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ELIZABETH A. MAULDIN DANNY W. SCOTT WILLIAM H. MILLER & CHRISTINA A. SMITH 《Veterinary dermatology》1997,8(3):191-202
A retrospective histopathological and immunopathological study was conducted on 86 dogs with Malassezia dermatitis. West Highland White terriers, English Setters, Shih Tzus, Basset Hounds, American Cocker Spaniels, spayed females, and castrated males were found to be at increased risk. The histopathological reaction pattern of lymphocytic superficial perivascular to interstitial dermatitis with parakeratotic hyperkeratosis, irregular epidermal hyperplasia, diffuse intercellular oedema and lymphocytic exocytosis was found to be consistent with a diagnosis of Malassezia dermatitis whether yeast were histologically visible (73.3% of the cases) or not (26.7%). Immunopathological studies revealed that 60– > 90% of the inflammatory cells within the epidermis, and 25–75% of those within the dermis were CD3+T lymphocytes, and that the only immunoglobulin-positive cells were dermal plasma cells. 相似文献
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中华鳖肝组织炎性细胞的浸润及其结构↑(*) 总被引:7,自引:1,他引:6
用组织化学和显微及亚显微生物技术,研究了患非寄生性肝病中华鳖(Trionyxsinensis)的外周血、肝静脉血血相变化和浸润肝组织炎性细胞的亚显微结构及其细胞免疫病理反应。结果表明,中华鳖的炎性细胞趋化性强、浸润面广。其剧烈的非特异性细胞免疫反应表现为:嗜中性粒细胞数量多、个体大、结构变化复杂,并在非特异性细胞免疫反应中发挥重要作用,其次是淋巴细胞、Kufer细胞;肝组织中被激活的白细胞在结构和数量上发生显著变化,并在浸润肝组织后聚集、吞噬、消化,发生强烈的细胞免疫反应。红细胞发生渗出性病理反应。 相似文献
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CVI 988/Rispens冷冻苗鸡胚胎免疫的免疫病理学机制 总被引:1,自引:1,他引:0
用CCI 988/Rispens冷冻苗免疫18日龄的鸡胚,观察淋巴器官的超微结构变化,揭示胚胎免疫的免疫病理学机制.结果显示:胚胎免疫组和胚胎免疫攻毒组的淋巴细胞活性增加,细胞核仁数目和胞浆内线粒体数目增多;非免疫攻毒组的淋巴细胞感染病毒,引起细胞核膜和线粒体受损,细胞有明显的退行性变化,表现为细胞大小不一,常染色质增加,异染色质减少.由此可见,18日龄胚胎免疫对淋巴器官的早期发育具有明显的免疫促进作用,可使雏鸡提前产生有效的免疫力. 相似文献
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Kyohei Yasuno Haruka Sakashita Ryosuke Kobayashi Saori Araki Rio Saito Mariko Shirota Junichi Kamiie Kinji Shitora 《Journal of toxicologic pathology》2013,26(2):203-208
Membranous glomerulonephropathy can be experimentally induced in rats, but spontaneous
cases have been rarely reported. In this report, we present a typical case of spontaneous
membranous glomerulonephropathy in a rat. A male Hatano low-avoidance (LAA) strain rat had
a tumor mass on the right auricle, and was sacrificed at 41 weeks of age. Urinary
screening by reagent strips revealed intense proteinuria. Histological tests revealed
frequent presence of irregularly sized eosinophilic hyaline materials on the capillary
wall and in the mesangium of renal glomeruli. Immunofluorescence revealed granular
deposits of IgG, IgM, and C3 in the glomeruli. Subepithelial dense deposits were observed
by electron microscopy accompanied by podocyte foot process effacement and occasional
irregular thickening of the glomerular basement membrane. The rat also developed chronic
lymphocytic pancreatitis, and the tumor mass on the right auricle was diagnosed as a
fibrosarcoma. Screening tests for antibodies against major infectious agents and
antinuclear antibody were negative. Western blot and indirect immunofluorescence analyses
suggested the presence of an autoantibody against the pancreatic component. The
glomerulopathy was considered an early stage of membranous glomerulonephropathy. 相似文献
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Richard C Weiss Fredric W Scott 《Comparative immunology, microbiology and infectious diseases》1981,4(2):175-189
Non-immune kittens passively immunized with feline serum containing high-titered antibodies reactive with feline infectious peritonitis virus (FIPV) developed a more rapid disease after FIPV challenge than did kittens pretreated with FIPV antibody-negative serum. Antibody-sensitized, FIPV challenged—kittens developed earlier clinical signs (including pyrexia, icterus, and thrombocytopenia) and died more rapidly than did non-sensitized, FIPV-challenged kittens. Mean survival time in sensitized kittens was significantly (P < 0.05) reduced compared to non-sensitized kittens (mean ± SEM, 10.0 ± 0.6 days vs. 28.8 ± 8.3 days, respectively). Lesions induced included fibrinous peritonitis, disseminated pyogranulomatous inflammation and necrotizing phlebitis and periphlebitis. FIPV antigen, immunoglobulin G, complement (C3) and fibrinogen were demonstrated in lesions by immunofluorescence microscopy.The pathogenesis of dengue hemorrhagic fever (DHF) in persons bears striking resemblance to that of FIP in experimental kittens. In both FIP and DHF, non-neutralizing antibody may promote acute disease by enhancement of virus infection in mononuclear phagocytes or by formation of immune complexes, activation of complement and secondary vascular disturbances. 相似文献
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NJ Cave 《New Zealand veterinary journal》2013,61(6):262-274
In the inflammatory bowel diseases (IBD) that affect dogs and cats there appears to be dysregulation of normal mucosal immunity, characterised by polyclonal lymphocytic infiltrates which are presumably specific for luminal antigens. There is an absence of a classical polarisation of either T-helper (Th) 1 or Th2 cytokine responses, although increased expression of mRNA for interleukin (IL) 2 and IL-12p40 and a shift towards mucosal immunoglobulin (Ig) G production are consistent findings, whilst variable responses are seen in tumour necrosis factor-α (TNF-α), IL-1, IL-4, IL-6, and interferon-γ (IFN-γ). Increased mucosal permeability and deranged intestinal motility are common sequelae. Despite obvious similarities with Crohn’s disease and ulcera- tive colitis in humans, important differences exist. Of these, the diffuse superficial nature but with no Th1 or Th2 bias, and the prevalence of proximal small intestinal disease are notable. Potential hypotheses for these disparities include specific differences in the types or locations of “agonistic” gut flora, diffuse abnormalities in microbial-host interactions, a greater importance of diet, or anatomical or cellular differences in mucosal immune responses. Although specific pathogens and genetic susceptibilities may be involved, quantitative or qualitative changes in the normal flora or abnormal responses to a normal flora are more likely to be involved in the immunopathogenesis. Dietary influences include a large source of antigen, promotion of abnormal microbial growth through Maillard compounds within canned diets, and specific macro- and micronutrient deficiencies. Although dependent on a histopathological diagnosis, limitations of biopsies procured endoscopically, lack of histopathological standardisation and difficulty distinguishing inflammation from neoplasia remain significant problems. Clinician-pathologist dialogue, immunohistochemistry, cytokine profiling and lymphocyte-clonality assessment may lead to more accurate diagnoses, a deeper understanding of the immunopathogenesis, and ultimately to new therapies or prevention of disease induction. 相似文献
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