Plasticity of innervation of the medulla of axillary lymph nodes in the rat after antigenic stimulation

The purpose of this investigation was to test the hypothesis that activation of the immune system in rats will lead to changes in the density of innervation in lymph nodes. In order to reduce the variability between animals, the rats were reared under sterile conditions and immunostimulation was effected by subcutaneous application of bovine albumin in a region draining to the axillary lymph nodes of both sides. Control animals received an equivalent application of sterile physiological saline. The animals were sacrificed 10 days and 27 days and 4 months after immunostimulation. The nerves in the axillary lymph nodes were quantified by light microscopy in silver impregnated sections and at the ultrastructural level on ultrathin sections. The survival times were chosen so that the first group was in the ascending phase of antibody production, the second group at the peak, and the third group in the declining phase. Both at the light and ultrastructural levels, there were statistically significant differences in the density of innervation of medulla between the groups, with a particularly pronounced increase in the group 4 months after immunostimulation. At the ultrastructural level, there was also an increase in the density of incompletely ensheathed axonal profiles in the parenchyma of the medulla, while the nerves associated with blood vessels were not increased. We conclude that immunostimulation leads to morphological changes in the innervation of the medulla of axillary lymph nodes, that are consistent with the concept of functional activation of the autonomic nervous system through the immune system. © 1994 Wiley-Liss, Inc.     

Engulfment of mast cell secretory granules on skin inflammation boosts dendritic cell migration and priming efficiency

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Ras homolog gene family H (RhoH) deficiency induces psoriasis-like chronic dermatitis by promoting TH17 cell polarization

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Granulocytic sarcoma presenting with lymph node infarction at disease onset

A completely infarcted lymph node is an unusual event. However, lymph node infarction should alert the pathologist to the considerable likelihood of malignant lymphoma. We report two unusual cases of acute myeloid leukemia presenting with granulocytic sarcoma at disease onset with a lymph node lesion exhibiting extensive lymph node infarction. The infarcted tissue contained numerous eosinophilic cell ghosts. There were some islands of degenerated, pyknotic medium-sized nuclei resembling lymphoblasts present in the necrotic area. By immunohistochemistry, these medium sized cells were CD3-, CD20-, CD34+, CD43+, CD45RO-, CD68-, CD79a- and myeloperoxidase+ in both cases. Differentiation of granulocytic sarcoma from malignant lymphomas is important for adequate therapy. The present cases indicate that granulocytic sarcoma should be added to the list of differential diagnoses for lymph node infarction.     

Anti-high endothelial venule monoclonal antibody HECA-452 recognizes plasmacytoid T cells and delineates an ”extranodular“ compartment in the reactive lymph node

So-called plasmacytoid T cells represent a subset of monocyte related cells, which share with endothelium the CD36⁺CD11b⁻ (OKM5⁺OKM1⁻) phenotype. The reactivity of plasmacytoid T cells with rat monoclonal antibody HECA-452, highly specific for high endothelial venules, was analyzed in reactive lymph nodes. In all cases, HECA-452 not only labelled the endothelium of high endothelial venules, but also strongly reacted with singular and clustered plasmacytoid T cells. The HECA-452 positivity for high endothelial venules and plasmacytoid T cells visualized a lymph node compartment extending from the subcapsular sinus to the corticomedullary junction. This compartment surrounded the composite nodule and was designated the ”extranodular“ compartment. The cooccurrence of plasmacytoid T cells and high endothelial venules in this extranodular compartment, together with their immunophenotypical similarities, may be indicative of functional co-operations.     

大鼠肠系膜淋巴结高内皮微静脉与淋巴迷路之间的网状纤维支架的研究

目的 研究大鼠肠系膜淋巴结内高内皮微静脉与淋巴迷路之间淋巴细胞归巢的通路.方法 用镀银染色光镜观察法和冻裂割断扫描电镜观察法观察健康、成熟Wistar大鼠肠系膜淋巴结的基质网状结构.结果 位于高内皮微静脉和淋巴迷路周围有网状纤维支架,在二者相临近部位有密集交织的网状纤维网.结论 淋巴结内高内皮微静脉和淋巴迷路之间密集交织的网状纤维网,为细胞的居留和迁移提供结构支持和适宜的微环境,可能是淋巴细胞归巢的重要通路.     

舌鳞癌术后颈部区域淋巴结的分析研究

目的：分析舌鳞癌颈淋巴结转移的发生规律，探讨舌癌特别是 cNo(临床不怀疑转移)患者的治疗原则。 方法： 通过对1985-2003年199例舌癌患者进行舌颌颈联合根治术的临床病理资料进行回顾性研究。 结果： 舌鳞癌的总体转移率为42.14%,cNo患者的颈淋巴结隐匿性转移率为26.83%,舌鳞癌的隐匿性转移与肿瘤ＴNM分期等密切相关。 结论： 临床上应根据原发灶的大小等综合考虑分析,选择合理的治疗方案。     

Lymphokine-activated killer cell function of peripheral blood mononuclear cells, spleen cells and regional lymph node cells in gastric cancer patients.

Lymphokine-activated killer (LAK) cells generated by culture of peripheral blood mononuclear cells (PBMC), spleen cells (SPC) and regional lymph node cells (LNC) with IL-2 for 4 days were examined for their functional capabilities in 29 patients with gastric carcinoma. The cytotoxic activity of LAK cells induced from LNC was significantly lower than that from either PBMC or SPC, although there was no difference between PBMC or SPC. The induction of mRNA of interferon-gamma (IFN-gamma) or tumour necrosis factor-alpha (TNF-alpha) and the production of these cytokines in the non-adherent LAK cells from LNC were also significantly reduced compared with those from PBMC or SPC. Further, the LAK cells from LNC secreted significantly lower levels of these cytokines when stimulated with tumour target, Raji cells, although the production of these cytokines was markedly increased by stimulation with the targets in all three cell populations. Phenotypic analysis of each cell population revealed a decreased proportion of the cells mediating natural killer (NK) activity, including CD16+, CD56+, and CD57+ cells in LNC either before or after culture, although OKIa1+ and CD25+ cells were uniformly increased in all cell populations after culture. Changes in subpopulations of CD4+ and CD8+ cells in LNC were not apparently different from PBMC or SPC. These results indicated the differential reactivity of each lymphocyte population to IL-2 and the reduced LAK cell function of LNC compared with PBMC or SPC in patients with gastric carcinoma.     

The developmentally regulated neural crest-associated glycotope HNK-1 predicts metastasis in cutaneous malignant melanoma

Aberrant glycosylation is a common feature of metastatic sub-clones of malignant tumours and in uveal melanoma in particular, the HNK-1 glycotope has been positively correlated with poor prognosis. So far, no such correlation has been investigated in cutaneous melanoma. In order to do so, HNK-1 expression was evaluated immunohistochemically in 100 primary cutaneous melanomas and correlated with metastasis after up to 10-years' follow-up. Furthermore, HNK-1 expression was analysed in metastatic deposits (19 distant cutaneous metastases and six sentinel lymph node metastases), as well as in benign nevi. Kaplan-Meier analysis revealed a positive association between HNK-1 expression and metastasis (p < 0.005) and multivariate Cox regression analysis adjusted for the standard prognostic markers ulceration and vertical tumour thickness confirmed HNK-1 expression as an independent prognostic marker. HNK-1 expression was preserved in 42% of the distant cutaneous metastases, but metastatic cells in lymph nodes were devoid of HNK-1 immunoreactivity. None of the benign pigmented lesions exhibited HNK-1 immunoreactivity. Expression of the HNK-1 glycotope in cutaneous malignant melanoma is an independent prognostic marker of metastasis. Differential HNK-1 expression at the metastatic sites implies that its expression is modulated by the surrounding environment. As HNK-1 is also transiently expressed during migration of melanocyte precursor cells derived from the neural crest, recapitulation of this transient expression might occur during metastatic spread of cutaneous malignant melanoma.     

Patterns of major histocompatibility complex class II expression by T cell subsets in different immunological compartments. 2. Altered expression and cell function following activation in vivo

This study characterizes antigen-induced phenotypic and functional aspects of major histocompatibility complex (MHC) class II expression on recirculating T cells in efferent lymph. In vivo secondary, but not primary challenge is associated with both kinetic and phenotypic alterations in class II expression by T cells. All three major T cell subsets, CD4⁺, CD8⁺ and T19⁺ (γδ T cell receptor), show an approximate four fold increase in the level of MHC class II expression during secondary responses. No changes in B cell expression of class II were seen. Resting efferent lymph T cells are predominantly either class II^? or DR⁺DQ^? but this changes to DR⁺DQ⁺ after antigenic challenge. The antigen-presenting function of these class II⁺ T cells was investigated at daily intervals after in vivo antigenic challenge. T cells from non-activated lymph nodes could not induce proliferation of antigen-specific T cells with soluble antigen but were weakly stimulatory in allo-mixed lymphocyte reaction (MLR) at high (> 2:1) stimulator cell ratios. Activated T cells isolated during secondary in vivo responses, and expressing increased quantities of MHC class II, were positive stimulator cells in the MLR. In contrast these cells could not present soluble antigen or trypsin-digested antigen to the T cell lines. In the MLR assays, the relative stimulation by class II⁺ T cells correlates with the levels of class II expression. We conclude from these experiments that both quantitative and qualitative changes in MHC class II, induced on T cells under physiological conditions, play a role in the regulation of the immune response in vivo but that that role is not simply one of presentation of soluble antigen.