In vivo generation of oligoclonal colitic CD4+ T-cell lines expressing a distinct T-cell receptor Vβ

Ana C. Abadía-Molina, Atsushi Mizoguchi, William Alvis Faubion, Ype P. De Jong, Svend T. Rietdijk, Martina Comiskey, Kareem Clarke, Atul K. Bhan, Cox Terhorst

Research output: Contribution to journalArticle

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Abstract

Background & Aims: Transplantation of wild-type (H-2k) bone marrow into tgε26 mice (BM→tgε26) induces colitis, characterized by T-helper cell type 1 activation in the lamina propria. Here we determined whether pathogenic T-cell clones could be derived by serial adoptive transfers into healthy tgε26 recipients, starting with the population of CD4+ cells in the mesenteric lymph nodes of BM→tgε26 mice. Methods: CD4+ cells purified from the mesenteric lymph nodes of colitic BM→tgε26 mice were adoptively transferred into a second group of healthy tgε26 recipients. Mesenteric lymph node CD4+ cells from the second group of mice were then used for consecutive transfers. Lamina propria CD4+ cells isolated from each mouse with colitis were analyzed for their cytokine profile and for their T-cell receptor Vβ repertoire. Results: CD4+ T cells maintained a dominant T-helper 1 phenotype after multiple transfers (≤8) into recipient tgε26 mice. A single T-cell receptor Vβ was enriched (as much as 90%) in 8 CD4 + T-cell lines: Vβ8S3, Vβ8S1/2, Vβ10S1, or Vβ14. Sequence analyses of the T-cell receptor Vβs showed clonality or the presence of a very restricted number of clones within each line. Adoptive transfers of the oligoclonal lines into either C3H × Rag-/- or severe combined immunodeficiency disease mice (H-2k) also induced colitis, whereas transfers into BALB/c × Rag-/- or severe combined immunodeficiency disease mice (H-2d) did not. Conclusions: Colitis-inducing CD4+ T-helper 1 cell clones can be obtained by enrichment through sequential adoptive transfers of CD4+ cells from mesenteric lymph nodes. Distinct dominant T-cell receptor Vβs in each cell line responded to antigens presented by class II major histocompatibility complex.

Original languageEnglish (US)
Pages (from-to)1268-1277
Number of pages10
JournalGastroenterology
Volume128
Issue number5
DOIs
StatePublished - May 2005
Externally publishedYes

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T-Cell Antigen Receptor
T-Lymphocytes
Cell Line
Colitis
Adoptive Transfer
Lymph Nodes
Severe Combined Immunodeficiency
Th1 Cells
Clone Cells
Bone Marrow
Mucous Membrane
Histocompatibility Antigens Class II
Major Histocompatibility Complex
Sequence Analysis
Transplantation
Cytokines
Phenotype

ASJC Scopus subject areas

  • Gastroenterology

Cite this

Abadía-Molina, A. C., Mizoguchi, A., Faubion, W. A., De Jong, Y. P., Rietdijk, S. T., Comiskey, M., ... Terhorst, C. (2005). In vivo generation of oligoclonal colitic CD4+ T-cell lines expressing a distinct T-cell receptor Vβ. Gastroenterology, 128(5), 1268-1277. https://doi.org/10.1053/j.gastro.2005.01.060

In vivo generation of oligoclonal colitic CD4+ T-cell lines expressing a distinct T-cell receptor Vβ. / Abadía-Molina, Ana C.; Mizoguchi, Atsushi; Faubion, William Alvis; De Jong, Ype P.; Rietdijk, Svend T.; Comiskey, Martina; Clarke, Kareem; Bhan, Atul K.; Terhorst, Cox.

In: Gastroenterology, Vol. 128, No. 5, 05.2005, p. 1268-1277.

Research output: Contribution to journalArticle

Abadía-Molina, AC, Mizoguchi, A, Faubion, WA, De Jong, YP, Rietdijk, ST, Comiskey, M, Clarke, K, Bhan, AK & Terhorst, C 2005, 'In vivo generation of oligoclonal colitic CD4+ T-cell lines expressing a distinct T-cell receptor Vβ', Gastroenterology, vol. 128, no. 5, pp. 1268-1277. https://doi.org/10.1053/j.gastro.2005.01.060
Abadía-Molina, Ana C. ; Mizoguchi, Atsushi ; Faubion, William Alvis ; De Jong, Ype P. ; Rietdijk, Svend T. ; Comiskey, Martina ; Clarke, Kareem ; Bhan, Atul K. ; Terhorst, Cox. / In vivo generation of oligoclonal colitic CD4+ T-cell lines expressing a distinct T-cell receptor Vβ. In: Gastroenterology. 2005 ; Vol. 128, No. 5. pp. 1268-1277.
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abstract = "Background & Aims: Transplantation of wild-type (H-2k) bone marrow into tgε26 mice (BM→tgε26) induces colitis, characterized by T-helper cell type 1 activation in the lamina propria. Here we determined whether pathogenic T-cell clones could be derived by serial adoptive transfers into healthy tgε26 recipients, starting with the population of CD4+ cells in the mesenteric lymph nodes of BM→tgε26 mice. Methods: CD4+ cells purified from the mesenteric lymph nodes of colitic BM→tgε26 mice were adoptively transferred into a second group of healthy tgε26 recipients. Mesenteric lymph node CD4+ cells from the second group of mice were then used for consecutive transfers. Lamina propria CD4+ cells isolated from each mouse with colitis were analyzed for their cytokine profile and for their T-cell receptor Vβ repertoire. Results: CD4+ T cells maintained a dominant T-helper 1 phenotype after multiple transfers (≤8) into recipient tgε26 mice. A single T-cell receptor Vβ was enriched (as much as 90{\%}) in 8 CD4 + T-cell lines: Vβ8S3, Vβ8S1/2, Vβ10S1, or Vβ14. Sequence analyses of the T-cell receptor Vβs showed clonality or the presence of a very restricted number of clones within each line. Adoptive transfers of the oligoclonal lines into either C3H × Rag-/- or severe combined immunodeficiency disease mice (H-2k) also induced colitis, whereas transfers into BALB/c × Rag-/- or severe combined immunodeficiency disease mice (H-2d) did not. Conclusions: Colitis-inducing CD4+ T-helper 1 cell clones can be obtained by enrichment through sequential adoptive transfers of CD4+ cells from mesenteric lymph nodes. Distinct dominant T-cell receptor Vβs in each cell line responded to antigens presented by class II major histocompatibility complex.",
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AU - Abadía-Molina, Ana C.

AU - Mizoguchi, Atsushi

AU - Faubion, William Alvis

AU - De Jong, Ype P.

AU - Rietdijk, Svend T.

AU - Comiskey, Martina

AU - Clarke, Kareem

AU - Bhan, Atul K.

AU - Terhorst, Cox

PY - 2005/5

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N2 - Background & Aims: Transplantation of wild-type (H-2k) bone marrow into tgε26 mice (BM→tgε26) induces colitis, characterized by T-helper cell type 1 activation in the lamina propria. Here we determined whether pathogenic T-cell clones could be derived by serial adoptive transfers into healthy tgε26 recipients, starting with the population of CD4+ cells in the mesenteric lymph nodes of BM→tgε26 mice. Methods: CD4+ cells purified from the mesenteric lymph nodes of colitic BM→tgε26 mice were adoptively transferred into a second group of healthy tgε26 recipients. Mesenteric lymph node CD4+ cells from the second group of mice were then used for consecutive transfers. Lamina propria CD4+ cells isolated from each mouse with colitis were analyzed for their cytokine profile and for their T-cell receptor Vβ repertoire. Results: CD4+ T cells maintained a dominant T-helper 1 phenotype after multiple transfers (≤8) into recipient tgε26 mice. A single T-cell receptor Vβ was enriched (as much as 90%) in 8 CD4 + T-cell lines: Vβ8S3, Vβ8S1/2, Vβ10S1, or Vβ14. Sequence analyses of the T-cell receptor Vβs showed clonality or the presence of a very restricted number of clones within each line. Adoptive transfers of the oligoclonal lines into either C3H × Rag-/- or severe combined immunodeficiency disease mice (H-2k) also induced colitis, whereas transfers into BALB/c × Rag-/- or severe combined immunodeficiency disease mice (H-2d) did not. Conclusions: Colitis-inducing CD4+ T-helper 1 cell clones can be obtained by enrichment through sequential adoptive transfers of CD4+ cells from mesenteric lymph nodes. Distinct dominant T-cell receptor Vβs in each cell line responded to antigens presented by class II major histocompatibility complex.

AB - Background & Aims: Transplantation of wild-type (H-2k) bone marrow into tgε26 mice (BM→tgε26) induces colitis, characterized by T-helper cell type 1 activation in the lamina propria. Here we determined whether pathogenic T-cell clones could be derived by serial adoptive transfers into healthy tgε26 recipients, starting with the population of CD4+ cells in the mesenteric lymph nodes of BM→tgε26 mice. Methods: CD4+ cells purified from the mesenteric lymph nodes of colitic BM→tgε26 mice were adoptively transferred into a second group of healthy tgε26 recipients. Mesenteric lymph node CD4+ cells from the second group of mice were then used for consecutive transfers. Lamina propria CD4+ cells isolated from each mouse with colitis were analyzed for their cytokine profile and for their T-cell receptor Vβ repertoire. Results: CD4+ T cells maintained a dominant T-helper 1 phenotype after multiple transfers (≤8) into recipient tgε26 mice. A single T-cell receptor Vβ was enriched (as much as 90%) in 8 CD4 + T-cell lines: Vβ8S3, Vβ8S1/2, Vβ10S1, or Vβ14. Sequence analyses of the T-cell receptor Vβs showed clonality or the presence of a very restricted number of clones within each line. Adoptive transfers of the oligoclonal lines into either C3H × Rag-/- or severe combined immunodeficiency disease mice (H-2k) also induced colitis, whereas transfers into BALB/c × Rag-/- or severe combined immunodeficiency disease mice (H-2d) did not. Conclusions: Colitis-inducing CD4+ T-helper 1 cell clones can be obtained by enrichment through sequential adoptive transfers of CD4+ cells from mesenteric lymph nodes. Distinct dominant T-cell receptor Vβs in each cell line responded to antigens presented by class II major histocompatibility complex.

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