Adoptive transfer of nontransgenic mesenteric lymph node cells induces colitis in athymic HLA‐B27 transgenic nude rats | Zendy

Hoentjen F. | Zendy; Tonkonogy S. L. | Zendy; Liu B. | Zendy; Sartor R. B. | Zendy; Taurog J. D. | Zendy; Dieleman L. A. | Zendy

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Adoptive transfer of nontransgenic mesenteric lymph node cells induces colitis in athymic HLA‐B27 transgenic nude rats

Author(s) -

Hoentjen F.,

Tonkonogy S. L.,

Liu B.,

Sartor R. B.,

Taurog J. D.,

Dieleman L. A.

Publication year - 2006

Publication title -

clinical & experimental immunology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.329

H-Index - 135

eISSN - 1365-2249

pISSN - 0009-9104

DOI - 10.1111/j.1365-2249.2006.03013.x

Subject(s) - adoptive cell transfer , colitis , mesenteric lymph nodes , immunology , lymph node , medicine , inflammatory bowel disease , t cell , pathology , immune system , disease

Summary HLA‐B27 transgenic (TG) rats develop spontaneous colitis when colonized with intestinal bacteria, whereas athymic nude (rnu/rnu) HLA‐B27 TG rats remain disease free. The present study was designed to determine whether or not HLA‐B27 expression on T cells is required for development of colitis after transfer of mesenteric lymph node (MLN) cells into rnu/rnu HLA‐B27 recipients. Athymic nontransgenic (non‐TG) and HLA‐B27 TG recipients received MLN cells from either TG or non‐TG rnu /+ heterozygous donor rats that contain T cells. HLA‐B27 TG rnu/rnu recipients receiving either non‐TG or TG MLN cells developed severe colitis and had higher caecal MPO and IL‐1β levels, and their MLN cells produced more IFN‐γ and less IL‐10 after in vitro stimulation with caecal bacterial lysate compared to rnu/rnu non‐TG recipients that remained disease free after receiving either TG or non‐TG cells. Interestingly, proliferating donor TG T cells were detectable one week after adoptive transfer into rnu/rnu TG recipients but not after transfer into non‐TG recipients. T cells from either non‐TG or TG donors induce colitis in rnu/rnu TG but not in non‐TG rats, suggesting that activation of effector T cells by other cell types that express HLA‐B27 is pivotal for the pathogenesis of colitis in this model.

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