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3 ression was higher in lesions from resistant tuberculoid as compared with susceptible lepromatous pat
4 ter frequency in patients with the localized tuberculoid as compared with the disseminated lepromatou
7 y expressed in lesions from the self-limited tuberculoid compared with expression in progressive lepr
8 ngly expressed in lesions from the localized tuberculoid form (T-lep) as compared with the disseminat
9 ing those diagnosed with the paucibacillary, tuberculoid form of disease, can be classified based on
10 ples of involved skin from patients with the tuberculoid form of leprosy or with reversal reactions,
14 rosy (L-lep) transition toward self-limiting tuberculoid leprosy (T-lep), mounting effective antimicr
15 antigen (HLA) class II genes in 54 cases of tuberculoid leprosy (TL) and 44 controls has shown a pos
16 crophages from patients with lepromatous and tuberculoid leprosy and from normal donors do not differ
18 at T cell activation in situ by M. leprae in tuberculoid leprosy leads to local up-regulation of CD40
21 ripheral blood mononuclear cells (PBMC) from tuberculoid leprosy patients (n = 59) and healthy lepros
22 ge of responders) ranging from 19 to 47% for tuberculoid leprosy patients and 21 to 64% for healthy l
25 7-1, B7-2, and CD28 transcripts dominated in tuberculoid leprosy patients, who have potent T cell res
27 inical manifestations seen in patients, from tuberculoid leprosy with robust production of Th1-type c
30 . leprae Ag by a T cell clone derived from a tuberculoid lesion in the context of monocyte APC result
31 ere preferentially expressed in self-healing tuberculoid lesions and mediated antimicrobial activity
32 the IL-12Rbeta2 was more highly expressed in tuberculoid lesions compared with lepromatous lesions.
33 c recall response of CD4+ T cell clones from tuberculoid lesions was blocked by anti-B7-1 mAb, but no
35 mAbs did not block activation of clones from tuberculoid lesions, suggesting that B7-1 may utilize an
38 ere predominant in skin lesions of resistant tuberculoid patients compared with the highly susceptibl
40 ongly expressed in immunologically resistant tuberculoid patients than in with unresponsive and susce
41 -18 augmented M. leprae-induced IFN-gamma in tuberculoid patients, but not lepromatous patients, whil
43 de Ags of mycobacteria in leprosy, comparing tuberculoid patients, who are able to restrict the patho