A second model of Cachexia/ multiple organ failure caused by the complete human p75 TNF receptor. This model is characterized by inflammation in pancreas, liver, lung, kidney, and hematopoietic abnormalities.(View the original article)

p75TNF-R-triggered multi-organ inflammation
and hematopoietic abnormalities develop even in the absence of TNF.
Histopathological analysis (H/E) in liver and pancreas of 4-mo-old heterozygous TgE1335 mice (TgE1335het) and 3-wkold TgE1335 homozygous (TgE1335hom) or homozygous TgE1335 3 TNF2/2 mice (TgE1335hom/TNF2/2). Lesions in heterozygous Tg1335 mice involve mainly the liver and pancreas where inflammatory infiltrates develop and persist chronically from 2–3 mo of age. In homozygous TgE1335 mice a more severe pathology develops, characterized by extensive periportal inflammation and tissue necrosis (asterisk) in the liver, and in a severely hypoplastic and inflamed pancreas. A similar histopathology evolves in homozygous TgE1335 transgenic mice bred into a null TNF background. Original magnification 3108. Spleen sections from homozygous TgE1335 mice are characterized by markedly reduced numbers of IgM1 B cells (brown) whereas CD31 T cell localization (blue) seems unaffected. A similar phenotype occurs even in the absence of endogenous TNF.