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1 ation with lymphocytes, and disappearance of microabscess.
2 s epidermotropic and produces intraepidermal microabscesses.
3 n the liver and an increase in the number of microabscesses.
4 tes become heavily infected and develop into microabscesses.
5 ted chronic steatohepatitis and superimposed microabscesses.
6 amatically increased PMN trafficking to skin microabscesses and lungs after ischemia-reperfusion, whe
7 s, hyperkeratosis, intraepidermal neutrophil microabscesses, and increased T helper type 1 (Th1)/Th17
8                     However, not all hepatic microabscesses are due to CMV infection.
9                                          The microabscesses are smaller and more numerous than in CMV
10 leukocytes, rather than forming disseminated microabscesses as seen for the wild type.
11 l infiltration, intraepithelial eosinophils, microabscesses, basal cell hyperplasia, and lamina propr
12 epidermis and superficial dermis, subcorneal microabscesses, basement membrane degradation, and angio
13                   ANCA lung capillaritis and microabscesses began within one day and evolved into gra
14  widespread polymorphonuclear leukocyte-rich microabscesses but without change in cytotoxic T-lymphoc
15                                      Munro's microabscesses contain polymorphonuclear leukocytes and
16   The persistence of leukocytes within liver microabscesses correlated with enhanced colonization and
17  macrophages, and numerous neutrophil-filled microabscesses developed, followed by tissue destruction
18 nflammatory cells and tissue damage, such as microabscesses, edema, and necrosis progressed following
19  keratinocytes is essential for neutrophilic microabscess formation and contributes to hyperprolifera
20 S mice with purified CD8(+) T cells restored microabscess formation and epidermal hyperproliferation.
21 nsplant patients with necrotizing lesions or microabscess formation at allograft biopsy.
22 e infected with Listeria had similar hepatic microabscess formation in terms of histologic appearance
23 cation of imiquimod in vivo led to epidermal microabscess formation, acanthosis, and increased IL-1al
24 n RAS was expressed on a Rag1-/- background, microabscess formation, inducible nitric oxide synthase
25 1alpha and IL-1R1 signaling is essential for microabscess formation, neutrophil recruiting chemokine
26     Here we investigate the basis for clonal microabscess formation, using in vitro and in silico mod
27 n, we explored the role of IL-1 signaling in microabscess formation.
28                              Neutrophil-rich microabscesses formed beneath the stratum corneum.
29  providing a conceptual framework for clonal microabscess generation, which was supported by a stocha
30                                 Disseminated microabscesses in major organs were found in animals tre
31 yperplasia, and the presence of eosinophilic microabscesses in the epithelium) were examined by revie
32  the liver, about 95% are granulomas with 5% microabscesses involving intrahepatic infection.
33                                  Parenchymal microabscesses (MA) in liver transplant biopsies are fre
34                 In 1992, we described "mini" microabscess (MMA) syndrome, a distinct clinical syndrom
35  patient developed cirrhosis and suppurative microabscesses of the liver and died of progressive live
36                       The number and area of microabscesses on the ears of E-/P-deficient mice were d
37 led hyperplasia of the epidermis, subcorneal microabscesses, orthohyperkeratosis, parakeratosis, and
38                                              Microabscess, severe necrosis, and early calcification w
39 calized with Thy-1(+) EC of small vessels in microabscesses, suggesting an interaction between CD97 a
40     Histopathologically, disseminated septic microabscesses surrounded by necrotic foci were found ex
41 n bacterial division, escape and founding of microabscesses that can seed other host niches.
42 is characterized in the liver by parenchymal microabscesses, usually containing CMV-infected cells.
43   Atypical lymphocytes in epidermal Pautrier microabscesses were positive for HTLV-1.
44 s is particularly evident in the edge of the microabscess, where hepatocytes are not yet destroyed by
45 the equilibrium between granulomas and liver microabscesses, with massive transfer of the infection t