acid-phosphatase and Graft-vs-Host-Disease

Interstitial pneumonia (IP) is a frequent and serious complication of bone marrow transplantation with a median time of onset about 2 months posttransplant. Most cases result either from toxicity of radiation and chemotherapy or from infection with pathogens such as cytomegalovirus. Described are two patients with chronic graft-versus-host disease (GVHD) who presented with late-onset IP 242 and 632 days posttransplant. Histologic examination of lung biopsy specimens disclosed a lymphoid interstitial pneumonia (LIP) in both cases. The major lymphocyte subset found in bronchoalveolar lavages and lung tissue was OKT8(+) and showed a positive dot staining for acid phosphatase. Contrary to peripheral blood mononuclear cells, most OKT8(+) lymphocytes in the lungs were OKT3(-). Since acute GVHD lesions are mediated mainly by cytotoxic T-lymphocytes, our data suggest that LIP in marrow-grafted patients may be a manifestation of chronic GVHD. It should be distinguished from the more common types of IP encountered following bone marrow transplantation.

Topics: Acid Phosphatase; Adolescent; Adult; Biopsy; Bone Marrow Transplantation; Graft vs Host Disease; Humans; Lung; Male; Pulmonary Fibrosis; Respiratory Function Tests; T-Lymphocytes

The effect of systemic immunologic stimulation on renal expression of the H-2K (class I) and Ia (class II) antigens of the mouse major histocompatibility complex was explored. We previously reported that graft-vs-host (GvH) disease in mice caused an increase in host renal Ia expression. In the present experiments, we demonstrated that Kk antigen expression also increased during GvH. Other immune stimuli (allogeneic tumor grafts or injections of allogeneic spleen cells) caused increased renal Ia (and, where studied, Kk) expression in the epithelium of some renal tubules, as demonstrated by indirect immunofluorescence (IIF) or immunoperoxidase (IIP) staining. The normal interstitial Ia staining was frequently diminished in the kidneys of mice given these stimuli. At least in the case of allogeneic tumor grafts, the changes in renal Ia and H-2K were dependent on host T cells, in that no similar change appeared in nude (nu/nu) mice bearing allogeneic tumor grafts. By histochemical techniques, most of the change was in proximal tubules. In semiquantitative absorption, the total renal Ia was usually increased (two- to 20-fold) in parallel with the IIF or IIP changes. Serial studies revealed that MHC product induction was frequently transient and was not associated with detectable histologic abnormalities. In cultured renal cells, increased Iak and Kk could be demonstrated by IIF after 4 days of culture in supernatants of lymphocytes stimulated with concanavalin A: the activity in these supernatants was probably not interleukin 2, but might have been IFN-gamma, because IFN-gamma also induced this change. We conclude that systemic immunologic stimuli alter MHC product expression in renal tubule epithelium and that this effect can be stimulated in vitro by supernatants of stimulated lymphocytes.

Topics: Acid Phosphatase; Animals; Carcinoma, Ehrlich Tumor; Cells, Cultured; Female; Fluorescent Antibody Technique; Graft vs Host Disease; H-2 Antigens; Histocompatibility Antigens Class II; Immunization; Immunoenzyme Techniques; Kidney; Lymphocyte Transfusion; Mice; Mice, Inbred A; Mice, Inbred BALB C; Mice, Inbred C3H; Mice, Inbred C57BL; Mice, Inbred DBA; Mice, Nude; Neoplasm Transplantation