TNF receptor p55 is required for elimination of inflammatory cells following control of intracellular pathogens.
Publication/Presentation Date
10-1-1999
Abstract
The elimination of lymphocytes within inflammatory lesions is a critical component in the resolution of disease once pathogens have been cleared. We report here that signaling through the TNF receptor p55 (TNFRp55) is required to eliminate lymphocytes from lesions associated with intracellular pathogens. Thus, TNFRp55-/- mice, but not Fas-deficient mice, maintained inflammatory lesions associated with either Leishmania major or Rhodococcus equi infection, although they developed a Th1 response and controlled the pathogens. Inflammatory cells from either L. major- or R. equi-infected C57BL/6 mice were sensitive to TNF-induced apoptosis, and conversely the number of apoptotic cells in the lesions from TNFRp55-/- mice was dramatically reduced compared with wild-type mice. Furthermore, in vivo depletion of TNF in wild-type mice blocked lesion regression following R. equi infection. Taken together, our results suggest that signaling through the TNFRp55, but not Fas, is required to induce apoptosis of T cells within inflammatory lesions once pathogens are eliminated, and that in its absence lesions fail to regress.
Volume
163
Issue
7
First Page
3883
Last Page
3889
ISSN
0022-1767
Published In/Presented At
Kanaly, S. T., Nashleanas, M., Hondowicz, B., & Scott, P. (1999). TNF receptor p55 is required for elimination of inflammatory cells following control of intracellular pathogens. Journal of immunology (Baltimore, Md. : 1950), 163(7), 3883–3889.
Disciplines
Medicine and Health Sciences
PubMedID
10490988
Department(s)
Department of Medicine
Document Type
Article