מח עצם

אני חולת לופוס האם אני יכולה לתרום מח עצם? כלומר אם אני מתאימה יקחו את הדם שלי למרות שיש לי אנטי באדי?

שלום רב לענ"ד אין לוקחים תרומת מח עצם מחולי מחלות אוטואימוניות. אם כבר, אז יש היום מאמרים ורעיונות אודות טיפול במחלות אוטואימוניות בהשתלת מח עצם . כמובן שזה מאוד ראשוני וכרוכות בזה בעיות רבות (יש סיכון בתהליך ההשתלה ועלותו מאוד גבוהה, אבל הרעיון קיים). ראי למשל את התקציר הבא: Acta Haematol 1998;99(3):116-32 Bone marrow transplantation for autoimmune diseases. Ikehara S First Department of Pathology, Kansai Medical University, Moriguchi City, Japan. Bone marrow transplantation (BMT) is now becoming a powerful strategy for the treatment of patients with autoimmune diseases. Using various animal models for autoimmune diseases, we have previously found that allogeneic BMT (not autologous BMT) can be used to treat autoimmune diseases such as systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), immune thrombocytic purpura, insulin-dependent diabetes mellitus (IDDM), chronic glomerulonephritis, and certain types of non-insulin-dependent diabetes mellitus. In contrast, we have found that the transplantation of T-cell-depleted bone marrow cells or partially purified hemopoietic stem cells (HSCs) from autoimmune-prone mice to normal mice leads to the induction of autoimmune diseases in the recipients. These findings have recently been confirmed even in humans; autoimmune diseases such as RA, SLE, multiple sclerosis, and Crohn's disease were resolved after allogeneic BMT. However, there have recently been reports on the rapid recurrence or persistence of autoimmune diseases after autologous BMT. Conversely, the adoptive transfer of autoimmune diseases such as myasthenia gravis, IDDM and Graves' disease by allogeneic BMT from donors to recipients has been reported. Based on these findings, we have proposed that autoimmune disease is 'a stem cell disorder'. To clarify the differences between normal and abnormal HSCs, we have established a new method for purifying HSCs. Using this method, we purified HSCs from normal and autoimmune-prone mice and compared the former with the latter. We have found that a major histocompatibility complex (MHC) restriction exists between normal HSCs and stromal cells, whereas there is no MHC restriction between abnormal HSCs and stromal cells either in vivo or in vitro; abnormal HSCs proliferate even in allogeneic environments. Abnormal HSCs thus appear to be more resilient than normal HSCs. In humans, BMT across MHC barriers has had a low success rate as a consequence of (1) graft-versus-host disease (GVHD), (2) graft rejection and (3) incomplete recovery of T cell functions. However, we have found that such problems can be overcome in mice. GVHD can be prevented if T-cell-depleted bone marrow cells are used. Graft rejection can be prevented by bone grafts to recruit donor stromal cells, since, as we have found, an MHC restriction exists between HSCs and stromal cells. In addition, we have found that stromal cells migrate from the bone marrow to the thymus, where they become engaged in positive selection. Therefore, the bone grafting to recruit donor stromal cells leads to a complete recovery of T cell functions, since T cells, which are positively selected by donor stromal cells in the thymus, can cooperate with donor B cells and antigen-presenting cells. In humans, it is well known that the success rate of BMT in patients more than 45 years old is low. Recently, we have found that the low success rate is due to the aging of the thymus, and that BMT plus embryonal thymus grafts can be used to treat late-onset autoimmune diseases in MRL/+ mice. Based on these findings, we would like to suggest that the transplantation of the embryonal thymus in conjunction with BMT will become a valuable strategy for treating older patients with various intractable diseases, including autoimmune diseases. We believe that similar conditions (to permit successful allogeneic BMT) to those in mice will be realized in humans in the near future. או התקציר הבא: Oncology (Huntingt) 1997 Jul;11(7):1001-14; 1017, discussion 1018-24 BMT for severe autoimmune diseases: an idea whose time has come. Burt RK Northwestern University Chicago, Illinois, USA. Most patients with autoimmune diseases are thought to have a a normal life expectancy, and thus are treated conservatively. However, these diseases have a diverse clinical course. A small subset of patients have "severe autoimmune diseases," or SADS, which are rapidly progressive and are associated with early mortality. If patients with SADS can be identified before they develop irreversible organ damage, aggressive intervention would be indicated. Consequently, patients with SADS are now being enrolled in experimental protocols of immune ablation and hematopoietic stem-cell rescue (ie, bone marrow transplantation [BMT] at several US institutions. For various reasons, including the high cost of BMT, it will probably be years before the benefits, if any, of this procedure are known.

כפי שכבר כתבתי לך - למיטב ידיעתי אינך מתאימה לתרומת מח עצם אבל..... הדבר נוסה. להלן תקציר של מאמר רלבנטי: Ann Rheum Dis 1996 Sep;55(9):638-41 Transplantation with allogenic bone marrow from a donor with systemic lupus erythematosus (SLE): successful outcome in the recipient and induction of an SLE flare in the donor. Sturfelt G, Lenhoff S, Sallerfors B, Nived O, Truedsson L, Sjoholm AG Department of Rheumatology, Lund University Hospital, Sweden. OBJECTIVE: To investigate the transfer of autoimmunity by allogenic bone marrow transplantation. METHODS: Bone marrow transplantation was performed in a 43 years old man with acute myeloid leukaemia (AML) in remission. The donor was his HLA identical brother who had a mild systemic lupus erythematosus (SLE). Autoantibodies, including antinuclear, anti-C1q, and anticardiolipin antibodies, were measured before and after transplantation. RESULTS: Transient mild graft versus host disease (GvHD) developed in the recipient in the weeks following transplantation. The donor had persistently high concentrations of anti-C1q antibodies to the collagenous region of the complement component C1q. Three months after transplantation the recipient developed antiC1q antibodies that persisted for two months. No other autoantibodies and no SLE-like manifestations appeared. Chronic GVHD started five months posttransplant and responded to intensified immunosuppressive treatment. Three years post-transplant the patient was in unmaintained remission. Within a few weeks after bone marrow donation the donor's disease was exacerbated with development of severe pulmonary alveolitis which required treatment with cyclophosphamide. CONCLUSIONS: When bone marrow transplantation was performed in a patient with AML with bone marrow from an HLA identical brother who had SLE, no evidence of transfer of disease was obtained. However, the recipient temporarily produced anti-C1q antibodies which was a characteristic feature of the donor's SLE and was probably produced by the transplant. The flare of the donor's SLE might be related to the bone marrow tap