Generalized Immunological Decline during Long-Term Experimental Infection with<i>Mycobacterium avium</i>

Gilbertson, Brad; Cheers, Christina

doi:10.1128/iai.70.12.7145-7148.2002

Cited by 3 publications

(2 citation statements)

References 13 publications

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“…The high rate of T‐cell apoptosis was preceded by a high rate of CD4 + and CD8 + T‐cell proliferation in vivo 25 suggesting the possibility of AICD. Both CD4 + and CD8 + T cells were steadily depleted from the spleen 26 and other tissues 27 . Ultimately, even the remaining T cells lost their ability to produce protective IFN‐γ and the mice became moribund, with bacterial numbers exceeding 10 9 /lung.…”

Section: Introductionmentioning

confidence: 99%

Apoptosis of CD4+ and CD8+ T cells during experimental infection with Mycobacterium avium is controlled by Fas/FasL and Bcl‐2‐sensitive pathways, respectively

2003

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Summary Both CD4 + and CD8 + T cells from mice infected with Mycobacterium avium suffered a high rate of apoptosis, beginning with the onset of the immune response and culminating in the loss of T cells from the tissues and loss of IFN-γ production. Fas expression increased over the course of infection on both T cell populations, as did their susceptibility to the induction of apoptosis in vitro by anti-Fas mAb. Nevertheless, although the rate of apoptosis among CD4 + T cells from infected mice was reduced to normal levels in lpr mice with a defective Fas, CD8 + T cells were unaffected, implying that Fas/FasL interaction was not important in these cells in vivo . Conversely, over-expression of B-cell lymphoma-2 (Bcl-2), which is known to protect T cells from apoptosis signalled through the TNF receptor or due to the withdrawal of cytokines, totally protected CD8 + T cells from infected mice but had no effect on CD4 + . It is of interest that these two contrasting pathways of T-cell apoptosis operate at the same time during a single infection.

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Section: Introductionmentioning

confidence: 99%

Apoptosis of CD4+ and CD8+ T cells during experimental infection with Mycobacterium avium is controlled by Fas/FasL and Bcl‐2‐sensitive pathways, respectively

2003

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“…In contrast, a less virulent strain (M. avium 2447) did not (9). In a different model of infection initiated by exposure to an intratracheal infection, Cheers and colleagues dissected the development of severe anergy associated with pronounced T-cell loss at late stages of M. avium infection (13,14,24). In the latter studies, such T-cell loss was observed at different sites of infection and was explained by the increase in apoptosis of T cells in infected animals (14).…”

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Gamma Interferon-Induced T-Cell Loss in VirulentMycobacterium aviumInfection

et al. 2005

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Infection by virulent Mycobacterium avium caused progressive severe lymphopenia in C57BL/6 mice due to increased apoptosis rates. T-cell depletion did not occur in gamma interferon (IFN-␥)-deficient mice which showed increased T-cell numbers and proliferation; in contrast, deficiency in nitric oxide synthase 2 did not prevent T-cell loss. Although T-cell loss was IFN-␥ dependent, expression of the IFN-␥ receptor on T cells was not required for depletion. Similarly, while T-cell loss was optimal if the T cells expressed IFN-␥, CD8؉ T-cell depletion could occur in the absence of T-cell-derived IFN-␥. Depletion did not require that the T cells be specific for mycobacterial antigen and was not affected by deficiencies in the tumor necrosis factor receptors p55 or p75, the Fas receptor (CD95), or the respiratory burst enzymes or by forced expression of bcl-2 in hematopoietic cells.

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Prevalence of Mycobacterium avium subspecies paratuberculosis (MAP) infection in suspected diarrhoeic buffaloes and cattle reporting at Veterinary University in India

Sharma

Gautam

Singh

et al. 2020

Comparative Immunology, Microbiology and Infectious Diseases

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Generalized Immunological Decline during Long-Term Experimental Infection withMycobacterium avium

Cited by 3 publications

References 13 publications

Apoptosis of CD4+ and CD8+ T cells during experimental infection with Mycobacterium avium is controlled by Fas/FasL and Bcl‐2‐sensitive pathways, respectively

Apoptosis of CD4+ and CD8+ T cells during experimental infection with Mycobacterium avium is controlled by Fas/FasL and Bcl‐2‐sensitive pathways, respectively

Gamma Interferon-Induced T-Cell Loss in VirulentMycobacterium aviumInfection

Prevalence of Mycobacterium avium subspecies paratuberculosis (MAP) infection in suspected diarrhoeic buffaloes and cattle reporting at Veterinary University in India

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