Abstract
Granulocyte macrophage-colony stimulating factor (GM-CSF) is a pleiotrophic proinflammatory cytokine that augments adaptive immunity by linking it to innate immunity. Experimental autoimmune gastritis is an animal model of human autoimmune gastritis and pernicious anaemia. We have previously shown that GM-CSF is expressed in the gastric mucosa of mice with gastritis initiated by neonatal thymectomy ( Gastroenterology 110 (1996) 1791) and that transgenic expression of GM-CSF in the stomach induces autoimmune gastritis in mice ( J. Immunol. 166 (2001) 2090). Here we have examined the development of autoimmune gastritis initiated by immunisation or by neonatal thymectomy in GM-CSF deficient mice. We found that gastritis develops in GM-CSF deficient mice initiated by neonatal thymectomy but not by immunisation with gastric antigen. These observations suggest that GM-CSF is not absolutely required for the initiation of autoimmunity and highlights the different conclusions that can be drawn using different disease models.
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