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The Immune Response to Chronic Myeloid Leukaemia (pp. 27-59) $25.00
Authors:  Clark, Richard E. (Royal Liverpool University Hospital, Liverpool)
Chronic myeloid leukaemia (CML) is an uncommon disease, characterised by the Philadelphia chromosome. This reciprocal translocation juxtaposes the ABL gene on chromosome 9q34 to the BCR gene on chromosome 22q11, resulting in the fusion gene BCRABL. The p210 gene product of BCR-ABL has enhanced tyrosine kinase activity, and is central to the pathogenesis of CML. It is also a novel antigen that is unique to leukaemic cells. Peptides derived from the BCR-ABL fusion junction may therefore be immunogenic, if appropriately presented to the immune system. The present article reviews the information that has accrued over the last decade on the immune response to CML. Some BCR-ABL junctional peptides have been shown to bind to Human Leukocyte Antigen (HLA) molecules, and these peptides will elicit specific T-lymphocyte responses in vitro, in both normal subjects and in CML patients. Circulating cytotoxic T lymphocytes (CTL) directed against BCR-ABL have been demonstrated in CML patients. Intriguingly, circulating BCR-ABL specific CTL have also been demonstrated in a proportion of normal subjects. This finding is consistent with the view that BCR-ABL rearrangement may be considerably more common than the prevalence of CML, suggesting that an host anti-BCR-ABL response may be important in preventing clinical CML. Mass spectroscopy has shown that CML cells express peptides from the BCR-ABL junction on the cell surface in association with HLA Class I molecules, at least for certain HLA types. Proteinase 3 and the Wilms tumour gene WT1 are also overexpressed in CML, and these are therefore leukaemia-associated antigens. Peptides from these proteins have been shown to elicit T cell responses in CML. Allogeneic stem cell transplantation may be curative in CML, and infusions of donor lymphocytes may restore durable molecular remissions for the minority of post-allograft relapses. The molecular targets that may confer remission after allografting may include donor responses against host minor histocompatibility antigens. Based on these collective observations, several immunotherapeutic strategies are currently in clinical trial. Although it is too early to know the place of immunotherapy in the management of CML, early data are at least encouraging. The role of immunotherapy might be facilitated by the advent of the 2- phenylaminopyrimidine imatinib mesylate (trade names Glivec or Gleevec), which targets the kinase domain in ABL and BCR-ABL, and which has been shown to be remarkably effective in a variety of settings of CML. 

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The Immune Response to Chronic Myeloid Leukaemia (pp. 27-59)