Unravelling the Genetic Basis of Susceptibility to Mycobacterial Infection

Levin, Michael; Newport, Melanie J.

doi:10.1002/(sici)1096-9896(199701)181:1<5::aid-path731>3.0.co;2-x

Cited by 6 publications

(1 citation statement)

References 19 publications

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“…gamma interferon, from T-lymphocytes is essential for the activation of cytolytic activity by the macrophages after phagocytosis (2)(3)(4)(5)(6)(7)(8)(9). Genetic factors also play a role in the type of lyinphocytic response to M. ^e;^a^ organisms (10)(11)(12)(13).…”

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Multibacillary leprosy: lesions with macrophages positive for S100 protein and dendritic cells positive for Factor 13a

1998

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In the defense against Mycobacterium leprae, macrophages play an essential part in the mechanism of bacterial lysis but require the presence of cytokines such as interleukin 2 and gamma interferon from lymphocytes in order to effectively kill the organisms in any number. While there have been many studies of the lymphocytes in lesions of leprosy, less attention has been given to the immunohistochemical characterization of the macrophage populations. In this study, the cutaneous lesions of 69 patients with leprosy (42 lepromatous, 5 mid-borderline, and 22 tuberculoid) were evaluated by immunohistochemistry for the expression of S100 protein, CD1a, CD68, muramidase, HLA-DR, and Factor 13a. The macrophages from lesions of polar, subpolar, and borderline lepromatous leprosy patients expressed S100 protein intensely and constantly. In contrast, the lesions of polar and subpolar tuberculoid leprosy had very few cells that were immunoreactive for S100 protein ('S100+') in the granulomas in the dermis. The macrophages in all lesions were reactive for CD68 and muramidase. In paraffin sections, macrophages of lepromatous lesions failed to stain for HLA-DR, whereas in tuberculoid lesions, they were strongly positive for HLA-DR. Three patients with histoid leprosy (relapse lesions) had lesions that were strongly positive for Factor 13a and were negative for S100 protein ('S100-'). Given the possible chemotactic and migration inhibition effects of the calcium-binding proteins of the S100 family, these data suggest a possibly important role for S100 protein in the accumulation of macrophages in lepromatous leprosy, and also reveal infection of Factor 13a + dermal dendritic cells in histoid leprosy.

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Multibacillary leprosy: lesions with macrophages positive for S100 protein and dendritic cells positive for Factor 13a

1998

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Invasive lobular and invasive ductal carcinoma of the breast show distinct patterns of vascular endothelial growth factor expression and angiogenesis

et al. 1998

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Angiogenesis is essential for tumour growth and important in tumour metastasis and prognosis. Vascular endothelial growth factor (VEGF) stimulates endothelial proliferation in vitro and angiogenesis in vivo. VEGF expression has been correlated with high vascularity in tumours, including carcinoma of the breast. This study investigated VEGF expression and vascularity of invasive lobular (n=10) and invasive ductal carcinoma (n=28), and pure ductal carcinoma in situ of the breast (n=33). VEGF protein expression was studied with immunohistochemistry and VEGF mRNA with in situ hybridization. Vascular density was assessed on sections stained for von Willebrand factor. There was more expression of both VEGF protein (P=0·006) and mRNA (P=0·002) in invasive ductal than in invasive lobular carcinoma. VEGF protein (rs=0·32, P=0·047) and mRNA (rs=0·56, P=0·04) correlated with vascular density in invasive ductal carcinoma. In invasive lobular carcinoma, vascular density did not correlate with VEGF mRNA (rs=0·15, P=0·35) and was inversely related to VEGF protein (rs=−0·57, P=0·04). There were no significant differences in vascular density between the two types of invasive carcinoma, suggesting that VEGF is important in angiogenesis in invasive ductal carcinoma, but that other angiogenic factors are important in invasive lobular carcinoma. Although VEGF protein was frequently expressed in ductal carcinoma in situ, no relationship was found between VEGF and the two patterns of angiogenesis previously described. © 1998 John Wiley & Sons, Ltd.

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