Autoimmune diseases and autoimmunity post-bone marrow transplantation

Abstract

BMT can both transmit and eliminate autoimmune diseases, and hence it has been suggested as an optional treatment for severe autoimmune conditions. In this communication we deal with the question of whether chronic GVHD is an autoimmune disease in itself, review the literature reports of autoimmune diseases following BMT in humans, and describe the autoimmune nature of the post-BMT state. Chronic GVHD, which is a frequent complication post-BMT, has clinical and pathogenic characteristics similar to autoimmune diseases, such as scleroderma and Sjogren's syndrome. Although the pathogenesis of chronic GVHD is not yet clear, thymic damage induced by acute GVHD may contribute to both the immunodeficiency and autoimmunity characterising chronic GVHD. A similar phenomenon is syngeneic GVHD, which results from an imbalance between autoreactive and autoregulatory lymphocytes. Additionally, other autoimmune diseases have been reported in post-BMT patients, and among these the most common are hypothyroidism, hyperthyroidism, myasthenia gravis and immune cytopenias. Although these diseases also occur also outside the post-BMT setting, they are unique with respect to pathogenesis (no association between myasthenia gravis and thymic pathology), diagnosis (symptoms of hyperthyroidism may be inadvertently related to other conditions), and prognosis (post-BMT autoimmune cytopenias may be fatal and treatment non-responsive). Nevertheless, many other autoimmune diseases have been reported after BMT, and these are mainly presented as case reports. Regarding the mechanism of post-BMT autoimmunity, the minority of cases stem from donor-related transfer of pathogenic lymphocytes or their progenitors, while most of the cases (either chronic GVHD or specific diseases) can be attributed to the immunologic imbalances characterising the post-BMT setting. The factors that may expose an individual to autoimmunity development post-BMT include genetic predisposition, an environmental factor such as CMV, and the nature of the donor who may aid in creating microchimerism and subsequently chronic GVHD and its related autoimmune manifestations.

Resolution of psoriasis following allogeneic bone marrow transplantation for chronic myelogenous leukemia: Case report and review of the literature

“…The cutaneous lesions of psoriasis are characterized by a hyperproliferation of keratinocytes in the epidermis, and it has been suggested that activated T cells play an important role in the disease's pathogenesis. In allogeneic bone marrow transplantation (BMT), the immune system of the host is effectively eliminated by a pre-conditioning regimen, and immunity after BMT is mostly of donor origin [3]. Therefore, it has been suspected that the course of autoimmune disease can be modified by allogeneic BMT.…”

Pure red cell aplasia with the onset of graft versus host disease

“…1 Post transplant, PRCA is usually a complication of major ABO incompatibility and may have an increased incidence after nonmyeloablative compared with myeloablative conditioning regimens. 2 While autoimmune haematological disorders including haemolytic anaemia and immune neutropenia, thrombocytopenia and pancytopenia due to peripheral destruction are well recognised post allograft, 3 often in the context of chronic graft versus host disease (GVHD), 4 to our knowledge PRCA as an immune complication in the absence of ABO incompatibility has not been reported. This case documents PRCA after an ABO-compatible nonmyeloablative allograft in the absence of any secondary causes.…”

Resolution of atopic dermatitis following allogeneic bone marrow transplantation for chronic myelogenous leukemia

“…Thus, it is likely that the course of autoimmune disorders can be modified by allogeneic BMT. 7 Atopic dermatitis is thought to be an autoimmune or allergic disease, as indicated by increasing evidence for the role of a cellular immune reaction in the pathogenesis. 1,2 In the present case, the immunosuppressive treatment used to prevent GVHD may have also influenced the clinical course of the atopic dermatitis.…”