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1 elevant mathematical models as they apply to autoimmune myocarditis.
2 ic differences controlling susceptibility to autoimmune myocarditis.
3 myocarditogenic peptide-induced experimental autoimmune myocarditis.
4  and cardiac function in murine experimental autoimmune myocarditis.
5 ce results in the spontaneous development of autoimmune myocarditis.
6 nd modulation of immune responses to prevent autoimmune myocarditis.
7  cell effector cells in a new mouse model of autoimmune myocarditis.
8 urified myosin, which normally causes severe autoimmune myocarditis.
9  of captopril on myosin-induced experimental autoimmune myocarditis.
10 of IL-10 in the induction and suppression of autoimmune myocarditis.
11 ity in mice with myosin-induced experimental autoimmune myocarditis.
12 myosin antibodies and their ability to cause autoimmune myocarditis.
13 cells are a critical APC in the induction of autoimmune myocarditis.
14 cTnI values were first measured in mice with autoimmune myocarditis.
15 ic T cells have proven effective in treating autoimmune myocarditis.
16  potential therapeutic strategy in viral and autoimmune myocarditis.
17  similar to that observed in AMP mice and in autoimmune myocarditis.
18                Conclusion: In a rat model of autoimmune myocarditis, (18)F-FOL shows specific uptake
19                              In experimental autoimmune myocarditis, a disease model dependent on CD4
20 portantly, CM is the autoantigen that causes autoimmune myocarditis, a heart autoimmune disease whose
21 ctivity is associated with cardiac damage in autoimmune myocarditis, an inflammatory heart disease ch
22 otoxic T lymphocytes contribute to viral and autoimmune myocarditis and cardiac allograft rejection.
23 vel therapeutic strategy in the treatment of autoimmune myocarditis and inflammatory cardiomyopathy.
24 cate that captopril ameliorates experimental autoimmune myocarditis and may act, at least in part, by
25 oped severe coxsackievirus B3 (CVB3)-induced autoimmune myocarditis and myocarditogenic peptide-induc
26 1(-/-);MRL-Fas(lpr) mice died as a result of autoimmune myocarditis and pneumonitis before developing
27 mice lacking the Fas(lpr) mutation developed autoimmune myocarditis and pneumonitis.
28 ults suggest that apoJ limits progression of autoimmune myocarditis and protects the heart from posti
29 use antimyosin autoantibodies are present in autoimmune myocarditis and rheumatic carditis, the purpo
30 tion of myocardial inflammation in rats with autoimmune myocarditis and studied the expression of FR-
31 tion receptors promotes CD4+ T-cell-mediated autoimmune myocarditis and subsequent inflammatory cardi
32 s critical for the induction of experimental autoimmune myocarditis and that it acts through compleme
33 on specifically and robustly in experimental autoimmune myocarditis, and thus allowed for an unpreced
34 ght mice were studied after the induction of autoimmune myocarditis by immunization with alpha-myosin
35 irect experimental evidence that spontaneous autoimmune myocarditis can occur in the absence of infec
36 356 patients treated with cemiplimab (due to autoimmune myocarditis, cardiac failure, cardio-respirat
37                                 Experimental autoimmune myocarditis (EAM) can be induced in the Lewis
38 ckievirus B3 (CVB3)-mediated or experimental autoimmune myocarditis (EAM) in BALB/c mice, followed by
39 n, a heart autoantigen, induced experimental autoimmune myocarditis (EAM) in susceptible animals.
40 ng in the development of murine experimental autoimmune myocarditis (EAM) induced by cardiac myosin i
41                                 Experimental autoimmune myocarditis (EAM) is induced in mice by immun
42      In this study, we used the experimental autoimmune myocarditis (EAM) model to determine the role
43  Inhibition of NET formation in experimental autoimmune myocarditis (EAM) of mice substantially reduc
44                                 Experimental autoimmune myocarditis (EAM) was initiated in BALB/c mic
45 deficient mice developed severe experimental autoimmune myocarditis (EAM), in which mice are immunize
46 stablished model of TnI-induced experimental autoimmune myocarditis (EAM), we demonstrated that both
47 12 and IL-23 on CD4+ T cells in experimental autoimmune myocarditis (EAM).
48 myosin leads to T cell-mediated experimental autoimmune myocarditis (EAMC) and DCM.
49                              In experimental autoimmune myocarditis, elevations in autoantigen-specif
50                     Appropriate treatment of autoimmune myocarditis following virus infection remains
51 riety of cardiomyopathies, but its effect on autoimmune myocarditis has not been addressed experiment
52 to the pro-inflammatory activity of IL-23 in autoimmune myocarditis, highlighting its unique role in
53  Herein, we demonstrate that ANT1 can induce autoimmune myocarditis in A/J mice by generating autorea
54 e the pathogenic effector cell population in autoimmune myocarditis in BALB/c mice.
55  their potential to aid in the management of autoimmune myocarditis in humans, possibly including pat
56 e found that the acute phase of experimental autoimmune myocarditis in IFN-gamma-KO mice was characte
57          Cardiac myosin-induced experimental autoimmune myocarditis in interferon (IFN)-gamma-knockou
58 s, we have developed a model of experimental autoimmune myocarditis in the A.SW mouse.
59 al hearts should result in a T cell-mediated autoimmune myocarditis in the healthy syngeneic rats.
60 tant stromal cells prevented exacerbation of autoimmune myocarditis in vivo.
61     We conclude that IFN-gamma deficiency in autoimmune myocarditis is associated with preferential e
62              It has been widely thought that autoimmune myocarditis is of infectious etiology, with t
63 nduction of TnI-AM or after establishment of autoimmune myocarditis, mice were treated with the immun
64  and 'molecular mimicry' in the CB-3-induced autoimmune myocarditis model, and instead favors the ide
65 rdiac injury through a modified experimental autoimmune myocarditis mouse model and an ischemia-reper
66 r T (Th17) cells after inducing experimental autoimmune myocarditis or myocardial infarction in mice.
67  myocardial inflammation in all experimental autoimmune myocarditis-positive animals.
68 i-CM sera and mAbs derived from experimental autoimmune myocarditis targeted the heart cell surface a
69                                 TnI-directed autoimmune myocarditis (TnI-AM), a CD4(+) T-cell-mediate
70 utoreactive T-cell responses in experimental autoimmune myocarditis via nitric oxide.
71                             A mouse model of autoimmune myocarditis was developed to study the role o
72                                 Experimental autoimmune myocarditis was induced in BALB/c mice by imm
73                                 Experimental autoimmune myocarditis was induced in BALB/c mice.
74 To test its ability to modify myosin-induced autoimmune myocarditis, we generated apoJ-deficient mice