Clinical investigation of pulmonary Mycobacterium avium complex infection in human T lymphotrophic virus type I carriers

Matsuyama, Wataru; Mizoguchi, Akira; Iwami, Fumiyuki; Koreeda, Yoshifusa; Wakimoto, Joeji; Kanazawa, Hironobu; Mori, S; Kawabata, Masaharu; Fukunaga, Hideaki; Osame, Mitsuhiro

doi:10.1136/thorax.55.5.388

Cited by 12 publications

(9 citation statements)

References 27 publications

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“…35 These findings are considered as evidence of immunodeficiency in HTLV-I-infected individuals, which is due to suppression of naive T lymphocytes. Recent studies by Matsuyama and colleagues 36 have demonstrated high seropositivity among patients with Mycobacterium avium complex (MAC) infection. Because defense against MAC infection depends on cell-mediated immunity, especially T lymphocytes, impaired cellmediated immunity in HTLV-I carriers might be responsible for increased susceptibility to MAC infection.…”

Section: Discussionmentioning

confidence: 99%

Impaired production of naive T lymphocytes in human T-cell leukemia virus type I–infected individuals: its implications in the immunodeficient state

Yasunaga

Sakai

Nosaka

et al. 2001

Blood

135

102

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Section: Discussionmentioning

confidence: 99%

Impaired production of naive T lymphocytes in human T-cell leukemia virus type I–infected individuals: its implications in the immunodeficient state

Yasunaga

Sakai

Nosaka

et al. 2001

Blood

135

102

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“…However, some subtle immune defects are apparent even in the otherwise healthy HTLV-1 infected population. Compared to individuals without HTLV-1 infection, parasite load is higher and chronic carriage more common in subjects with strongyloidiasis and HTLV-1 co-infection (reviewed in13), Mycobacterium avium complex infection causes more extensive pulmonary lesions in HTLV-1 infected subjects,14 and HTLV-1 infected subjects are at increased risk for bladder or kidney infections, possibly related to neurological dysfunction 15,16. A detailed understanding of the immuno-pathophysiology underlying HTLV-1 disease associations is lacking, in part because many studies have been narrowly focused.…”

Section: Introductionmentioning

confidence: 99%

Human T cell leukemia virus type 1 infection drives spontaneous proliferation of natural killer cells

et al. 2010

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Most human T cell leukemia virus type 1 (HTLV-1) infected subjects remain asymptomatic throughout their lives, with a few individuals developing HTLV-1 associated myelopathy/tropical spastic paraparesis (HAM/TSP) or adult T cell leukemia. Lymphocytes from about half of HTLV-1 infected subjects spontaneously proliferate in vitro, and how this phenomenon relates to symptomatic disease outcome and viral burden is poorly understood. Spontaneous proliferation was measured in lymphocyte subsets, and these findings were correlated with HTLV-1 proviral load and Tax expression in PBMCs. We found that in addition to previously described vigorous CD8+ T cell spontaneous proliferation, natural killer (NK) cells spontaneously proliferated to a similar high level, resulting in expansion of CD56-expressing NK cells. Spontaneous NK cell proliferation positively correlated with HTLV-1 proviral load but not with Tax expression or the presence of HAM/TSP. The strongest correlate with clinical outcome in this cohort was the ability of cells to express Tax, while HTLV-1 proviral load was more closely related to spontaneous NK cell proliferation. These results demonstrate that spontaneous proliferation, Tax expression, and proviral load are inter-related but not equivalent, and that spontaneous lymphocyte proliferation is not restricted to T cells, the targets of HTLV-1 infection.

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“…5 HTLV-I infection affects not only the peripheral blood lymphocytes but also the lymphocytes in the lungs 1314 Taken together, we think that the enhanced inhibitory effect of MAC GPL observed in this in vitro study is one of the reasons why MAC spreads more widely in lungs of individuals infected with HTLV-I 2. It may be necessary to treat pulmonary MAC infection in HTLV-I carriers even if there are no immunological abnormalities in the clinical data.…”

Section: Discussionmentioning

confidence: 71%

“…Blood samples were obtained from 29 individuals who had recovered from pulmonary MAC infection, 10 of whom also had HTLV-I (all women, mean (SD) age 70.1 (10.2) years) and 19 who did not have HTLV-I (16 women, mean (SD) age 70.9 (9.5) years) 2. They had neither systemic nor local underlying disorders which might predispose to pulmonary MAC infection such as alcoholism and residual pulmonary damage from previous infection, nor any unexplained pulmonary diseases or other pathogens.…”

Section: Methodsmentioning

confidence: 99%

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Enhanced inhibition of lymphocyte activation by Mycobacterium avium complex in human T lymphotrophic virus type I carriers

Matsuyama

Hamasaki²,

Mizoguchi³

et al. 2001

Thorax

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Background-We have previously reported that disseminated pulmonary Mycobacterium avium complex (MAC) infection is more common in human T lymphotrophic virus type I (HTLV-I) carriers than in non-carriers. However, the reason for this remains unclear. It has been shown that glycopeptidelipid (GPL), one of the lipid components of the cell envelope of MAC, is able to reduce the lymphocyte blastogenic response to mitogens. The purpose of this study was to clarify whether or not the inhibitory eVect of GPL diVers between HTLV-I carriers and non-carriers. Methods-Peripheral blood lymphocytes were obtained from 29 patients who had recovered from pulmonary MAC infection (10 of whom also had HTLV-I infection) and the lymphocyte counts and T cell subpopulations of the peripheral blood lymphocytes in HTLV-I carriers and noncarriers were compared. The inhibitory eVect of GPL on the lymphocyte blastogenic response to phytohaemagglutinin (PHA) was tested in these 29 cases and in 15 healthy controls who had never suVered from MAC (seven of whom also had HTLV-I infection). All HTLV-I positive cases were carriers. Results-There was no significant diVerence in the numbers or subset proportions of T cells between HTLV-I carriers and non-carriers. Lymphocyte activation by PHA was significantly inhibited by GPL in MAC positive and negative HTLV-I carriers compared with MAC negative noncarriers and MAC negative healthy controls (p<0.001). Conclusions-We suggest that MAC infection leads to strong inhibition of lymphocyte activation in HTLV-I carriers. This may account, in part, for the severity of pulmonary MAC infection in HTLV-I carriers.

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Clinical investigation of pulmonary Mycobacterium avium complex infection in human T lymphotrophic virus type I carriers

Cited by 12 publications

References 27 publications

Impaired production of naive T lymphocytes in human T-cell leukemia virus type I–infected individuals: its implications in the immunodeficient state

Impaired production of naive T lymphocytes in human T-cell leukemia virus type I–infected individuals: its implications in the immunodeficient state

Human T cell leukemia virus type 1 infection drives spontaneous proliferation of natural killer cells

Enhanced inhibition of lymphocyte activation by Mycobacterium avium complex in human T lymphotrophic virus type I carriers

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