ライフサイエンスコーパス: HTLV-I infection

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1 ere enrolled and prospectively evaluated for HTLV-I infection.

2 in neurodegenerative disease associated with HTLV-I infection.

3 cell fratricide with particular reference to HTLV-I infection.

4 aparesis (HAM/TSP) are known to be caused by HTLV-I infection.

5 protein PDLIM2 may determine the outcome of HTLV-I infection.

6 contribute to the pathology associated with HTLV-I infection.

7 stent nuclear expression of c-Rel induced by HTLV-I infection.

8 a rabbit 20 months into a course of chronic HTLV-I infection.

9 /Tax and PDLIM2 may determine the outcome of HTLV-I infection.

10 tory genes could influence susceptibility to HTLV-I infection.

11 own about the innate immunity of the host to HTLV-I infection.

12 would not be effective for the treatment of HTLV-I infections.

13 aused by human T-cell leukemia virus type I (HTLV-I) infection.

14 l models to describe the in vivo dynamics of HTLV-I infection, an explanation is offered for the slow

15 ted findings included a relationship between HTLV-I infection and cardiac disease history (OR=1.4; 95

16 ous lymphoproliferative lesion resulted from HTLV-I infection and further establishes the New Zealand

17 an inflammatory neurologic disease caused by HTLV-I infection and has been associated with elevated l

18 he IL-2 signal transduction pathway and that HTLV-I infection and oncogenic transformation can lead t

19 r cancers and other diseases associated with HTLV-I infection and/or PDLIM2 deregulation.

20 actionated T cell subsets (CD4+ and CD8+) in HTLV-I infections and suggests that 1) clonal expansion

21 Mathematical modelling of HTLV-I infection, as is often the case in biology, is se

22 and maternal cells may influence the risk of HTLV-I infection by breast-feeding, perhaps because anti

23 However, current methods used to determine HTLV-I infection do not differentiate between HTLV-I asy

24 e the differences in host immune response to HTLV-I infection in 2 populations.

25 sequilibrium with it, may affect the risk of HTLV-I infection in a recessive manner.

26 C/-1116G) were significantly associated with HTLV-I infection in children independent of maternal pro

27 review presents an overview of the impact of HTLV-I infection in general, and Tax expression in parti

28 lammatory neurologic disease associated with HTLV-I infection, in which chronically activated, HTLV-I

29 e of these findings to the neuropathology of HTLV-I infection is discussed.

30 Japanese population within an area in which HTLV-I infection is endemic.

31 HTLV-I infection may modify the risk of specific disease

32 Thus, p53 stabilization in HTLV-I infection occurs in the absence of genetic mutati

33 To investigate whether HTLV-I infection of certain cells can modulate HIV-1 inf

34 that human T cell lymphotropic virus type I (HTLV-I) infection of CD4(+)CD25(+) Tregs in patients wit

35 nd host immunity during the chronic phase of HTLV-I infection offers important insights regarding the

36 volved in human T lymphotropic virus type I (HTLV-I) infections, peripheral blood T cell subsets were

37 children, human T lymphotropic virus type I (HTLV-I) infection was found to be associated with signif

38 ated with human T lymphotropic virus type I (HTLV-I) infection was investigated in a Japanese populat

39 bility to human T lymphotropic virus type I (HTLV-I) infection, we examined common variants in 11 imm

40 TLV-I pathogenicity given the association of HTLV-I infection with autoimmune-like diseases.

41 spite the lack of epidemiologic data linking HTLV-I infection with CTCL, the molecular data still inv

42 The association of HTLV-I infection with the most common variant, CCR2-64I,

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