Search PubMed⌕ Search

Biomedical subjects

D Benjamin

Publications and source records attributed to D Benjamin.

At least 55 records · Page 3Linked to original sources
PubMed1996

Monocyte chemoattractant protein-1 mRNA expression in hemangiomas and vascular malformations.

Hemangiomas are vascular tumors that appear at or shortly after birth and undergo a rapid growth before involuting. During the proliferative phase, hemangiomas are infiltrated by macrophages, cells that are capable of initiating angiogenesis. Vascular malformations grow slowly, commensurate with the child, and do not regress or become infiltrated by macrophages. We demonstrate by in situ hybridization increased monocyte chemoattractant protein-1 (MCP-1) mRNA expression during hemangioma and vascular malformation growth. We found markedly upregulated expression of MCP-1 mRNA in all proliferative hemangioma specimens, expressed by alpha-actin perivascular smooth muscle cells and interstitial HAM 56+ macrophages. In contrast, 9 of 10 clinically involuting hemangiomas displayed no expression of MCP-1 mRNA. We found no expression of MCP-1 mRNA in vascular malformations, which correlates with the minimal monocytic infiltration of these lesions. We also showed that dexamethasone and interferon-alpha downregulate MCP-1 mRNA in cultured human vascular smooth muscle cells. Glucocorticoids can be efficacious in 30-50% of cases when given in the proliferative phase of hemangioma growth, but have no beneficial effect on vascular malformations. Interferon-alpha has been used to dramatically induce regression of steroid-refractory hemangiomas. Both of these agents' beneficial action on proliferative hemangiomas may, in part, result from reduced MCP-1 production and reduced influx of angiogenic macrophages.

Blood Vessels↗
PubMed1996

IL-12 expression in AIDS-related lymphoma B cell lines.

IL-12 is a 70-kDa heterodimer formed by the 40-kDa heavy chain (p40) and the 35-kDa light chain (p35). Twenty-five Burkitt's lymphoma cell lines (CL) and seven normal lymphoblastoid B CL were studied. The Burkitt's CL included AIDS-associated B CL (AABCL) (7 EBV+/2 EBV-) and non-AABCL (8 EBV+/8 EBV-). Reverse transcription-PCR detected p40 in EBV+ AABCL (7 of 7), EBV+ non-AABCL (3 of 8), and normal lymphoblastoid B CL (6 of 6) but not in EBV- CL (0 of 10). p35 mRNA was detected in 30 of 30 CL. Constitutive secretion of p40 was found in 7 of 7 EBV+ AABCL (range, 341-18,086 pg/ml) and p70 in 3 of 7 EBV+ AABCL (range, 25-197 pg/ml), but in only 1 of 8 EBV+ non-AABCL and 0 of 7 normal lymphoblastoid CL. PMA stimulated p40 secretion in 7 of 7 EBV+ AABCL and p70 secretion in 5 of 7 EBV+ AABCL. PMA also triggered p40 and p70 secretion in 2 EBV+ non-AABCL and in 3 of 7 normal lymphoblastoid CL. No IL-12 secretion was detected in 10 EBV- CL, including EBV- AABCL. The CL produced IL-10, a known inhibitor of IL-12, but anti-IL-10 Abs did not neutralize IL-12. Similarly, neutralizing anti-IFN gamma Abs or IFN gamma did not affect B cell IL-12. For IL-12R studies, reverse transcription-PCR and 125I-IL-12 binding assays were performed. Although all CL tested showed mRNA accumulation for one of the IL-12R components, IL-12 binding sites were detected in only 1 of 30 CL. Our data suggest that: 1) AABCL constitutively secrete large amounts of IL-12, contrasting with low IL-12 production by HIV-1 infected PBMC; 2) lack of IL-12 expression in EBV- AABCL suggests that in vivo exposure of B cells to HIV-1 only does not induce IL-12 secretion and that both HIV-1 and EBV are required; 3) the autocrine-negative effect of IL-10 on IL-12 in monocytes and the enhancing effect of IFN gamma on IL-12 secretion do not apply to B cells derived from AIDS patients.

Acquired Immunodeficiency Syndrome↗