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1  that, in this case, will mount a pathogenic autoimmune reaction.
2 ay activate nonparenchymal cells and provoke autoimmune reaction.
3 a burgdorferi, or rather a self-perpetuating autoimmune reaction.
4 ombination competent retrovirus, cancer, and autoimmune reaction.
5 in during mitosis, which may help to prevent autoimmune reaction.
6  may be a manifestation of a small RNA-based autoimmune reaction.
7 collective, and they potentially cause fewer autoimmune reactions.
8 ariants of HLA genes that contribute to many autoimmune reactions.
9 olerant to self-antigens, thereby preventing autoimmune reactions.
10  immune response, mediating inflammation and autoimmune reactions.
11 duction of colitis by infections, drugs, and autoimmune reactions.
12                    There were no symptomatic autoimmune reactions.
13 eliminated to avoid harmful inflammatory and autoimmune reactions.
14 be a component of antimicrobial immunity and autoimmune reactions.
15 ced to a single complex demonstrated various autoimmune reactions.
16 opment of strategies for controlling harmful autoimmune reactions.
17 ; predominance of stimulatory signals favors autoimmune reactions.
18 at dominant T cell stimulation might promote autoimmune reactions.
19 ate in the development of such tissue-driven autoimmune reactions.
20 the body (self-antigens), thereby minimizing autoimmune reactions.
21 immunoinflammatory pathways and the onset of autoimmune reactions.
22 es, a phenomenon that might serve to inhibit autoimmune reactions.
23 ial for adaptive immune responses as well as autoimmune reactions.
24 r its homologous regions can also trigger an autoimmune reaction against aquaporin-4 and inflammation
25 sis of CAA-ri may be mediated by a selective autoimmune reaction against cerebrovascular Abeta, direc
26 e most common autoimmune liver diseases, the autoimmune reaction against hepatocytes and biliary epit
27 lass I antigen expression and may trigger an autoimmune reaction against MHC class II antigens throug
28                           Suppression of the autoimmune reaction against pancreatic beta cells was ev
29 oss of motor neurons in the spinal cord, and autoimmune reaction against these cells.
30 ation, anergic cells can induce a pathologic autoimmune reaction against tissue expressing the same A
31 efense against intruding microorganisms, and autoimmune reactions against intraocular antigens.
32 neoplastic neurological syndromes arise from autoimmune reactions against nervous system antigens due
33  in non-malignant cells, which can result in autoimmune reactions against non-malignant cells from th
34 chanistic insights connecting stress-induced autoimmune reactions against the brain and stress suscep
35  autoantibodies and IFN-a, which leads to an autoimmune reaction and exacerbates lupus-like symptoms.
36  beneficial effect on T1D by attenuating the autoimmune reaction and improving beta cell health.
37                 The association of zinc with autoimmune reactions and cancers as diseases with increa
38 nd fungal infections) or pathological (e.g., autoimmune reactions and contact sensitivity reactions s
39 terleukin-6 (IL-6) is critical to triggering autoimmune reactions and contributes substantially to bi
40 y mechanisms of CD8-mediated tissue-specific autoimmune reactions and to identify potential treatment
41 in the control of graft-versus-host disease, autoimmune reactions, and the growth of certain tumors.
42  the mammalian immune system from developing autoimmune reactions by forming a self-tolerant repertoi
43 monstrating the activation of heart-specific autoimmune reactions by ICI therapy.
44 atments for multiple sclerosis (MS) focus on autoimmune reactions causing demyelination, it is possib
45 tic disorders are thought to be caused by an autoimmune reaction directed against 'onconeural' antige
46 nt eradication of the spirochete suggests an autoimmune reaction downstream of the original bacterial
47 oreactive T cells and may restrict bystander autoimmune reactions following the innate immune respons
48                    The Tg, a known target of autoimmune reactions in ATh, was cleaved at lower levels
49 nt and potential prevention of cell-mediated autoimmune reactions in skin.
50  CD4(+)Foxp3(+) T-reg to effectively control autoimmune reactions in the target organ, it may also be
51  and for its propensity to engender untoward autoimmune reactions, including serum sickness-like dise
52 s and macrophages participating in allo- and autoimmune reactions, including the perivascular inflamm
53 y plasmacytoid DCs and B cells amplifies the autoimmune reaction leading to disease manifestations.
54 red toxic properties and the induction of an autoimmune reaction must be found.
55 ence suggests that it may be triggered by an autoimmune reaction or, conversely, initiate an autoimmu
56 new biomarkers that predict the onset of the autoimmune reaction preceding autoantibody positivity or
57 t they also highlight that in vivo during an autoimmune reaction, RA suppresses autoimmunity mainly b
58                                              Autoimmune reactions reflect an imbalance between effect
59 rs and minimizing potential risks, including autoimmune reactions resembling Omenn syndrome.
60           The T-cell activity and associated autoimmune reaction seem to induce epithelial and stroma
61                                          The autoimmune reaction that targets neutrophil serine prote
62 nosis, perhaps because the host can tolerate autoimmune reactions that destroy tumour cells at some c
63 V-1 KOS) infection triggers T cell-dependent autoimmune reactions to corneal tissue.
64             Celiac disease, characterized by autoimmune reactions to dietary gluten, affects up to 3
65 induce atherosclerosis via the mechanisms of autoimmune reactions to HSP60 expressed on arterial endo
66  study was to investigate the involvement of autoimmune reactions to native and post-translationally
67                               In conclusion, autoimmune reactions to native and post-translationally
68           Regulatory T cells protect against autoimmune reactions to self antigens and assist in the
69 The cause of BD remains unknown, although an autoimmune reaction triggered by an infectious agent in
70 hat tissues acquire the ability to attenuate autoimmune reactions upon repeated responses to antigens
71 an be processed and presented to initiate an autoimmune reaction, we surmise that cell death triggere
72 issue and are primed to attenuate subsequent autoimmune reactions when antigen is re-expressed.
73   However, autoantibodies indicate an active autoimmune reaction, wherein the immune tolerance is alr
74         T cell inhibitory mechanisms prevent autoimmune reactions, while cancer immunotherapy aims to
75 us self-protein results in a severe systemic autoimmune reaction with skin inflammation, wasting, and