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1 ulate in the lesions of individuals with the lepromatous (also known as disseminated) form of human l
2 indicate that macrophages from patients with lepromatous and tuberculoid leprosy and from normal dono
4 h robust production of Th1-type cytokines to lepromatous disease, characterized by elevated levels of
6 of patients with the clinically progressive lepromatous form of leprosy; in contrast, galectin-3 was
7 In contrast, lesions from patients with the lepromatous form of the disease who lack effective cell-
9 increased in the lesions of the progressive, lepromatous form vs the self-limited, tuberculoid form o
11 onocytes in individuals with the progressive lepromatous form, except during reversal reactions in wh
15 in the lesions of subjects with progressive lepromatous (L-lep) versus the self-limited tuberculoid
16 in Winchester, UK, showing skeletal signs of lepromatous leprosy (LL) have been studied using a multi
18 tured human pathogen associated with diffuse lepromatous leprosy and a reactional state known as Luci
19 eprosum (ENL), which occurs in patients with lepromatous leprosy and is characterized by neutrophil i
20 oor cellular immune response associated with lepromatous leprosy and may have important implications
23 ymorphonuclear leukocytes from patients with lepromatous leprosy iodinate ingested bacteria normally.
26 immune defect leading to the development of lepromatous leprosy resides in the lymphocyte or in the
27 in skin lesions of patients with progressive lepromatous leprosy, correlating and colocalizing with I
28 0-CD40L interaction, which is not evident in lepromatous leprosy, probably participates in the cell-m
30 Multibacillary disease is similar to human lepromatous leprosy, with variable/high levels of antibo
35 suggested that the absence of expression in lepromatous lesions was most likely due to local factors
37 urthermore, IL-10, a cytokine predominant in lepromatous lesions, blocked the IFN-gamma up-regulation
42 have recently been recognized as a model of lepromatous neuritis; the major site of early accumulati
44 ere significantly up-regulated in lesions of lepromatous patients suffering from the disseminated for
45 leprae-induced IL-12 production by PBMC from lepromatous patients was not dependent on CD40L-CD40 lig
46 ant tuberculoid as compared with susceptible lepromatous patients, and, in vitro, monocytes produced
47 sion in ENL when compared with nonreactional lepromatous patients, both locally in the skin lesions a
48 e responsive to IL-12; however, T cells from lepromatous patients, the susceptible form of leprosy, d
49 nsiveness against mycobacterial lipid Ags in lepromatous patients, we used T cell clones to probe the
50 d IFN-gamma in tuberculoid patients, but not lepromatous patients, while IL-4 production was not indu
51 , who are able to restrict the pathogen, and lepromatous patients, who have disseminated infection.
52 was more strongly expressed in lesions from lepromatous patients, who manifest specific T cell anerg
56 (Lophocebus aterrimus) were inoculated with lepromatous tissue that had been serially passaged in fo
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