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1 ombination competent retrovirus, cancer, and autoimmune reaction.
2 may be a manifestation of a small RNA-based autoimmune reaction.
3 that, in this case, will mount a pathogenic autoimmune reaction.
4 ay activate nonparenchymal cells and provoke autoimmune reaction.
5 a burgdorferi, or rather a self-perpetuating autoimmune reaction.
6 immunoinflammatory pathways and the onset of autoimmune reactions.
7 olerant to self-antigens, thereby preventing autoimmune reactions.
8 duction of colitis by infections, drugs, and autoimmune reactions.
9 There were no symptomatic autoimmune reactions.
10 eliminated to avoid harmful inflammatory and autoimmune reactions.
11 be a component of antimicrobial immunity and autoimmune reactions.
12 ced to a single complex demonstrated various autoimmune reactions.
13 opment of strategies for controlling harmful autoimmune reactions.
14 ; predominance of stimulatory signals favors autoimmune reactions.
15 at dominant T cell stimulation might promote autoimmune reactions.
16 ate in the development of such tissue-driven autoimmune reactions.
17 the body (self-antigens), thereby minimizing autoimmune reactions.
18 es, a phenomenon that might serve to inhibit autoimmune reactions.
19 ariants of HLA genes that contribute to many autoimmune reactions.
20 r its homologous regions can also trigger an autoimmune reaction against aquaporin-4 and inflammation
21 sis of CAA-ri may be mediated by a selective autoimmune reaction against cerebrovascular Abeta, direc
22 lass I antigen expression and may trigger an autoimmune reaction against MHC class II antigens throug
25 ation, anergic cells can induce a pathologic autoimmune reaction against tissue expressing the same A
28 nd fungal infections) or pathological (e.g., autoimmune reactions and contact sensitivity reactions s
29 terleukin-6 (IL-6) is critical to triggering autoimmune reactions and contributes substantially to bi
30 y mechanisms of CD8-mediated tissue-specific autoimmune reactions and to identify potential treatment
31 in the control of graft-versus-host disease, autoimmune reactions, and the growth of certain tumors.
32 tic disorders are thought to be caused by an autoimmune reaction directed against 'onconeural' antige
33 nt eradication of the spirochete suggests an autoimmune reaction downstream of the original bacterial
34 oreactive T cells and may restrict bystander autoimmune reactions following the innate immune respons
37 CD4(+)Foxp3(+) T-reg to effectively control autoimmune reactions in the target organ, it may also be
38 and for its propensity to engender untoward autoimmune reactions, including serum sickness-like dise
39 s and macrophages participating in allo- and autoimmune reactions, including the perivascular inflamm
40 y plasmacytoid DCs and B cells amplifies the autoimmune reaction leading to disease manifestations.
42 ence suggests that it may be triggered by an autoimmune reaction or, conversely, initiate an autoimmu
43 t they also highlight that in vivo during an autoimmune reaction, RA suppresses autoimmunity mainly b
49 induce atherosclerosis via the mechanisms of autoimmune reactions to HSP60 expressed on arterial endo
50 study was to investigate the involvement of autoimmune reactions to native and post-translationally
53 The cause of BD remains unknown, although an autoimmune reaction triggered by an infectious agent in
54 hat tissues acquire the ability to attenuate autoimmune reactions upon repeated responses to antigens
55 an be processed and presented to initiate an autoimmune reaction, we surmise that cell death triggere
57 us self-protein results in a severe systemic autoimmune reaction with skin inflammation, wasting, and
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