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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-
10 increased in the lesions of the progressive, lepromatous form vs the self-limited, tuberculoid form o
12 onocytes in individuals with the progressive lepromatous form, except during reversal reactions in wh
16 in the lesions of subjects with progressive lepromatous (L-lep) versus the self-limited tuberculoid
19 cess whereby some patients with disseminated lepromatous leprosy (L-lep) transition toward self-limit
20 in Winchester, UK, showing skeletal signs of lepromatous leprosy (LL) have been studied using a multi
24 tured human pathogen associated with diffuse lepromatous leprosy and a reactional state known as Luci
25 eprosum (ENL), which occurs in patients with lepromatous leprosy and is characterized by neutrophil i
26 oor cellular immune response associated with lepromatous leprosy and may have important implications
30 ymorphonuclear leukocytes from patients with lepromatous leprosy iodinate ingested bacteria normally.
32 ular exhaustion to the hyporesponsiveness of lepromatous leprosy patients by evaluating the classical
34 immune defect leading to the development of lepromatous leprosy resides in the lymphocyte or in the
36 in skin lesions of patients with progressive lepromatous leprosy, correlating and colocalizing with I
37 0-CD40L interaction, which is not evident in lepromatous leprosy, probably participates in the cell-m
39 Multibacillary disease is similar to human lepromatous leprosy, with variable/high levels of antibo
44 suggested that the absence of expression in lepromatous lesions was most likely due to local factors
46 urthermore, IL-10, a cytokine predominant in lepromatous lesions, blocked the IFN-gamma up-regulation
51 have recently been recognized as a model of lepromatous neuritis; the major site of early accumulati
53 ere significantly up-regulated in lesions of lepromatous patients suffering from the disseminated for
54 leprae-induced IL-12 production by PBMC from lepromatous patients was not dependent on CD40L-CD40 lig
55 contribute to the hyporesponsive profile of lepromatous patients, and that PD-1 blockade could contr
56 ant tuberculoid as compared with susceptible lepromatous patients, and, in vitro, monocytes produced
57 AG-3 is increased in the skin lymphocytes of lepromatous patients, as well as membrane-bound and solu
58 sion in ENL when compared with nonreactional lepromatous patients, both locally in the skin lesions a
59 e responsive to IL-12; however, T cells from lepromatous patients, the susceptible form of leprosy, d
60 nsiveness against mycobacterial lipid Ags in lepromatous patients, we used T cell clones to probe the
61 d IFN-gamma in tuberculoid patients, but not lepromatous patients, while IL-4 production was not indu
62 , who are able to restrict the pathogen, and lepromatous patients, who have disseminated infection.
63 was more strongly expressed in lesions from lepromatous patients, who manifest specific T cell anerg
69 (Lophocebus aterrimus) were inoculated with lepromatous tissue that had been serially passaged in fo