ライフサイエンスコーパス: tuberculoid

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1 Analogous to the tuberculoid and lepromatous forms of leprosy, CD may hav

2 , IL-12Rbeta1 expression was similar in both tuberculoid and lepromatous lesions.

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

5 binding in M. leprae-activated T cells from tuberculoid but not from lepromatous patients.

6 was up-regulated by Mycobacterium leprae in tuberculoid but not in lepromatous patients.

7 ngly expressed in lesions from the localized tuberculoid form (T-lep) as compared with the disseminat

8 ing those diagnosed with the paucibacillary, tuberculoid form of disease, can be classified based on

9 ples of involved skin from patients with the tuberculoid form of leprosy or with reversal reactions,

10 ssive, lepromatous form vs the self-limited, tuberculoid form of leprosy.

11 during T cell activation, in contrast to the tuberculoid form.

12 In tuberculoid lepromatous lesions, DC-SIGN+ cells were pos

13 antigen (HLA) class II genes in 54 cases of tuberculoid leprosy (TL) and 44 controls has shown a pos

14 crophages from patients with lepromatous and tuberculoid leprosy and from normal donors do not differ

15 ort describes elements resembling borderline tuberculoid leprosy in humans.

16 at T cell activation in situ by M. leprae in tuberculoid leprosy leads to local up-regulation of CD40

17 Therefore, T cell responsiveness in tuberculoid leprosy may be mediated by the ability of HL

18 ripheral blood mononuclear cells (PBMC) from tuberculoid leprosy patients (n = 59) and healthy lepros

19 ge of responders) ranging from 19 to 47% for tuberculoid leprosy patients and 21 to 64% for healthy l

20 In contrast, tuberculoid leprosy patients had only minor signal trans

21 We found that the majority of tuberculoid leprosy patients responded to peptides corre

22 7-1, B7-2, and CD28 transcripts dominated in tuberculoid leprosy patients, who have potent T cell res

23 proteins induced good IFN-gamma responses in tuberculoid leprosy patients.

24 inical manifestations seen in patients, from tuberculoid leprosy with robust production of Th1-type c

25 Skin biopsy was consistent with borderline tuberculoid leprosy with type 1 lepra reaction.

26 sociated, respectively, with lepromatous and tuberculoid leprosy.

27 . leprae Ag by a T cell clone derived from a tuberculoid lesion in the context of monocyte APC result

28 ere preferentially expressed in self-healing tuberculoid lesions and mediated antimicrobial activity

29 the IL-12Rbeta2 was more highly expressed in tuberculoid lesions compared with lepromatous lesions.

30 c recall response of CD4+ T cell clones from tuberculoid lesions was blocked by anti-B7-1 mAb, but no

31 T cell clones from tuberculoid lesions were CD4+CD28+ or CD4+CD28-, and T c

32 mAbs did not block activation of clones from tuberculoid lesions, suggesting that B7-1 may utilize an

33 in-3 was almost undetectable in self-limited tuberculoid lesions.

34 levels on monocytes from the blood of either tuberculoid or lepromatous leprosy patients.

35 ere predominant in skin lesions of resistant tuberculoid patients compared with the highly susceptibl

36 IL-12 release from PBMC of tuberculoid patients stimulated with Mycobacterium lepra

37 ongly expressed in immunologically resistant tuberculoid patients than in with unresponsive and susce

38 -18 augmented M. leprae-induced IFN-gamma in tuberculoid patients, but not lepromatous patients, whil

39 T cells from tuberculoid patients, the resistant form of leprosy, are

40 de Ags of mycobacteria in leprosy, comparing tuberculoid patients, who are able to restrict the patho

41 lepromatous (L-lep) versus the self-limited tuberculoid (T-lep) disease.

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