HISTOPATHOLOGIC SEQUENCE OF EVENTS IN ADULT MICE UNDERGOING LETHAL GRAFT VERSUS HOST REACTION DEVELOPED ACROSS H-2 AND-OR NON-H-2 HISTOCOMPATIBILITY BARRIERS

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  • 1 January 1979
    • journal article
    • research article
    • Vol. 96  (1) , 121-142
Abstract
The sequence of histologic events in graft-vs-host reaction (GVHR) caused by major and/or minor histoincompatibilities was studied. GVHR may manifest itself in the form of 2 distinct multiphasic disease entities, depending on whether the donor cells are incompatible with the host for major and minor histocompatibility antigens (major GVHR) or for minor histocompatibility antigens alone (minor GVHR). The acute or major GVHR has 4 phases: a transient phase of aplasia; a repopulation phase; a proliferative phase involving lymphoid, presumably immunocompetent, cells; and a phase of acute organ rejection (terminal). The chronic or minor GVHR is characterized by 6 phases: a transient phase of aplasia; a repopulation phase; a phase of proliferation and tissue infiltration by lymphoid, presumably immunocompetent cells; a phase of major immunologic injuries; a phase of repair; and a terminal phase with advanced sclerosis and proliferative glomerulonephritis. In acute or major GVHR the disease was manifested by the tissue reactions characteristic of acute organ rejection. Lesions were seen in the kidney, liver, bone marrow, lymph nodes, spleen, thymus, intestine and skin. In the chronic or minor GVHR, tissue injuries were more widespread, affecting the collagen, vessel walls, adipose tissue, renal glomeruli, heart muscle, fascias of skeletal muscles, lymph nodes, spleen, thymus, bone marrow, intestine, skin, esophageal mucosa and urinary tract. A pronounced plasma cell proliferation was a striking feature in the minor GVHR. Its evolution coincided with advanced thymic epithelial atrophy. The destruction of thymic epithelium apparently resulted in depletion of suppressor T [thymus-derived] cells and, consequently, in an unopposed proliferation of plasma cells.