Mucosal T cells regulate Paneth and intermediate cell numbers in the small intestine of T. spiralis-infected mice
M. Kamal
*Division of Gastroenterology and †School of Biological Sciences , University of Nottingham, UK, ‡Department of Pathology, University of California, Irvine, USA, §Institute of Animal Health, Compton, UK and ¶Gastrointestinal Unit, Massachusetts General Hospital and Harvard Medical School, Boston, USA
Search for more papers by this authorD. Wakelin
*Division of Gastroenterology and †School of Biological Sciences , University of Nottingham, UK, ‡Department of Pathology, University of California, Irvine, USA, §Institute of Animal Health, Compton, UK and ¶Gastrointestinal Unit, Massachusetts General Hospital and Harvard Medical School, Boston, USA
Search for more papers by this authorA. J. Ouellette
*Division of Gastroenterology and †School of Biological Sciences , University of Nottingham, UK, ‡Department of Pathology, University of California, Irvine, USA, §Institute of Animal Health, Compton, UK and ¶Gastrointestinal Unit, Massachusetts General Hospital and Harvard Medical School, Boston, USA
Search for more papers by this authorA. Smith
*Division of Gastroenterology and †School of Biological Sciences , University of Nottingham, UK, ‡Department of Pathology, University of California, Irvine, USA, §Institute of Animal Health, Compton, UK and ¶Gastrointestinal Unit, Massachusetts General Hospital and Harvard Medical School, Boston, USA
Search for more papers by this authorD. K. Podolsky
*Division of Gastroenterology and †School of Biological Sciences , University of Nottingham, UK, ‡Department of Pathology, University of California, Irvine, USA, §Institute of Animal Health, Compton, UK and ¶Gastrointestinal Unit, Massachusetts General Hospital and Harvard Medical School, Boston, USA
Search for more papers by this authorY. R. Mahida
*Division of Gastroenterology and †School of Biological Sciences , University of Nottingham, UK, ‡Department of Pathology, University of California, Irvine, USA, §Institute of Animal Health, Compton, UK and ¶Gastrointestinal Unit, Massachusetts General Hospital and Harvard Medical School, Boston, USA
Search for more papers by this authorM. Kamal
*Division of Gastroenterology and †School of Biological Sciences , University of Nottingham, UK, ‡Department of Pathology, University of California, Irvine, USA, §Institute of Animal Health, Compton, UK and ¶Gastrointestinal Unit, Massachusetts General Hospital and Harvard Medical School, Boston, USA
Search for more papers by this authorD. Wakelin
*Division of Gastroenterology and †School of Biological Sciences , University of Nottingham, UK, ‡Department of Pathology, University of California, Irvine, USA, §Institute of Animal Health, Compton, UK and ¶Gastrointestinal Unit, Massachusetts General Hospital and Harvard Medical School, Boston, USA
Search for more papers by this authorA. J. Ouellette
*Division of Gastroenterology and †School of Biological Sciences , University of Nottingham, UK, ‡Department of Pathology, University of California, Irvine, USA, §Institute of Animal Health, Compton, UK and ¶Gastrointestinal Unit, Massachusetts General Hospital and Harvard Medical School, Boston, USA
Search for more papers by this authorA. Smith
*Division of Gastroenterology and †School of Biological Sciences , University of Nottingham, UK, ‡Department of Pathology, University of California, Irvine, USA, §Institute of Animal Health, Compton, UK and ¶Gastrointestinal Unit, Massachusetts General Hospital and Harvard Medical School, Boston, USA
Search for more papers by this authorD. K. Podolsky
*Division of Gastroenterology and †School of Biological Sciences , University of Nottingham, UK, ‡Department of Pathology, University of California, Irvine, USA, §Institute of Animal Health, Compton, UK and ¶Gastrointestinal Unit, Massachusetts General Hospital and Harvard Medical School, Boston, USA
Search for more papers by this authorY. R. Mahida
*Division of Gastroenterology and †School of Biological Sciences , University of Nottingham, UK, ‡Department of Pathology, University of California, Irvine, USA, §Institute of Animal Health, Compton, UK and ¶Gastrointestinal Unit, Massachusetts General Hospital and Harvard Medical School, Boston, USA
Search for more papers by this authorAbstract
Secretions of Paneth, intermediate and goblet cells have been implicated in innate intestinal host defense. We have investigated the role of T cells in effecting alterations in small intestinal epithelial cell populations induced by infection with the nematode Trichinella spiralis. Small intestinal tissue sections from euthymic and athymic (nude) mice, and mice with combined deficiency in T-cell receptor β and δ genes [TCR(β/δ)−/–] infected orally with T. spiralis larvae, were examined by electron microscopy and after histochemical and lineage-specific immunohistochemical staining. Compared with uninfected controls, Paneth and intermediate cell numbers increased significantly in infected euthymic and nude mice but not infected TCR(β/δ)−/– mice. Transfer of mesenteric lymph node cells before infection led to an increase in Paneth and intermediate cells in TCR(β/δ)−/– mice. In infected euthymic mice, Paneth cells and intermediate cells expressed cryptdins (α-defensins) but not intestinal trefoil factor (ITF), and goblet cells expressed ITF but not cryptdins. In conclusion, a unique, likely thymic-independent population of mucosal T cells modulates innate small intestinal host defense in mice by increasing the number of Paneth and intermediate cells in response to T. spiralis infection.
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