We studied the Ca(2+)-capture ability of follicular dendritic cells (FDCs) in tonsillar secondary lymphoid follicles (LFs) and the expression of six Ca(2+)-binding proteins (CBPs), caldesmon, S-100 protein, calcineurin, calbindin-D, calmodulin, and annexin VI in LFs of various lymphoid tissues and caldesmon and S-100 protein in neoplastic follicles of follicular lymphomas. First, Ca(2+)-capture cytochemistry revealed extensive Ca(2+) capture in the nuclei and cytoplasm of FDCs, but little or none in follicular lymphocytes. All six CBPs were localized immunohistochemically in the LFs and were always present in the basal light zone. Immunoelectron microscopic staining of FDCs was classified into two patterns: caldesmon was distributed in the peripheral cytoplasm like a belt; S-100 protein, calcineurin, calbindin-D, and calmodulin were distributed diffusely in the cytosol. Annexin VI was, however, negative on FDCs. Immunocytochemistry also demonstrated CBP-positive FDCs within FDC-associated clusters isolated from germinal centers. In situ hybridization revealed diffuse calmodulin mRNA expression throughout the secondary LFs. These data indicate that the CBPs examined may regulate Ca(2+) in the different subcellular sites of FDCs, and the roles of CBPs may be heterogeneous. We also investigated the distribution of caldesmon and S-100 protein in follicular lymphomas on paraffin-embedded tissue sections. FDCs within grades I and II neoplastic follicles clearly expressed caldesmon, but not S-100 protein, except a part of grade II neoplastic follicles. FDCs within grade III follicles showed no caldesmon, but frequently expressed S-100 protein. These results demonstrate that the caldesmon and S-100 protein staining patterns of grade I follicular lymphomas are different from those of grade III follicular lymphomas and suggest that FDC networks in grade I neoplastic follicles may be similar to those in the light zone within non-neoplastic follicles, FDC networks in grade III neoplastic follicles may be similar to those in dark and basal light zones within non-neoplastic follicles, and grade II follicles may be intermediate between grade I and grade III follicles.
JC EH lin xp ematopathol Original article INTRODUCTIONBlastic plasmacytoid dendritic cell neoplasm (BPDCN) is a relatively rare hematological malignancy, 1 accounting for 0.44% of all hematological malignancies and 0.7% of all cutaneous lymphomas.2 BPDCN is a clinically aggressive tumor derived from the precursors of plasmacytoid dendritic cells (pDC).1 It usually occurs at the age of 50-70 and is rare in pediatric patients; the ratio of male to female patients is 2.5-2.7:1, and the median survival is 12-14 months. 1-4The clinical features and evolution of BPDCN are rather homogenous and categorized into dermatopathic (>90% of cases) and leukemic patterns. 5 The dermatopathic pattern is characterized by a deceptive indolent onset dominated by skin lesions, which is the prominent and only detectable clinical feature in nearly 50% of patients, followed by tumor dissemination. Conversely, the leukemic variant is characterized by an elevated white blood cell count, circulating neoplastic cells, and massive bone marrow (BM) infiltration. Pure leukemic presentation is very rare (7% of 756 cases) and is mostly associated with multiple skin lesions. Other manifestations are related with tumor infiltration into the lymph nodes (localized and generalized lymphadenopathy), spleen, and liver. Notably, BPDCN can be precisely diagnosed by the immunohistochemical scoring system using CD4, CD56, and Blastic plasmacytoid dendritic cell (pDC) neoplasm (BPDCN) is a relatively rare hematological malignancy with significantly complex clinicopathological features that are still unclear. This study aimed to analyze the clinicopathological data of BPDCN and evaluate immunohistochemical detection of minimal bone marrow (BM) involvement. In this study, we examined skin and BM lesions from 6 patients with BPDCN. Neoplastic cells tested positive for CD303 (polyclonal, 100%; monoclonal, 40%) in the skin lesions and for CD303 (polyclonal, 100%; monoclonal, 67%) in the BM clots. Although immunostaining of CD4, CD56, CD123, CD303, and TCLl detected minimal BM involvement in 3 patients, morphological identification was challenging in the BM clots stained with hematoxylin-eosin. In conclusion, our results demonstrate the significance of observing BM smears to detect neoplastic cells and that immunohistochemical examination, including CD303 antibodies, is useful to detect minimal BM involvement. This study is the first to report the expression of thymic stromal lymphopoietin (TSLP) and its receptor in BPDCN cells. Therefore, the TSLP/TSLP receptor axis may be associated with the proliferation of BPDCN, and consequently, the survival of patients.
A 53‐year‐old Japanese man, with a history of developing urticaria (once after consuming mackerel and 10 times after consuming boiled burdock, carrot, curry, and rice), presented with redness over his entire body and dyspnea 1 h after eating boiled burdock. Physical examination revealed a low blood pressure of 64/29 mmHg and stridor, together with striking redness of the whole body; he was diagnosed to be in anaphylactic shock. He recovered from the anaphylactic shock with subcutaneous injection of epinephrine (1 mg) and an intravenous drip of lactate Ringer's solution containing hydrocortisone (100 mg) and dexamethasone (8 mg). Laboratory examination and skin prick test were performed 3 weeks after his first visit. The total immunoglobulin E (radioimmunosobent test) level was 190 IU/mL, and specific immunoglobulin E for mackerel and carrot was found to be negative. Skin prick test was performed on the volar forearm with burdock, carrot, and turmeric after he had not taken any medication for 1 week. It was also conducted in normal healthy persons at the same time. A skin prick was made with a PRICK‐LANCETTER® (made in Sweden) using 1% histamine chloride solution and 0.9% saline solution as positive (3+) and negative (–) controls, respectively. For skin prick tests, burdock and carrot were employed in their boiled and raw conditions. Turmeric powder was diluted to 1% and 10% in petrolatum. Skin prick tests were judged according to the recommendations of the European Academy of Allergy and Clinical Immunology (Shono M. The skin test learned in Finland. Hifubyou‐Shinryoh 1999; 25 (3): 255–269; Bernstein IL. Proceedings of the task force on guidelines for standardizing old and new technologies used for the diagnosis and treatment of allergic diseases. J Allergy Clin Immunol 1988; 82: 487–526). The results of the skin prick tests (Table 1) were positive for raw and boiled burdock and carrot, but negative for turmeric (Fig. 1). Two normal healthy controls showed negative responses to all substances. Results of skin prick test Wheal size (mm) Score Boiled burdock3 × 4(3+)Boiled carrot3 × 3(3+)Raw burdock3 × 4(3+)Raw carrot3 × 3(3+)1% turmeric diluted with petrolatum0 × 0(–)10% turmeric diluted with petrolatum0 × 0(–)1% histamine chloride4 × 4(3+)Normal saline–(–) 1 Skin prick tests performed on the flexor surface of the forearm (left: 1, boiled burdock; 2, boiled carrot; 3, raw burdock; 4, raw carrot; right: 5, 1% turmeric; 6, 10% turmeric; 7, histamine chloride; 8, normal saline) This is the first case report of anaphylaxis due to burdock.
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