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Induction of syngeneic graft‐versus‐host disease in LPS hyporesponsive C3H/HeJ mice
Author(s) -
Flanagan Diana Lowery,
Gross Rachel,
Jennings C. Darrell,
Caywood Betty E.,
Goes Sarah,
Kaplan Alan M.,
Bryson J. Scott
Publication year - 2001
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1189/jlb.70.6.873
Subject(s) - biology , immunology , secretion , transplantation , ratón , tumor necrosis factor alpha , disease , immune system , lipopolysaccharide , endocrinology , medicine
Syngeneic GVHD (SGVHD) develops following syngeneic bone marrow transplantation and treatment with cyclosporine A. Previous studies have demonstrated a role for IL‐12, IFN‐γ, and TNF‐α in the development of murine SGVHD. Macrophages can be activated to secrete IL‐12 and TNF‐α via a T‐cell‐dependent or T‐cell‐independent pathway (LPS or bacterial products). Studies were designed to determine if LPS participated in the development of SGVHD in C3H/HeN (LPS‐responsive) and C3H/HeJ (LPS‐hyporesponsive) mice. C3H/HeJ and C3H/HeN mice had similar levels of disease induction and pathology. Following induction of SGVHD, treatment of C3H/HeN, but not C3H/HeJ, mice with a sublethal dose of LPS resulted in mortality. However, neutralization of IL‐12 abrogated the development of disease in C3H/HeJ mice, demonstrating that activated macrophages and their products participated in the development of SGVHD in these animals. These data suggested that LPS responsiveness was not a predisposing factor for SGVHD induction.