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CD27 promotes survival of activated T cells and complements CD28 in generation and establishment of the effector T cell pool.

Hendriks J, Xiao Y, Borst J - J. Exp. Med. (2003)

Bottom Line: In the primary response, CD27 and CD28 impact to a similar extent on expansion of virus-specific T cells in draining lymph nodes.Unlike CD28, CD27 does not affect cell cycle activity, but promotes survival of activated T cells throughout successive rounds of division at the site of priming and may do so at the site of infection as well.CD27 was found to rescue CD28(-/-) T cells from death at the onset of division, explaining its capacity to support a T cell response in absence of CD28.

View Article: PubMed Central - PubMed

Affiliation: Division of Immunology, The Netherlands Cancer Institute, 1066 CX Amsterdam, Netherlands.

ABSTRACT
CD27, like CD28, acts in concert with the T cell receptor to support T cell expansion. Using CD27(-/-) mice, we have shown earlier that CD27 determines the magnitude of primary and memory T cell responses to influenza virus. Here, we have examined the relative contributions of CD27 and CD28 to generation of the virus-specific effector T cell pool and its establishment at the site of infection (the lung), using CD27(-/-), CD28(-/-), and CD27/CD28(-/-) mice. We find that primary and memory CD8+ T cell responses to influenza virus are dependent on the collective contribution of both receptors. In the primary response, CD27 and CD28 impact to a similar extent on expansion of virus-specific T cells in draining lymph nodes. CD27 is the principle determinant for accumulation of virus-specific T cells in the lung because it can sustain this response in CD28(-/-) mice. Unlike CD28, CD27 does not affect cell cycle activity, but promotes survival of activated T cells throughout successive rounds of division at the site of priming and may do so at the site of infection as well. CD27 was found to rescue CD28(-/-) T cells from death at the onset of division, explaining its capacity to support a T cell response in absence of CD28.

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In vivo primary and memory T cell responses to influenza virus in the presence or absence of CD27 and/or CD28. Wild-type, CD27−/−, CD28−/−, and CD27−/−/CD28−/− mice were infected intranasally with influenza virus. Cells were isolated from the lung, DLNs, and spleen on the indicated days after infection. They were counted, stained with anti-CD8 mAb and NP366–374/H2-Db tetramers, and analyzed by flow cytometry. Each symbol represents an individual mouse (four per group) and dashes represent mean values. (A) Primary response. (B) Memory response. The complete experiment was performed two times with reproducible results.
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fig1: In vivo primary and memory T cell responses to influenza virus in the presence or absence of CD27 and/or CD28. Wild-type, CD27−/−, CD28−/−, and CD27−/−/CD28−/− mice were infected intranasally with influenza virus. Cells were isolated from the lung, DLNs, and spleen on the indicated days after infection. They were counted, stained with anti-CD8 mAb and NP366–374/H2-Db tetramers, and analyzed by flow cytometry. Each symbol represents an individual mouse (four per group) and dashes represent mean values. (A) Primary response. (B) Memory response. The complete experiment was performed two times with reproducible results.

Mentions: Wild-type, CD27−/−, CD28−/−, and CD27/CD28−/− double deficient mice were infected and analyzed 6, 8, 10, or 14 d later for the presence of virus-specific CD8+ T cells. In the lung, accumulation of wild-type virus-specific T cells became detectable at day 6 and peaked at days 8–10 after infection (Fig. 1 A). In CD28−/− mice, the T cell response at this site was partially intact, whereas it was almost completely abrogated upon additional CD27 deletion. Apparently, CD27 can support the virus-specific CD8+ T cell response in the lung in absence of CD28. Accumulation of virus-specific CD8+ T cells in the lung of CD27−/− mice was in fact much lower than in CD28−/− mice, indicating that CD27 is a major determinant for the CD8+ T cell response at the site of infection. The response at the site of priming, the mediastinal lung DLNs, was strongly reduced in both CD27−/− and CD28−/− mice compared with wild-type mice, and virtually absent in CD27/CD28−/− mice, indicating that both receptors make crucial and in part complimentary contributions to generation of the virus-specific CD8+ T cell pool. Strikingly, in the spleen, CD27 deficiency only had a minor effect, whereas CD28 deletion strongly reduced the response. Accumulation of virus-specific CD8+ T cells in the spleen appeared fully dependent on the collective contribution of CD27 and CD28. In the absence of both molecules, increase in tetramer+ T cells was virtually undetectable.


CD27 promotes survival of activated T cells and complements CD28 in generation and establishment of the effector T cell pool.

Hendriks J, Xiao Y, Borst J - J. Exp. Med. (2003)

In vivo primary and memory T cell responses to influenza virus in the presence or absence of CD27 and/or CD28. Wild-type, CD27−/−, CD28−/−, and CD27−/−/CD28−/− mice were infected intranasally with influenza virus. Cells were isolated from the lung, DLNs, and spleen on the indicated days after infection. They were counted, stained with anti-CD8 mAb and NP366–374/H2-Db tetramers, and analyzed by flow cytometry. Each symbol represents an individual mouse (four per group) and dashes represent mean values. (A) Primary response. (B) Memory response. The complete experiment was performed two times with reproducible results.
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Related In: Results  -  Collection

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getmorefigures.php?uid=PMC2194245&req=5

fig1: In vivo primary and memory T cell responses to influenza virus in the presence or absence of CD27 and/or CD28. Wild-type, CD27−/−, CD28−/−, and CD27−/−/CD28−/− mice were infected intranasally with influenza virus. Cells were isolated from the lung, DLNs, and spleen on the indicated days after infection. They were counted, stained with anti-CD8 mAb and NP366–374/H2-Db tetramers, and analyzed by flow cytometry. Each symbol represents an individual mouse (four per group) and dashes represent mean values. (A) Primary response. (B) Memory response. The complete experiment was performed two times with reproducible results.
Mentions: Wild-type, CD27−/−, CD28−/−, and CD27/CD28−/− double deficient mice were infected and analyzed 6, 8, 10, or 14 d later for the presence of virus-specific CD8+ T cells. In the lung, accumulation of wild-type virus-specific T cells became detectable at day 6 and peaked at days 8–10 after infection (Fig. 1 A). In CD28−/− mice, the T cell response at this site was partially intact, whereas it was almost completely abrogated upon additional CD27 deletion. Apparently, CD27 can support the virus-specific CD8+ T cell response in the lung in absence of CD28. Accumulation of virus-specific CD8+ T cells in the lung of CD27−/− mice was in fact much lower than in CD28−/− mice, indicating that CD27 is a major determinant for the CD8+ T cell response at the site of infection. The response at the site of priming, the mediastinal lung DLNs, was strongly reduced in both CD27−/− and CD28−/− mice compared with wild-type mice, and virtually absent in CD27/CD28−/− mice, indicating that both receptors make crucial and in part complimentary contributions to generation of the virus-specific CD8+ T cell pool. Strikingly, in the spleen, CD27 deficiency only had a minor effect, whereas CD28 deletion strongly reduced the response. Accumulation of virus-specific CD8+ T cells in the spleen appeared fully dependent on the collective contribution of CD27 and CD28. In the absence of both molecules, increase in tetramer+ T cells was virtually undetectable.

Bottom Line: In the primary response, CD27 and CD28 impact to a similar extent on expansion of virus-specific T cells in draining lymph nodes.Unlike CD28, CD27 does not affect cell cycle activity, but promotes survival of activated T cells throughout successive rounds of division at the site of priming and may do so at the site of infection as well.CD27 was found to rescue CD28(-/-) T cells from death at the onset of division, explaining its capacity to support a T cell response in absence of CD28.

View Article: PubMed Central - PubMed

Affiliation: Division of Immunology, The Netherlands Cancer Institute, 1066 CX Amsterdam, Netherlands.

ABSTRACT
CD27, like CD28, acts in concert with the T cell receptor to support T cell expansion. Using CD27(-/-) mice, we have shown earlier that CD27 determines the magnitude of primary and memory T cell responses to influenza virus. Here, we have examined the relative contributions of CD27 and CD28 to generation of the virus-specific effector T cell pool and its establishment at the site of infection (the lung), using CD27(-/-), CD28(-/-), and CD27/CD28(-/-) mice. We find that primary and memory CD8+ T cell responses to influenza virus are dependent on the collective contribution of both receptors. In the primary response, CD27 and CD28 impact to a similar extent on expansion of virus-specific T cells in draining lymph nodes. CD27 is the principle determinant for accumulation of virus-specific T cells in the lung because it can sustain this response in CD28(-/-) mice. Unlike CD28, CD27 does not affect cell cycle activity, but promotes survival of activated T cells throughout successive rounds of division at the site of priming and may do so at the site of infection as well. CD27 was found to rescue CD28(-/-) T cells from death at the onset of division, explaining its capacity to support a T cell response in absence of CD28.

Show MeSH
Related in: MedlinePlus