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1 variety of animal models of inflammatory and immune disease.
2 ion of advances in our armamentarium against immune disease.
3 d had no genomic evidence of any known, rare immune disease.
4 ng variable immune mosaics and heterogeneous immune disease.
5 iagnosis, and care for patients with genetic immune disease.
6 s, by congenital infections or maternal allo-immune disease.
7 ad broad clinical impact in the treatment of immune disease.
8 onmental risk factor associated with chronic immune disease.
9 d in cancer, cardiac, neurodegenerative, and immune disease.
10 bnormal cells in infection, cancer, or other immune disease.
11 owledge has rapidly been translated to human immune disease.
12 nd that decreased Foxp3 expression can cause immune disease.
13 s, including inflammatory, neurological, and immune diseases.
14 alth and a range of immune-mediated and auto-immune diseases.
15 in the IL-10 promoter and has been linked to immune diseases.
16 novel target for therapeutic intervention of immune diseases.
17 o our understanding of immune mechanisms and immune diseases.
18 and are essential for the prevention of auto-immune diseases.
19 isms and contribute to autoantibody-mediated immune diseases.
20 M-1) has been implicated in inflammatory and immune diseases.
21 some also show linkage to other inflammatory immune diseases.
22 n the etiology of cardiovascular, renal, and immune diseases.
23 resenting a significant target in cancer and immune diseases.
24 d susceptibility of females to IFNy-mediated immune diseases.
25 l in treatments of cancer, inflammation, and immune diseases.
26 s have emerged as potential targets for auto-immune diseases.
27 e of the human body to implanted devices and immune diseases.
28 enerative medicine, brain, cancer, skin, and immune diseases.
29 ngly recognized in the management of chronic immune diseases.
30 e of traits related to inflammatory and auto-immune diseases.
31 e little effect on allergic diseases or auto-immune diseases.
32 p explain how genetic variants predispose to immune diseases.
33 eral pathologies ranging from sepsis to auto-immune diseases.
34 iscuss biomarkers relevant to AIH from other immune diseases.
35  genetic architecture of schizophrenia to 19 immune diseases.
36 rtunities for preclinical studies in various immune diseases.
37 ncies, hematological deficiencies, and other immune diseases.
38 in novel preventative strategies for chronic immune diseases.
39 nced understanding of human inflammatory and immune diseases.
40 iety of diseases ranging from cancer to auto-immune diseases.
41 ant IRF3-dependent gene expression linked to immune diseases.
42 seases such as diabetes and inflammatory and immune diseases.
43 es encoding these proteins that give rise to immune diseases.
44 nvariant NKT cells, as well as its impact on immune diseases.
45 gets to treat GVHD and other T-cell-mediated immune diseases.
46  therapeutic potentials for neurological and immune diseases.
47 naling pathways regulating cell migration in immune diseases.
48 and striking association with immune and non-immune diseases.
49  of molecular events underlying vascular and immune diseases.
50 nhibitory molecule for T cell activation and immune diseases.
51  response and pathogen-induced T-cell-driven immune diseases.
52  function and the aetiology of various human immune diseases.
53 paB) for its involvement in inflammatory and immune diseases.
54 ications in therapeutic treatment of various immune diseases.
55 cancers but also for genetic, infectious and immune diseases.
56 the hypothesis that myositis may be an 'allo-immune' disease.
57 is associated with human inflammatory(8) and immune diseases(9,10) as well as responses to immunother
58 ar Kv1 antibodies mainly associated with non-immune disease aetiologies, poor longitudinal clinical-s
59                        Uveitis is a systemic immune disease and a common cause of blindness.
60  and dysregulation is frequently observed in immune disease and cancer.
61 tibility loci occurs between different human immune diseases and by comparing conserved regions with
62 iduals, might also be relevant in other auto-immune diseases and cancer.
63 otrienes, inflammatory mediators involved in immune diseases and defense.
64 ender rats well suited for reproducing human immune diseases and evaluating therapeutic strategies, d
65 dentify novel TF-cytokine regulatory axes in immune diseases and immune cell lineage development.
66 T cell activation, which has implications in immune diseases and immunotherapy.
67 ammation and tissue damage in IL-23-mediated immune diseases and it suggests the GM-CSF-eosinophil ax
68 vel insights into mechanisms of (auto-/allo-)immune diseases and more rationally designed antibody-ba
69 e levels in predisposition and expression of immune diseases and on mechanisms of glucocorticoid effe
70 o the epidemiological association of certain immune diseases and schizophrenia.
71  we observed genetic correlation between six immune diseases and schizophrenia: inflammatory bowel di
72                While shared features of some immune diseases and the concept of immunologic resilienc
73                              We investigated immune diseases and the risk of classical HL in a popula
74 proaches to medical interventions for ocular immune diseases and vaccination methods.
75 s been implicated in a range of oncology and immune diseases and, as such, small-molecule inhibition
76 etes, CVD, hypertension, infectious disease, immune disease, and nephrotoxic drugs use at baseline.
77 s including different types of cancer, (auto)immune diseases, and also viral infections.
78 an diseases, including neurodegenerative and immune diseases, and cancer.
79 hallenges such as infectious diseases, (auto)immune diseases, and cancer.
80 r the treatment of certain viral infections, immune diseases, and cancer.
81 of the gastrointestinal (GI) tract, systemic immune diseases, and cancers.
82 in resistance, obesity, cardiovascular risk, immune diseases, and even mood and behavior.
83 optosis may cause diseases, such as cancers, immune diseases, and neurodegenerative disorders.
84  in human cancers, congenital abnormalities, immune diseases, and neurodevelopmental syndromes.
85 been implicated in the pathology of cancers, immune diseases, and neuronal disorders.
86                                   Concurrent immune diseases are common, and immunoglobulin A nephrop
87 transformative for kinase inhibitors in auto-immune diseases, as several inhibitors have finally prog
88 ndent eQTLs showed significant enrichment in immune disease-associated genetic variants, and they imp
89                                              Immune disease-associated variants are enriched within r
90 by a shared genetic region, and STAT1 /STAT4-immune disease-associated variants modulate IFN-gamma- a
91 ur results represent an in-depth analysis of immune-disease-associated variants across a comprehensiv
92                                              Immune-disease-associated variants are enriched in activ
93        Our results point towards the role of immune-disease-associated variants in early rather than
94 ts previously reported to be associated with immune diseases at genome-wide significance.
95 IL-13 signaling is a key driver of type2/Th2 immune diseases (atopic/allergic diseases).
96 c approach to modulate immune recognition in immune disease beyond HIV.
97 studies highlight the role of metabolites in immune diseases, but it remains unknown how much of this
98      Thus, decreased Foxp3 expression causes immune disease by subverting the suppressive function of
99  been shown to have therapeutic efficacy for immune diseases by preferentially expanding distinct T c
100 e of immune-mediated conditions such as auto-immune disease, cancer and response to infection.
101 ic sclerosis (SSc or scleroderma) is an auto-immune disease characterized by skin fibrosis.
102 eart disease, chronic lung disease, impaired immune disease, chronic renal disease, stroke, and cance
103                            The occurrence of immune disease comorbidities in Alzheimer's disease (AD)
104  to test the hypothesis that comorbid type 2 immune diseases confer protection against morbidity and
105 n of IRAK1 and type I interferons in various immune diseases, controlling IRAK1 activation via inhibi
106                        The clustering of the immune disease diffusion profiles reveals shared shared
107      DRB4*0103 is associated with concurrent immune diseases, DRB1*0301 with a poor treatment respons
108 eal repurposing of TOP inhibition to reverse immune diseases driven by SP140 loss.
109  not predict the development of long-lasting immune diseases during DI, in contrast to 2 months of he
110 ramework can facilitate the interrogation of immune disease GWAS hits and propose that the combinatio
111                  The role of DOCK11 in human immune disease has been long suspected but, to the best
112 d genes with downstream targets enriched for immune disease heritability, including many missed by ex
113  discoveries in the field of human monogenic immune diseases highlight critical genes and pathways go
114 thways associated with the immune system and immune disease in both organs.
115 ls, is emerging as an important mechanism of immune disease in both young and older patients.
116           Multiple sclerosis (MS) is an auto-immune disease in which the body's immune system attacks
117 ng bacterial genera are also associated with immune diseases in humans, laying a path for future stud
118 our inability to recapitulate the biology of immune diseases in vitro.
119 sms, particularly with respect to TG-related immune diseases, in which development of isozyme-specifi
120 nd SP140 splice variants are associated with immune diseases including Crohn's disease, multiple scle
121 AR, the gene that encodes ADAR1, cause human immune diseases, including Aicardi-Goutieres syndrome (A
122  that PIDs can also predispose to cancer and immune diseases, including allergy, autoimmunity, and in
123 pendent elements with risk loci for multiple immune diseases, including multiple sclerosis, inflammat
124 y a disorder of lipid metabolism but also an immune disease involving CD1.
125    Atherosclerosis is a chronic inflammatory/immune disease involving multiple cell types including m
126   However, the mechanism by which SHED treat immune diseases is not fully understood.
127 rising number of liver, cardiometabolic, and immune diseases, little is known about the genetic regul
128 zation of molecular trait QTLs at 345 unique immune disease loci.
129 ly, among QTL variants that colocalized with immune-disease loci, only 7% were gene expression QTL, w
130 autoimmune hepatitis by male sex, concurrent immune diseases, lower serum gamma-globulin and immunogl
131  ASD: sex, maternal familial history of auto-immune diseases, maternal immunization to CMV, IgG CMV l
132 n, also serving as a resource for dissecting immune disease mechanisms.
133 t for the treatment of inflammatory and auto-immune diseases, metabolic diseases, and resistant cance
134 n linked to several conditions, such as auto-immune diseases, metabolic syndrome, sleep disorders, an
135 has been found to be elevated in a number of immune disease models.
136 nserved regions with experimental autoimmune/immune disease models.
137 ave been found to be elevated in a number of immune disease models.
138              Translational opportunities for immune disease monitoring are driving the rapid developm
139          For old men with an inflammatory or immune disease (n=10), mean old to young ratios of T-cel
140 nventional T cells, which contributed to the immune diseases observed in these mice.
141                                         Many immune diseases occur at different rates among people wi
142 ontrol of this potentially debilitating auto-immune disease of the central nervous system.
143          Psoriasis is a chronic inflammatory immune disease of the skin characterized by a complex in
144 able goal in autoimmunity, and perhaps other immune diseases of activation.
145 o ablate the immune system in viral-mediated immune diseases or virus-initiated autoimmune disease ma
146 ion, proliferation, chemotaxis and invasion, immune-diseases, oxidative stress, regulation and cell s
147 present and greater flexibility for modeling immune disease pathogenesis and immunotherapies in PI mi
148  site of inflammation as a result of chronic immune diseases, pathogenic infection, and tissue injury
149  aggregation and has been implicated in auto-immune disease pathology.
150 y, we validated our method against the human immune disease pathway.
151 nvironment and microorganisms that determine immune disease phenotypes.
152 ogram of cell death that plays a key role in immune disease processes.
153  afflicted with certain rheumatological auto-immune diseases produce autoantibodies directed against
154     TGs are also autoantigens in a number of immune diseases, resulting in the production of autoanti
155 ppreciated following the genotyping of large immune disease sample sets on a shared SNP array: the 'I
156               A comparative analysis with 15 immune diseases showed that T1D is more similar genetica
157   One obstacle precluding the development of immune-disease specific "humanized" mice is that optimal
158 o build new models and therapies for related immune diseases such as allergies, fibrosis, and metabol
159 eceptor (TCR) that is critically involved in immune diseases such as autoimmune arthritis.
160                                      Chronic immune diseases, such as asthma, are highly prevalent.
161 herapeutic implications for the treatment of immune diseases, such as autoimmunity and allergy.
162 PN2) increase the risk of developing chronic immune diseases, such as inflammatory bowel disease (IBD
163  use of adoptive T(reg) cell therapy for non-immune diseases, such as neurological disorders and tiss
164 y region, while BATF and ESRRA overlap other immune disease susceptibility regions, validating our ap
165 rs in neutrophil transcriptional control and immune disease susceptibility.
166 asis and multiple sclerosis (MS) are complex immune diseases that are mediated by T cells and share m
167 of the interleukin-1 (IL-1) pathway leads to immune diseases that can result in chronic tissue and or
168 anifestations (EHM), mainly due to a complex immune disease, that damage small and medium vessels, ca
169 ine adjuvant development and inflammatory or immune disease therapy.
170  specific subfunctions of Treg cells and the immune diseases they regulate can be influenced by FoxP3
171                  We collected information on immune diseases through telephone interviews and perform
172 ies involving fibroblasts, ranging from auto-immune diseases to fibrosis and cancer.
173  in a variety of clinical contexts from auto-immune diseases to malignancy.
174 cination of patients with inflammatory (auto)immune diseases under anti-tumor necrosis factor (TNF) t
175    TREX1 mutations, previously implicated in immune disease, untether TREX1 from the ER, disrupt TREX
176 uted the diffusion profiles of more than 100 immune diseases using a multilayer network that includes
177 of common variants between schizophrenia and immune diseases using cross-trait LD score regression.
178                                              Immune disease was analyzed using flow cytometry of tiss
179 ole of statins in allergic diseases and auto-immune diseases, we conducted a Mendelian randomization
180             The comorbidities among the five immune diseases were best explained by biological pleiot
181 y triggers tissue injury and inflammation in immune diseases, which occur predominantly in females fo
182                                    Of the 11 immune diseases with available genome-wide summary stati
183 n (HSCT) is a curative therapy for blood and immune diseases with potential for many settings beyond
184  ATP6AP1 (Ac45) has been implicated in human immune diseases, yet the mechanism underlying how Ac45 r

 
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