Direct Analysis of the Dynamics of the Intestinal Mucosa CD8 T Cell Response to Systemic Virus Infection

Masopust, David; Jiang, Jiu; Shen, Hao; Lefrançois, Leo

doi:10.4049/jimmunol.166.4.2348

Cited by 138 publications

(123 citation statements)

References 64 publications

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“…This result is consistent with the observations of others, showing that the memory CTL response after boosting is approximately 50% of the recall response (28). At the peak of the primary response to Env after vaccination with vPE16, ϳ6% of CD8 ϩ cells stained with MHC-I Env tetramers, compared to ϳ40% for VSV-Env-vaccinated mice (16).…”

supporting

confidence: 81%

Robust Recall and Long-Term Memory T-Cell Responses Induced by Prime-Boost Regimens with Heterologous Live Viral Vectors Expressing Human Immunodeficiency Virus Type 1 Gag and Env Proteins

Haglund

Leiner

Kerksiek

et al. 2002

J Virol

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We investigated long-term memory and recall cellular immune responses to human immunodeficiency virus type 1 (HIV-1) Env and Gag proteins elicited by recombinant vesicular stomatitis viruses (VSVs) expressing Env and Gag. More than 7 months after a single vaccination with VSV-Env, ϳ6% of CD8 ؉ splenocytes stained with major histocompatibility complex class I tetramers containing the Env p18-I10 immunodominant peptide and showed a memory phenotype (CD44 Hi ). The level of tetramer-positive cells in memory was about 14% of the peak primary response. Recall responses elicited in these mice 5 days after boosting with a heterologous recombinant vaccinia virus expressing HIV-1 Env showed that 40 to 45% of CD8 ؉ splenocytes were tetramer positive and activated (CD62L Lo ), and these cells produced gamma interferon after stimulation with Env peptide, indicating that they were functional. Five months after the boost, the long-term memory cell population (tetramer positive, CD44 Hi ) constituted 30% of the CD8 ؉ splenocytes. Recall responses to HIV-1 Gag were examined in mice primed with VSV recombinants expressing HIV-1 Gag protein and boosted with a vaccinia virus recombinant expressing Gag. Using this protocol, we found that ϳ40% of CD8 ؉ splenocytes were activated (CD62L Lo ) and specific for a Gag immunodominant peptide (tetramer positive). The high-level Gag recall response elicited by the vaccinia virus-Gag was greater than that obtained by boosting with a VSV-Gag vector with a different VSV glycoprotein. The corresponding levels of CD44 Hi memory cells were also higher long after boosting with vaccinia virus-Gag than after boosting with a glycoprotein exchange VSV-Gag. Our results show that VSV vectors elicit high-level memory CTL responses and that these can be amplified as much as six-to sevenfold using a heterologous boosting vector.

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supporting

confidence: 81%

Robust Recall and Long-Term Memory T-Cell Responses Induced by Prime-Boost Regimens with Heterologous Live Viral Vectors Expressing Human Immunodeficiency Virus Type 1 Gag and Env Proteins

Haglund

Leiner

Kerksiek

et al. 2002

J Virol

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“…Thus, although many cells responding late after infection had lost CFSE, the retention of a population of CFSE ϩ cells suggested that antigen levels were limiting late after infection. We also measured CD11a expression, since this integrin is upregulated upon T-cell activation and remains at high levels on memory CD8 T cells (31). Bona-fide memory OT-I cells generated by primary infection were uniformly CD11a high , and most OT-I cells derived from transfer late after infection expressed similarly high levels of CD11a (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…Donor CFSE-labeled cells were detected using their CD45 allele status. Ova-specific cells were detected using H-2K b tetramers containing the Ova-derived SIINFEKL peptide as previously described (1,31). For staining, lymphocytes were suspended in PBS-0.2% bovine serum albumin (BSA)-0.01% NaN 3 at a concentration of ϳ1 ϫ 10 7 /ml.…”

Section: Methodsmentioning

confidence: 99%

Persistent Antigen Presentation after Acute Vesicular Stomatitis Virus Infection

Turner

Cauley

Khanna

et al. 2007

J Virol

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Long-term antigen expression is believed to play an important role in modulation of T-cell responses to chronic virus infections. However, recent studies suggest that immune responses may occur late after apparently acute infections. We have now analyzed the CD8 T-cell response to vesicular stomatitis virus (VSV), which is thought to cause to an infection characterized by rapid virus clearance by innate and adaptive immune system components. Unexpectedly, virus-encoded antigen was detectable more than 6 weeks after intranasal VSV infection in both draining and nondraining lymph nodes by adoptively transferred CD8 T cells. Infection with Listeria monocytogenes expressing the same antigen did not result in prolonged antigen presentation. Weeks after VSV infection, discrete T-cell clustering with dendritic cells within the lymph node was observed after transfer of antigen-specific CD8 T cells. Moreover, memory CD8 T cells as defined by phenotype and function were generated from naïve CD8 T cells entering the response late after infection. These findings suggested that protracted antigen presentation after an apparently acute virus infection may contribute to an ongoing antiviral immune response.

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“…Studies comparing the kinetics of primary and secondary T cell responses in the same animal have shown that the contraction phase of the secondary CD8 ϩ T cell response is prolonged compared with that of the primary response (17,48,(61)(62)(63)(64). Studies by Grayson et al have demonstrated that memory T cells are more resistant than naive T cells to apoptosis (47) and have elevated levels of the antiapoptotic factor Bcl-2 (65).…”

Section: Discussionmentioning

confidence: 99%

Duration of Infection and Antigen Display Have Minimal Influence on the Kinetics of the CD4+ T Cell Response to Listeria monocytogenes Infection

Corbin

Harty

2004

The Journal of Immunology

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The T cell response to infection consists of clonal expansion of effector cells, followed by contraction to memory levels. It was previously thought that the duration of infection determines the magnitude and kinetics of the T cell response. However, recent analysis revealed that transition between the expansion and contraction phases of the Ag-specific CD8+ T cell response is not affected by experimental manipulation in the duration of infection or Ag display. We studied whether the duration of infection and Ag display influenced the kinetics of the Ag-specific CD4+ T cell response to Listeria monocytogenes (LM) infection. We found that truncating infection and Ag display with antibiotic treatment as early as 24 h postinfection had minimal impact on the expansion or contraction of CD4+ T cells; however, the magnitudes of the Ag-specific CD4+ and CD8+ T cell responses were differentially affected by the timing of antibiotic treatment. Treatment of LM-infected mice with antibiotics at 24 h postinfection did not prevent generation of detectable CD4+ and CD8+ memory T cells at 28 days after infection, vigorous secondary expansion of these memory T cells, or protection against a subsequent LM challenge. These results demonstrate that events within the first few days of infection stimulate CD4+ and CD8+ T cell responses that are capable of carrying out the full program of expansion and contraction to functional memory, independently of prolonged infection or Ag display.

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Direct Analysis of the Dynamics of the Intestinal Mucosa CD8 T Cell Response to Systemic Virus Infection

Cited by 138 publications

References 64 publications

Robust Recall and Long-Term Memory T-Cell Responses Induced by Prime-Boost Regimens with Heterologous Live Viral Vectors Expressing Human Immunodeficiency Virus Type 1 Gag and Env Proteins

Robust Recall and Long-Term Memory T-Cell Responses Induced by Prime-Boost Regimens with Heterologous Live Viral Vectors Expressing Human Immunodeficiency Virus Type 1 Gag and Env Proteins

Persistent Antigen Presentation after Acute Vesicular Stomatitis Virus Infection

Duration of Infection and Antigen Display Have Minimal Influence on the Kinetics of the CD4+ T Cell Response to Listeria monocytogenes Infection

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