The host response in graft versus host disease. I. Radiosensitive T cells of host origin inhibit parental anti-F1 cytotoxicity in murine chronic graft versus host disease.

Abstract

Murine graft versus host (GVH) disease takes two forms depending on the parental/F1 strain combination employed. Acute lethal GVH disease is characterized by anemia, lymphopenia, hypogammaglobulinemia, profound anti-F1 cytotoxicity, and the loss of cytotoxic potential against third-party alloantigen. In contrast to this, chronic GVH disease is characterized by polyclonal B cell activation, auto-antibody production, no anti-F1 cytotoxicity, and retained cytotoxicity against allotargets. We now report that this marked disparity in disease expression results from a radio-sensitive host mechanism which protects the F1 mouse from parental anti-F1 cytotoxicity in mice undergoing chronic GVH disease. Cellular analysis revealed that protection in chronic GVH disease is mediated by a phenotypically complex system of genetically unrestricted radiosensitive T cells of F1 origin. These cells fail to functionally emerge in mice undergoing acute lethal GVH disease.

• Authors: A B Singh, K Hiehle, M Singh, A E Jetzt, S M O'Connell, R A Mann
• Journal: Cellular immunology (Cell Immunol) Vol. 151 Issue 1 Pg. 24-38 (Oct 01 1993) ISSN: 0008-8749 [Print] Netherlands
• PMID: 8402929 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S.)

Chemical References

• H-2 Antigens

Topics

• Acute Disease
• Animals
• Chronic Disease
• Crosses, Genetic
• Cytotoxicity, Immunologic (physiology)
• Graft vs Host Disease (genetics, immunology)
• H-2 Antigens (immunology)
• Male
• Mice
• Mice, Inbred Strains
• Radiation Tolerance
• Self Tolerance
• T-Lymphocytes (immunology, radiation effects)