The Critical Need for CD4 Help in Maintaining Effective Cytotoxic T Lymphocyte Responses

Kalams, Spyros A.; Walker, Bruce D.

doi:10.1084/jem.188.12.2199

Cited by 607 publications

(442 citation statements)

References 50 publications

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“…It is well known that CTL and NK cells can lyse tumor cells directly by either releasing granzyme B or by inducing apoptosis through the Fas-FasL or TNF-TNFR system [18][19][20]. CD4+T cells can secrete cytokines and lead to tumor cell growth arrest [21][22][23]. As discussed above, we found that T cells were activated and resistant to AICD after immunization.…”

Section: Discussionsupporting

confidence: 63%

“…Accumulating evidence has demonstrated that tumor regression was induced in cancer patients treated with IL-2 plus IFN-γ [26,27]. This supports the idea that it is very important to enhance anti-tumor T-cell responses in the tumor immunotherapy [18][19][20][21][22][23].…”

Section: Introductionmentioning

confidence: 58%

“…Activated cytotoxic T lymphocytes (CTL) can lyse tumor cells directly, either by releasing granzyme B or by inducing apoptosis through Fas-Fas ligand (FasL) pathway [18][19][20]. In addition, CD4+T cells can secrete cytokines that lead to immune rejection of tumor cells [21][22][23]. However, the activity of T cells is down-regulated in patients with malignant tumors.…”

Section: Introductionmentioning

confidence: 99%

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Immunization with autologous T cells enhances in vivo anti-tumor immune responses accompanied by up-regulation of GADD45β

Wang

Cao

et al. 2006

Cell Res

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Immunization with inactivated autoreactive T cells may induce idiotype anti-idiotypic reactions to deplete autoreactive T cells, which are involved in autoimmune diseases. However, it is unknown whether attenuated activated healthy autologous T-cell immunization could increase anti-tumor immune responses. To this end, C57Bl/6 mice were immunized with attenuated activated autologous T cells. The splenocytes from immunized mice showed a higher proliferative ability than that from naive mice. The special phenotype analysis showed that there were more CD8+ T cells and CD62L+ T cells in immunized mice after 24 h of culture with 10% fetal calf serum complete medium in vitro (P<0.01). These results demonstrated that this immunization may activate T cells in vivo. Furthermore, the splenocytes from immunized mice revealed resistance to activation-induced cell death (AICD) in vitro. To further study the relative genes that are responsible for the higher proliferation and resistance to AICD, the expression of Fas/Fas ligand (FasL) and GADD45b was measured by real-time PCR. The results indicated that GADD45b transcription was higher in the splenocytes from immunized mice than that in the naive mice. In addition, the Fas expression showed a parallel higher, but FasL did not change obviously. To investigate the biologic functions induced by immunization in vivo, a tumor model was established by EL-4 tumor cell inoculation in C57/Bl mice. Mice receiving autologous T-cell immunization had significantly inhibited tumor growth in vivo (P<0.01). This study implicated that immunization with attenuated activated autologous T cells enhances anti-tumor immune responses that participate in tumor growth inhibition.

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Section: Discussionsupporting

confidence: 63%

Section: Introductionmentioning

confidence: 58%

Section: Introductionmentioning

confidence: 99%

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Immunization with autologous T cells enhances in vivo anti-tumor immune responses accompanied by up-regulation of GADD45β

Wang

Cao

et al. 2006

Cell Res

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“…The generation of sustained effector responses can depend on the availability of help [14][15][16]. This applies both to antibody and to cytotoxic T lymphocyte (CTL) responses.…”

Section: Generation Of Effector Responsesmentioning

confidence: 99%

Infection dynamics in HIV-specific CD4 T cells: Does a CD4 T cell boost benefit the host or the virus?

Wodarz

Hamer²

2007

Mathematical Biosciences

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Recent experimental data have shown that HIV specific CD4 T cells provide a very important target for HIV replication. We use mathematical models to explore the effect of specific CD4 T cell infection on the dynamics of virus spread and immune responses. Infected CD4 T cells can provide antigen for their own stimulation. We show that such auto-catalytic cell division can significantly enhance virus spread, and can also provide an additional reservoir for virus persistence during anti-viral drug therapy. In addition, the initial number of HIV-specific CD4 T cells is an important determinant of acute infection dynamics. A high initial number of HIVspecific CD4 T cells can lead to a sudden and fast drop of the population of HIV-specific CD4 T cells which results quickly in their extinction. On the other hand, a low initial number of HIVspecific CD4 T cells can lead to a prolonged persistence of HIV specific CD4 T cell help at higher levels. The model suggests that boosting the population of HIV-specific CD4 T cells can increase the amount of virus-induced immune impairment, lead to less efficient anti-viral effector responses, and thus speed up disease progression, especially if effector responses such as CTL have not been sufficiently boosted at the same time.

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“…120 Thus, more studies are needed to clarify the role of HIV-specific CD4 þ T-cell help for a persistent and effective HIV-specific CD8 þ T-cell response as it has been previously proposed. 121 This is further supported by recent data from murine studies emphasizing the importance of CD4 þ T-cell help in clonal expansion and survival of CTL responses. 122 …”

Section: Loss Of Hiv-specific Cd4 þ T-cell Helpmentioning

confidence: 64%

Apoptosis of HIV-specific CD8+ T cells: an HIV evasion strategy

2005

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The Critical Need for CD4 Help in Maintaining Effective Cytotoxic T Lymphocyte Responses

Cited by 607 publications

References 50 publications

Immunization with autologous T cells enhances in vivo anti-tumor immune responses accompanied by up-regulation of GADD45β

Immunization with autologous T cells enhances in vivo anti-tumor immune responses accompanied by up-regulation of GADD45β

Infection dynamics in HIV-specific CD4 T cells: Does a CD4 T cell boost benefit the host or the virus?

Apoptosis of HIV-specific CD8+ T cells: an HIV evasion strategy

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