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      KCI등재 SCOPUS SCIE

      Expression and Function of TLR2 on CD4 Versus CD8 T Cells

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      https://www.riss.kr/link?id=A103884182

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      다국어 초록 (Multilingual Abstract)

      Background: Toll-like receptors (TLRs) play a fundamental
      role in innate immunity through their capacity to recognize
      pathogen-associated molecular patterns. Also, TLRs that are
      expressed in T cells are reported to function as co-stimulatory
      receptors. However, the functional capacity of TLRs
      on CD4 T and CD8 T cells has not been directly compared.
      Here we compared CD4 and CD8 T cell responses to TLR2
      ligand plus TCR-mediated stimulation. Methods: TLR2 expression
      was analyzed on T cell subsets under naïve and alloantigen-
      primed conditions. We analyzed the effects of
      TLR2 co-stimulation on proliferation and survival of T cell
      subsets in vitro when stimulated with soluble anti-CD3 in the
      presence or absence of synthetic ligand Pam3CSK4. Results:
      TLR2 expression on CD8 T cells was induced following activation;
      this expression was much higher than on CD4 T cells.
      Thus, the molecule was constitutively expressed on Listeriaspecific
      memory CD8 T cells. Based on these expression levels,
      proliferation and survival were markedly elevated in CD8
      T cells in response to the TLR2 co-stimulation by Pam3CSK4
      compared with those in CD4 T cells. Conclusion: Our data
      show that TLR2 co-stimulation is more responsible for proliferation
      and survival of CD8 T cells than for that of CD4 T
      cells.
      번역하기

      Background: Toll-like receptors (TLRs) play a fundamental role in innate immunity through their capacity to recognize pathogen-associated molecular patterns. Also, TLRs that are expressed in T cells are reported to function as co-stimulatory receptors...

      Background: Toll-like receptors (TLRs) play a fundamental
      role in innate immunity through their capacity to recognize
      pathogen-associated molecular patterns. Also, TLRs that are
      expressed in T cells are reported to function as co-stimulatory
      receptors. However, the functional capacity of TLRs
      on CD4 T and CD8 T cells has not been directly compared.
      Here we compared CD4 and CD8 T cell responses to TLR2
      ligand plus TCR-mediated stimulation. Methods: TLR2 expression
      was analyzed on T cell subsets under naïve and alloantigen-
      primed conditions. We analyzed the effects of
      TLR2 co-stimulation on proliferation and survival of T cell
      subsets in vitro when stimulated with soluble anti-CD3 in the
      presence or absence of synthetic ligand Pam3CSK4. Results:
      TLR2 expression on CD8 T cells was induced following activation;
      this expression was much higher than on CD4 T cells.
      Thus, the molecule was constitutively expressed on Listeriaspecific
      memory CD8 T cells. Based on these expression levels,
      proliferation and survival were markedly elevated in CD8
      T cells in response to the TLR2 co-stimulation by Pam3CSK4
      compared with those in CD4 T cells. Conclusion: Our data
      show that TLR2 co-stimulation is more responsible for proliferation
      and survival of CD8 T cells than for that of CD4 T
      cells.

      더보기

      다국어 초록 (Multilingual Abstract)

      Background: Toll-like receptors (TLRs) play a fundamental
      role in innate immunity through their capacity to recognize
      pathogen-associated molecular patterns. Also, TLRs that are
      expressed in T cells are reported to function as co-stimulatory
      receptors. However, the functional capacity of TLRs
      on CD4 T and CD8 T cells has not been directly compared.
      Here we compared CD4 and CD8 T cell responses to TLR2
      ligand plus TCR-mediated stimulation. Methods: TLR2 expression
      was analyzed on T cell subsets under naïve and alloantigen-
      primed conditions. We analyzed the effects of
      TLR2 co-stimulation on proliferation and survival of T cell
      subsets in vitro when stimulated with soluble anti-CD3 in the
      presence or absence of synthetic ligand Pam3CSK4. Results:
      TLR2 expression on CD8 T cells was induced following activation;
      this expression was much higher than on CD4 T cells.
      Thus, the molecule was constitutively expressed on Listeriaspecific
      memory CD8 T cells. Based on these expression levels,
      proliferation and survival were markedly elevated in CD8
      T cells in response to the TLR2 co-stimulation by Pam3CSK4
      compared with those in CD4 T cells. Conclusion: Our data
      show that TLR2 co-stimulation is more responsible for proliferation
      and survival of CD8 T cells than for that of CD4 T
      cells.
      번역하기

      Background: Toll-like receptors (TLRs) play a fundamental role in innate immunity through their capacity to recognize pathogen-associated molecular patterns. Also, TLRs that are expressed in T cells are reported to function as co-stimulatory recep...

      Background: Toll-like receptors (TLRs) play a fundamental
      role in innate immunity through their capacity to recognize
      pathogen-associated molecular patterns. Also, TLRs that are
      expressed in T cells are reported to function as co-stimulatory
      receptors. However, the functional capacity of TLRs
      on CD4 T and CD8 T cells has not been directly compared.
      Here we compared CD4 and CD8 T cell responses to TLR2
      ligand plus TCR-mediated stimulation. Methods: TLR2 expression
      was analyzed on T cell subsets under naïve and alloantigen-
      primed conditions. We analyzed the effects of
      TLR2 co-stimulation on proliferation and survival of T cell
      subsets in vitro when stimulated with soluble anti-CD3 in the
      presence or absence of synthetic ligand Pam3CSK4. Results:
      TLR2 expression on CD8 T cells was induced following activation;
      this expression was much higher than on CD4 T cells.
      Thus, the molecule was constitutively expressed on Listeriaspecific
      memory CD8 T cells. Based on these expression levels,
      proliferation and survival were markedly elevated in CD8
      T cells in response to the TLR2 co-stimulation by Pam3CSK4
      compared with those in CD4 T cells. Conclusion: Our data
      show that TLR2 co-stimulation is more responsible for proliferation
      and survival of CD8 T cells than for that of CD4 T
      cells.

      더보기

      참고문헌 (Reference)

      1 Marsland BJ, "Toll-like receptors: paving the path to T cell-driven autoimmunity?" 19 : 611-614, 2007

      2 Medzhitov R, "Toll-like receptors and innate immunity" 1 : 135-145, 2001

      3 Takeda K, "Toll-like receptors" 21 : 335-376, 2003

      4 Gelman AE, "Toll-like receptor ligands directly promote activated CD4+ T cell survival" 172 : 6065-6073, 2004

      5 Steinman RM, "Tolerogenic dendritic cells" 21 : 685-711, 2003

      6 Gelman AE, "The adaptor molecule MyD88 activates PI-3 kinase signaling in CD4+ T cells and enables CpG oligodeoxynucleotide-mediated costimulation" 25 : 783-793, 2006

      7 Kerfoot SM, "TLR4 contributes to disease-inducing mechanisms resulting in central nervous system autoimmune disease" 173 : 7070-7077, 2004

      8 Komai-Koma M, "TLR2 is expressed on activated T cells as a costimulatory receptor" 101 : 3029-3034, 2004

      9 Cottalorda A, "TLR2 engagement on CD8 T cells lowers the threshold for optimal antigen-induced T cell activation" 36 : 1684-1693, 2006

      10 Imanishi T, "TLR2 directly triggers Th1 effector functions" 178 : 6715-6719, 2007

      1 Marsland BJ, "Toll-like receptors: paving the path to T cell-driven autoimmunity?" 19 : 611-614, 2007

      2 Medzhitov R, "Toll-like receptors and innate immunity" 1 : 135-145, 2001

      3 Takeda K, "Toll-like receptors" 21 : 335-376, 2003

      4 Gelman AE, "Toll-like receptor ligands directly promote activated CD4+ T cell survival" 172 : 6065-6073, 2004

      5 Steinman RM, "Tolerogenic dendritic cells" 21 : 685-711, 2003

      6 Gelman AE, "The adaptor molecule MyD88 activates PI-3 kinase signaling in CD4+ T cells and enables CpG oligodeoxynucleotide-mediated costimulation" 25 : 783-793, 2006

      7 Kerfoot SM, "TLR4 contributes to disease-inducing mechanisms resulting in central nervous system autoimmune disease" 173 : 7070-7077, 2004

      8 Komai-Koma M, "TLR2 is expressed on activated T cells as a costimulatory receptor" 101 : 3029-3034, 2004

      9 Cottalorda A, "TLR2 engagement on CD8 T cells lowers the threshold for optimal antigen-induced T cell activation" 36 : 1684-1693, 2006

      10 Imanishi T, "TLR2 directly triggers Th1 effector functions" 178 : 6715-6719, 2007

      11 Wong P, "Rapid development of T cell memory" 172 : 7239-7245, 2004

      12 Rahman AH, "MyD88 plays a critical T cell-intrinsic role in supporting CD8 T cell expansion during acute lymphocytic choriomeningitis virus infection" 181 : 3804-3810, 2008

      13 Dougan M, "Immune therapy for cancer" 27 : 83-117, 2009

      14 Lee EK, "Essential roles of toll-like receptor 4 signaling in arthritis induced by type II collagen antibody and LPS" 17 : 325-333, 2005

      15 Asprodites N, "Engagement of Toll-like receptor-2 on cytotoxic T-lymphocytes occurs in vivo and augments antitumor activity" 22 : 3628-3637, 2008

      16 Wong P, "CD8 T cell responses to infectious pathogens" 21 : 29-70, 2003

      17 Meng G, "Antagonistic antibody prevents toll-like receptor 2-driven lethal shock-like syndromes" 113 : 1473-1481, 2004

      18 Quigley M, "A critical role for direct TLR2-MyD88 signaling in CD8 T-cell clonal expansion and memory formation following vaccinia viral infection" 113 : 2256-2264, 2009

      19 Shuford WW, "4-1BB costimulatory signals preferentially induce CD8+ T cell proliferation and lead to the amplification in vivo of cytotoxic T cell responses" 186 : 47-55, 1997

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      학술지 이력

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      2016-01-01 평가 우수등재학술지 선정 (계속평가)
      2012-01-01 평가 등재 1차 FAIL (등재유지) KCI등재
      2009-01-01 평가 등재학술지 선정 (등재후보2차) KCI등재
      2008-01-01 평가 등재후보 1차 PASS (등재후보1차) KCI등재후보
      2007-01-01 평가 등재후보학술지 유지 (등재후보2차) KCI등재후보
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      학술지 인용정보

      학술지 인용정보
      기준연도 WOS-KCI 통합IF(2년) KCIF(2년) KCIF(3년)
      2016 0.36 0.36 0.29
      KCIF(4년) KCIF(5년) 중심성지수(3년) 즉시성지수
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