PubMed · 8409867
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J Dunlay. 1993. Bronchitis.. https://pubmed.ncbi.nlm.nih.gov/8409867/
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Autoimmune diabetes is caused by the CD4(+), T helper 1 (Th1) cell-mediated apoptosis of insulin-producing beta cells. We have previously shown that Th2 T cells bearing the same T cell receptor (TCR) as the diabetogenic Th1 T cells invade islets in neonatal nonobese diabetic (NOD) mice but fail to cause disease. Moreover, when mixed in excess and cotransferred with Th1 T cells, Th2 T cells could not protect NOD neonates from Th1-mediated diabetes. We have now found, to our great surprise, the same Th2 T cells that produced a harmless insulitis in neonatal NOD mice produced intense and generalized pancreatitis and insulitis associated with islet cell necrosis, abscess formation, and subsequent diabetes when transferred into immunocompromised NOD.scid mice. These lesions resembled allergic inflamation and contained a large eosinophilic infiltrate. Moreover, the Th2-mediated destruction of islet cells was mediated by local interleukin-10 (IL-10) production but not by IL-4. These findings indicate that under certain conditions Th2 T cells may not produce a benign or protective insulitis but rather acute pathology and disease. Additionally, these results lead us to question the feasibility of Th2-based therapy in type I diabetes, especially in immunosuppressed recipients of islet cell transplants.
Granulocytic sarcomas are localized deposits of myeloid leukemia cells that may precede or occur concurrently with disseminated disease. In either event, the origins of the cells comprising the malignancy are the same. Published reports of granulocytic sarcomas have described, in the majority of cases, a morphology typical of AML-M2 and the presence of the t(8;21)(q22;q21) typical of that FAB type. In a smaller number of cases, the inv(16)(p13q22) characteristic of AML-M4 has been recorded in cells with a myelomonocytic appearance. We report two patients with granulocytic sarcomas showing monocytic morphology in which the malignant cells showed t(9;11)(p22;q23) typical of AML-M5. This abnormality is seen in up to 7% of childhood AML, but has not previously been reported in granulocytic sarcoma. The detection of this cytogenetic abnormality facilitated the precise characterization of the malignant cells and selection of the most appropriate therapy, emphasizing the value of cytogenetic analysis in cases of granulocytic sarcoma.
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