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The idiopathic inflammatory myopathies (IIM) are a heterogeneous group of neuromuscular disorders subdivided into polymyositis (PM), sporadic inclusion body myositis (sIBM) and dermatomyositis (DM). Chemokines play an essential role in sustained inflammation associated with IIM. We studied the distribution of the alpha-chemokine receptors CXCR1, 2, 3 and their ligands interferon-gamma (IFN-gamma)-inducible T cell alpha chemoattractant (I-TAC), IFN-gamma-inducible protein of 10 kDa (IP-10), monokine induced by IFN-gamma (MIG) and growth-related oncogene (GRO) in IIM using immunohistochemistry, immunofluorescence and Western blotting. Abundant expression of IP-10 was observed on macrophages and T cells surrounding and invading non-necrotic muscle fibers in PM and sIBM and in T cells in perimysial infiltrates of DM. IP-10 was also localized to blood vessel endothelial cells in all inflammatory and normal muscle tissues. The distribution of other alpha-chemokines was variable: Only low levels of MIG and I-TAC were detected; GRO was localized to the endomysial infiltrates of some PM and sIBM samples, but not in DM. Muscle tissues were invariably CXCR1 negative, while a subset of inflammatory cells in all IIM were CXCR2 positive. Strong CXCR3 expression was observed on the majority of T cells in each IIM. We describe the differential repertoire of alpha-chemokines in IIM, and offer additional proof of the predominance of Th1-driven reactions in the immunopathogenesis of all three diagnostic subgroups. We suggest the Th1-mediated immunity in general, and the CXCR3/IP-10 interaction in particular, as potential targets for novel therapeutic intervention in IIM.

After kidney transplantation, thrombotic microangiopathy (TMA) can occur de novo or as recurrent disease. Risk factors for de novo posttransplant TMA include ischemia-reperfusion injury, immunosuppressive drugs, viral infections, acute humoral rejection, and complement gene abnormalities. Cytomegalovirus infection as a trigger for posttransplant TMA in kidney transplant recipients has only been reported in 7 cases, all of them between 4 weeks and 8 years after transplantation. We describe a new case of de novo TMA in association with cytomegalovirus infection 25 years after kidney transplantation.

A 67-year-old female presents with a small mass in the anterior mediastinum on chest computed tomography. A biopsy proves the mass to be a spindle-cell-type or type A thymoma. Subsequently the patient develops fever and severe Coombs-positive haemolytic anaemia. She is initially treated with oral corticosteroids. Because of persistence of the haemolysis subsequent thymectomy is performed. Haemolysis disappears almost instantly and does not return after discontinuation of the oral corticosteroids. Review of the literature reveals only 17 other cases of thymoma-associated autoimmune haemolytic anaemia.

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