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Specifically primed systemic T cells mediate colitis in mice. Splenic CD4+ CD45RBlow T cells are strongly implicated in colitis through production of tumour necrosis factor α (TNFα), according to results obtained in severe combined immunodeficient (SCID) mice.
SCID mice fed ovalbumin developed the hallmarks of colitis when reconstituted with splenic T cells from immunocompetent donor mice primed with ovalbumin. CD4+ T cells were more abundant in the large intestine than the spleen and small intestine, and they included a large proportion of CD45RBlow T cells. Those from the large intestine showed extensive staining for interferon γ (IFNγ) and TNFα and contained mRNA for both cytokines, though only antibody to TNFα prevented colitis after challenge with ovalbumin. Induced colitis was antigen specific. So SCID mice reconstituted with splenic CD4+ CD45RB+ T cells primed with ovalbumin or another protein showed severe colitis only with ovalbumin, and mononuclear cells isolated from spleen and large intestine showed ovalbumin specific proliferation in vitro. Finally, SCID mice reconstituted with primed CD4+ CD45RBlow T cells developed severe colitis with ovalbumin and showed abundant TNFα secreting cells compared with mice reconstituted with non-primed CD4+ CD45RBlow T cells .
BALB/c mice were primed subcutaneously with antigen. A week later CD4+ CD45RB+ or CD4+ CD45RBlow T cells were obtained by FACS sorting of a single cell suspension from the spleen for adoptive transfer to SCID mice by venous injection.
Previous studies have suggested interaction between spleen and colon in colitis but not which specific CD4+ T cells.