 nd 87 controls from the prospective Diabetes Autoimmunity Study in the Young (DAISY) cohort.
252 ated with persistence, tumor metastasis, and autoimmunity, such as soluble CD163 (sCD163), chitinase-
253  may thus be crucial players in exacerbating autoimmunity targeting the heart.
254                     In contrast to models of autoimmunity that are less dependent on IFN-gamma, ampic
255 activity in a mouse model of T cell-mediated autoimmunity that mimics multiple sclerosis (MS).
256               Mice with established anti-MPO autoimmunity that received CD4(+) T cells transferred fr
257                                           In autoimmunity, these same pathways can be targeted to opp
258       While Th17 T cells are associated with autoimmunity, they are present around many different sol
259  failure disorders linked to T-cell-mediated autoimmunity; they are associated with an increased risk
260 presumed primary MN associated with signs of autoimmunity (three of 16 patients); only one of the 14
261           IgG immune complexes (ICs) promote autoimmunity through binding fragment crystallizable (Fc
262 n shaping the T cell repertoire and limiting autoimmunity through both thymic clonal deletion and Tre
263 of dietary fiber have been shown to suppress autoimmunity through mechanisms that include enhanced re
264 1, MKK1/2, and MPK4, triggers cell death and autoimmunity through the nucleotide-binding leucine-rich
265 nts with autoimmune diseases and may promote autoimmunity through the presentation of self-antigen to
266 4, TT4) and triiodothyronine (fT3, TT3), and autoimmunity [thyroid peroxidase and thyroglobulin antib
267 rs that contribute to progression from islet autoimmunity to clinical type 1 diabetes.
268 ty as an important checkpoint in translating autoimmunity to inflammation.
269 s and can be used to predict transition from autoimmunity to inflammatory arthritis.
270 sis affects the transition from asymptomatic autoimmunity to inflammatory disease are incompletely ch
271                          Research implicates autoimmunity to nonmyelin self-antigens as important con
272                  These findings suggest that autoimmunity to RBPs, such as hnRNP A1, play a role in n
273                  Data from our lab implicate autoimmunity to the RNA binding protein (RBP) heterogene
274  < 8.5 x 10(-8)) with progression from islet autoimmunity to type 1 diabetes.
275 pe 1 diabetes, a childhood disease involving autoimmunity toward multiple islet antigenic peptides.
276 expansion of the MHC gene family, associated autoimmunity trade-offs, hitchhiking of deleterious muta
277 ne responses in infectious disease, allergy, autoimmunity, transplantation, and cancer.
278        The therapeutic use of Abs in cancer, autoimmunity, transplantation, and other fields is among
279 stion of significant clinical importance for autoimmunity, tumor immunology, and infectious disease.
280                                 The enhanced autoimmunity upon deletion of STAT3 in B cells is also r
281                                              Autoimmunity usually appears in genetically susceptible
282 l tissues upon dietary intake and to promote autoimmunity via the Th17 cell axis.
283                                    Increased autoimmunity was associated with specific expansion of t
284 precision medicine therapeutic approaches in autoimmunity, we explored the ability of p110delta inhib
285                      To provide evidence for autoimmunity, we searched for AHAs and AIDAs in ARVC.
286                               In preclinical autoimmunity, we show a marked enrichment of an interfer
287 eles are associated with severe, early-onset autoimmunity; we show that heterozygous carriage of an A
288    Immune parameters defining heart-specific autoimmunity were investigated in experimental TnI-AM an
289 id infiltrations, inflamatory conditions, or autoimmunity were somewhat more likely to have an identi
290  biomarkers of thyroid function but not with autoimmunity, which were within normal ranges for health
291 xes, and they outline a general mechanism of autoimmunity with autoantibodies being produced by ignor
292 tients suggests a susceptibility to systemic autoimmunity with important implications in monitoring a
293      Biallelic deficiency precipitated fatal autoimmunity with intense autoantibody production and dy
294 form of autoimmunity, presents as widespread autoimmunity with T and B cell responses to multiple org
295 -immune interactions during inflammation and autoimmunity, with a focus on barrier function and CD4(+
296  (SuperTreg cells) that can resolve advanced autoimmunity, with Brg1 re-expression in a minor fractio
297                    Neither scenario provoked autoimmunity, with no evidence of immunohistopathology a
298 ncy may increase future risk of infection or autoimmunity, with premature immunosenescence mediated t
299 opoietic cell transplantation that resembles autoimmunity, with unclear pathogenesis and few effectiv
300 en-specific donor T(regs) and controls islet autoimmunity without long-term immunosuppression.

 
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