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1 recruitment in vivo (e.g., in B cell-related immune disorders).
2 itical immune proteins, yielding a syndromic immune disorder.
3 s are viable and exhibit no obvious signs of immune disorder.
4 proved to be unaffected by any T-lymphopenic immune disorder.
5 d/or function in immune cells, leading to an immune disorder.
6 ned as an allergic Th2-mediated inflammatory immune disorder.
7 F-alpha found in these patients suggested an immune disorder.
8 Foxp3 expression in T(r) cells with various immune disorders.
9 w therapy for the treatment of several human immune disorders.
10 has been associated with numerous cancer and immune disorders.
11 in transplantation and other T cell mediated immune disorders.
12 a constellation of rare, autosomal recessive immune disorders.
13 NAs is essential for protection against auto-immune disorders.
14 e treatment for hematologic malignancies and immune disorders.
15 eases, including psychiatric, metabolic, and immune disorders.
16 other mouse models designed to reflect human immune disorders.
17 eurologic, psychiatric, cardiometabolic, and immune disorders.
18 with various diseases, including cancer and immune disorders.
19 genetic risk for both neurodevelopmental and immune disorders.
20 rs exhibited higher polygenicity compared to immune disorders.
21 generative, cardiovascular, nutritional, and immune disorders.
22 ent is essential in the treatment of several immune disorders.
23 el susceptibility to infectious diseases and immune disorders.
24 ll differentiation in normal homeostasis and immune disorders.
25 immunomodulatory drugs to treat a variety of immune disorders.
26 ption for tuning the immune system to target immune disorders.
27 be targeted in diseases such as cancers and immune disorders.
28 patients suffering from autoantibody-driven immune disorders.
29 ies targeting Bregs for better management of immune disorders.
30 s suis can be beneficial in treating various immune disorders.
31 otential therapeutic target for Treg-related immune disorders.
32 ditions such as liver diseases, diabetes and immune disorders.
33 th development of childhood asthma and other immune disorders.
34 fficacy and underlying mechanisms of MSCs in immune disorders.
35 rincipal driver of multiple inflammatory and immune disorders.
36 stry can inform therapies to resolve complex immune disorders.
37 ses, including cancer, neurological and auto-immune disorders.
38 therapies can be applied to treat additional immune disorders.
39 buting to risk, with some loci shared across immune disorders.
40 ontributing risk factor for autoimmunity and immune disorders.
41 for high-risk hematological malignancies and immune disorders.
42 NKG2D and the pathogenesis of organ-specific immune disorders.
43 e effective in the treatment of several auto-immune disorders.
44 athogenesis of various inflammatory and auto-immune disorders.
45 s may lead to new therapeutic strategies for immune disorders.
46 ceptibility to several inflammatory and auto-immune disorders.
47 to new therapies for intestinal and systemic immune disorders.
48 ssociated extraintestinal manifestations and immune disorders.
49 facilitate the therapeutic use of iTregs in immune disorders.
50 ponse to disease and into the development of immune disorders.
51 therapeutic agent specific for CTL-mediated immune disorders.
52 novel therapeutic strategy for CTL-mediated immune disorders.
53 eles are functionally significant in complex immune disorders.
54 s cancers, human immunodeficiency virus, and immune disorders.
55 ctions in other intestinal and nonintestinal immune disorders.
56 nvolved in the pathogenesis of XLP and other immune disorders.
57 studies of antiadhesion therapies in various immune disorders.
58 egard to both the initiation and severity of immune disorders.
59 est priority targets for study in other auto-immune disorders.
60 -17 cells) and has been linked to many human immune disorders.
61 or therapeutic intervention in metabolic and immune disorders.
62 uals or the implications of such for chronic immune disorders.
63 lipids and to reduce inflammation in certain immune disorders.
64 severe combined immunodeficiency, the first immune disorder accepted for population-based screening,
65 thrombocytopenia (HIT), a potentially fatal immune disorder affecting 1-5% of patients receiving hep
68 c syndrome, were clustered together, whereas immune disorder and chronic kidney disease displayed a d
73 worst, the ability to rapidly diagnose rare immune disorders and ensure delivery of precision medici
76 omas in individuals with acquired and innate immune disorders and is strongly associated with Hodgkin
77 m is therefore desirable in the treatment of immune disorders and lymphocyte cancers, but little is k
78 ed as a serum marker of T cell activation in immune disorders and of tumor burden in Tac-expressing m
80 urthermore, the broad spectrum of underlying immune disorders and the type of graft represent importa
82 eprint for the study of paediatric blood and immune disorders, and a reference for harnessing the the
87 e diagnostic workup of patients with complex immune disorders, and is as essential, if not more so, d
88 tal cytokine linking innate and Th2 adaptive immune disorders, and is upregulated by environmental po
90 ty and immunopathology, in allergy and other immune disorders, and recent progress towards defining t
91 ding consideration of underlying genetic and immune disorders, and use hypothetical patient cases to
93 th defects; endocrine, metabolic, blood, and immune disorders; and HIV/AIDS were the most overfunded
94 ital roles in the immune system, and several immune disorders are associated with disturbances of the
96 g infective endocarditis, rather than a host immune disorder, as the cause of infective endocarditis
100 s finding opens new avenues for treatment of immune disorders based on selective targeting of activat
101 of ESCRT dysfunctions, including infections, immune disorders, cancers and neurological diseases.
102 ere combined immunodeficiency (X-SCID) is an immune disorder caused by mutations in the IL2RG gene an
104 rrors of immunity (MEI) encompass a group of immune disorders caused by somatic or gonosomal gene var
106 hronic granulomatous disease (CGD), a severe immune disorder characterized by the inability of phagoc
107 s a rare, rapidly fatal, autosomal recessive immune disorder characterized by uncontrolled activation
108 of Usp21 specifically in Treg cells display immune disorders characterized by spontaneous T-cell act
109 lymphoproliferative disease (XLP) is a rare immune disorder commonly triggered by infection with Eps
110 netic variation in patients with unexplained immune disorders could uncover novel, actionable genetic
111 drug target for the treatment of a number of immune disorders due to the central role that they play
112 at included endocrine, metabolic, blood, and immune disorders (EMBI disorders), chronic kidney diseas
113 xic T-cell-mediated tissue damage in complex immune disorders exhibiting upregulation of IL15 and IL2
115 igodendrocytes, may develop in patients with immune disorders following reactivation of chronic benig
116 the multitude of other HSC-driven blood and immune disorders for which transplant can be disease-alt
117 mammalian CLR, in pneumonic sepsis, a deadly immune disorder frequently associated with a nonresolvin
118 ilities in the modulation of a wide range of immune disorders, from autoimmune diseases to cytokine s
119 gh the causal role of mosaicism in monogenic immune disorders has been recognized for over two decade
121 gest that the genetic risk for noninfectious immune disorders has gradually increased over millennia
122 kage searches of autoimmune and inflammatory/immune disorders have identified a large number of non-m
124 ent cytotoxicity led to the life-threatening immune disorder hemophagocytic lymphohistiocytosis (HLH)
125 rtant role in the most frequent drug-induced immune disorder, heparin-induced thrombocytopenia (HIT).
126 individuals from conditions such as primary immune disorders, HIV, or posttransplant immunosuppressi
128 dings that CD is primarily a T cell-mediated immune disorder in which CD4(+) T cells that recognize g
129 ugh successful therapies have been found for immune disorders in animal studies, few have passed the
132 D11 mutations cause several distinct primary immune disorders in human subjects, including severe com
133 NSTs are linked to several developmental and immune disorders in humans, and in pathogenic microbes t
134 ld establish therapeutic targets for several immune disorders in which estrogens play a prominent rol
135 that has been reported to be associated with immune disorders, in the modulation of carotid vasodilat
137 e importance of understanding how underlying immune disorders including immunodepression, autoimmunit
138 ved between neurodevelopmental disorders and immune disorders, including both positive and negative c
139 and might be developed for the treatment of immune disorders, including inflammatory bowel diseases.
140 We systematically investigated patterns of immune disorders, including predominantly T helper 17-(s
141 Factors contributing to ASCVD in women with immune disorders, including traditional risk factors, dy
142 ons including oculocutaneous telangiectasia, immune disorders, increased susceptibly to cancer and re
143 orary thought holds that asthma is a complex immune disorder involving innate as well as adaptive imm
144 ly epidemic with use of the term gay-related immune disorder is misleading regarding which population
145 e activities of regulatory B (Breg) cells in immune disorders is an emerging therapeutic strategy for
150 a number of cancers, metabolic syndrome, and immune disorders, making it an important target for the
151 hogens found in patients with AIDS and other immune disorders, N-[(2,4-diaminopteridin-6-yl)methyl]di
152 tigen (HLA) and non-HLA genes and with other immune disorders, notably juvenile diabetes and thyroid
154 -gamma are implicated in the pathogenesis of immune disorders of the central nervous system (CNS).
156 different causes, including inflammatory and immune disorders, oxidative stress, and nephrotoxins, am
157 riables specific to populations with chronic immune disorders, particularly in women, is emphasized.
159 1 psychiatric diagnoses or cardiovascular or immune disorders performed a functional neuroimaging tas
160 , adds significant disease burden in primary immune disorders (PID) and inborn errors of immunity (IE
161 Inborn errors of immunity (IEI), or primary immune disorders (PIDs), predispose individuals to infec
164 inked to various metabolic, inflammatory and immune disorders, regulatory proteins controlling macrop
167 wing evidence that rituximab has efficacy in immune disorders resulting from autoantibody formation.
169 odeficiency often coincides with hyperactive immune disorders such as autoimmunity, lymphoproliferati
170 s are widely used agents in the treatment of immune disorders such as rheumatoid arthritis and inflam
171 nce of infection can lead to pathogenesis of immune disorders, such as Aicardi-Goutieres syndrome.
173 hat may be exploited in treatment of chronic immune disorders, such as multiple sclerosis and inflamm
174 ustering of neurodevelopmental disorders and immune disorders suggest shared genetic risk factors.
175 he corresponding cytokines used by different immune disorders suggest unique targets for drug discove
176 rs was associated with liability for several immune disorders, suggesting that vertical pleiotropy re
177 ytopenia is a relatively common drug-induced immune disorder that can have life-threatening consequen
178 ommon variable immunodeficiency (CVID) is an immune disorder that not only causes increased susceptib
179 enetically heterogeneous autosomal recessive immune disorder that results when the critical regulator
180 gut microbiota dysbiosis is associated with immune disorders, the underlying mechanism remains unkno
182 ota, known as dysbiosis, can trigger several immune disorders through the activity of T cells that ar
184 and adding endocrine, metabolic, blood, and immune disorders to the health conditions causing SHS.
185 A connection between OST dysregulation and immune disorders was demonstrated in Trex1(-/-) mice, TR
186 m five neurodevelopmental disorders and four immune disorders, we conducted genome-wide, local geneti
187 Around 50%-90% of genetic variants of the immune disorders were shared with neurodevelopmental dis
188 apies are especially adaptable for blood and immune disorders, where clinical methods allow haematopo
193 ucosal surface is illustrated by the primary immune disorder, X-linked agammaglobulinemia in which pa