Transmission of human T-lymphotrophic virus type I infection to a neonatal infant by transfusion of washed and irradiated red cells

Human T-lymphotropic virus type I and/or II (HTLV-I/II) may be transmitted by the transfusion of blood and blood components. Several factors are critical to the efficiency of transmission. These include the number of contaminating white cells, the component volume, and the age of the component. After look-back notification, there was an investigation of the HTLV-I/II serostatus of three patients who had received blood from a donor now found to be positive for HTLV-I antibodies by enzyme immunoassay and Western blot. The donor red cell unit was group O negative and cytomegalovirus antibody negative; it was washed and irradiated at 2800 cGy and aliquoted into six small-volume transfusions for four neonatal infants. Three of the four patients were available for testing 3.5 years after their exposure. The fourth neonatal infant died on Day 11 of life. The three tested infants received 14, 14, and 44 mL of component, respectively. HTLV-I seroconversion was documented by enzyme immunoassay and Western blot (p19, p24) and occurred only in the patient receiving 44 mL. On the basis of quality control data, it is estimated that the affected infant received 8 × 10(7) white cells in the 44-mL aliquot. Washing and irradiation will not necessarily eliminate HTLV-I transmission.     

FOXP3+ T regulatory cells in lesions of oral lichen planus correlated with disease activity

Objective:  The aim of this study was to determine the correlation between the number of FOXP3⁺ T cell in lesions and the disease activity of patients with oral lichen planus (OLP).
Materials and Methods:  The expression of FOXP3 was investigated using immunohistochemical staining and real-time RT-PCR in 23 OLP lesions and 12 controls. Changes of FOXP3⁺ Treg in peripheral blood from three patients' pre and post-treatment were assessed using flow cytometry.
Results:  Few FOXP3⁺ cells were detected in controls, but an increased number of FOXP3⁺ cells were observed in lesions ( n  = 20, 40.99 ± 24.68 cells per high-power field – hpf). Furthermore, the frequency of FOXP3⁺ Treg in reticular OLP ( n  = 7, 63.6 ± 23.2 cells per hpf) was significantly higher than that in erythematous/erosive OLP ( n  = 13, 28.8 ± 16.8 cells per hpf, P  = 0.001). In addition, negative correlation was found between the number of FOXP3⁺ Treg and disease activity (correlation oefficient = −0.557, P  = 0.013). The proportion of FOXP3⁺ Treg showed remarkable increase in peripheral blood from patients after treatment (1.39 ± 0.71% vs 4.91 ± 1.59%).
Conclusions:  These data indicated that FOXP3⁺ Treg were involved in the pathogenesis of OLP and correlated with disease's subtype and activity.     

Pentoxifylline inhibits integrin-mediated adherence of interleukin-2- activated human peripheral blood lymphocytes to human umbilical vein endothelial cells, matrix components, and cultured tumor cells

Peripheral blood lymphocytes (PBLs) cultured in the presence of recombinant human interleukin-2 (rhIL-2) develop a natural killer (NK) cell phenotype (CD16+, CD56+, CD3-) and are referred to as lymphokine- activated killer cells (LAK). In developing the LAK phenotype, enhanced adherence to matrix components and endothelial cells have been described. In this report we investigated the functional behavior of adhesion receptors in rhIL-2-activated PBLs by in vitro adhesion assay and by flow cytometry. Compared to PBLs, IL-2-activated PBLs had increased integrin-mediated adherence to: (1) fibronectin (FN), (2) human umbilical vein endothelial (HUVE) cells, and (3) cultured melanoma and pancreatic tumor cell lines. This increase in adherence was mediated by increased surface expression of members of the beta 1 and beta 2 integrin subfamilies, as determined by flow cytometric analysis. No induction of an activation-dependent beta 1 (CD29) epitope was detected. We also investigated the effects of the methylxanthine derivative pentoxifylline (PTX) on PBLs and rhIL-2-activated PBL adhesion. PBLs co-cultivated in the presence of rhIL-2 (1,000 U/mL) and PTX exhibited reduced adherence to FN, HUVE and cultured tumor cell lines. This inhibition by PTX was concentration- and time-dependent. The increased expression of integrins induced by rhIL-2 was only in part inhibited by PTX, suggesting that PTX induced a subpopulation of integrins that are expressed but functionally inactive.     

Neuroendocrine carcinomas of the lung: clinical, radiologic, and pathologic correlation

Neuroendocrine carcinomas of the lung are characterized by differentiation toward Kulchitsky cells and are classified as Kulchitsky-cell carcinoma (KCC) I (classic carcinoid), KCC II (atypical carcinoid), and KCC III (small-cell carcinoma). The clinical, computed tomographic (CT), and pathologic findings in 31 patients with KCC were reviewed. KCC I lesions generally occurred in younger (56 years +/- 18) nonsmoking women, were small (1.8 cm +/- 0.7 in diameter on CT scans), and were associated with lymphadenopathy in one of ten patients. KCC II tumors were found predominantly in older (66 years +/- 12) smoking men and were larger (3.9 cm +/- 1.3 in diameter, P less than .001); four of ten patients had CT evidence of lymphadenopathy. KCC III tumors occurred in older (66 years +/- 8) smoking men and were large (4.2 cm +/- 1.0); 11 of 11 patients had massive lymphadenopathy. Clinical, radiologic, or pathologic overlap was noted in three patients. Sputum cytologic and fine-needle and bronchoscopic biopsy findings were often nondiagnostic or misleading, particularly for KCC II lesions. CT of the chest provides additional discriminating information in the preoperative diagnosis of neuroendocrine lung carcinomas.