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Journal articles on the topic 'Immune pathology'

Author: Grafiati
Published: 4 June 2021
Last updated: 20 February 2023

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1

TOMONAGA, Masao. "Immune Pathology of Myelodysplastic Syndromes." Internal Medicine 40, no. 10 (2001): 985–86. http://dx.doi.org/10.2169/internalmedicine.40.985.

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2

COOKE, T. D. V., and B. CHIR. "Immune Pathology in Polyarticular Osteoarthritis." Clinical Orthopaedics and Related Research &NA;, no. 213 (December 1986): 41???49. http://dx.doi.org/10.1097/00003086-198612000-00006.

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3

Kozakowski, N., H. Herkner, G. A. Bohmig, Z. Kikic, D. J. Cooper, K. Eller, A. H. Kirsch, et al. "PATHOLOGY: IMMUNE AND INFLAMMATORY MECHANISMS." Nephrology Dialysis Transplantation 29, suppl 3 (May 1, 2014): iii448—iii450. http://dx.doi.org/10.1093/ndt/gfu171.

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4

Bucelli, Robert C., and Alan Pestronk. "Immune myopathies with perimysial pathology." Neurology - Neuroimmunology Neuroinflammation 5, no. 2 (January 18, 2018): e434. http://dx.doi.org/10.1212/nxi.0000000000000434.

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ObjectiveImmune myopathies with perimysial pathology (IMPP) have a combination of damage to perimysial connective tissue and muscle fiber necrosis, more prominent near the perimysium. We studied the clinical and laboratory correlates of patients with pathologically defined IMPP.MethodsThis is a retrospective chart and pathology review of 57 consecutive patients with IMPP myopathology and, for comparison, 20 patients with dermatomyositis with vascular pathology (DM-VP).ResultsCompared with DM-VP, IMPP patients more commonly had interstitial lung disease (ILD) (p < 0.01), Raynaud phenomenon (p < 0.05), mechanic's hands (p < 0.05), arthralgias (p < 0.001), and a sustained response to immunomodulatory therapy (p < 0.05), and less frequently had a concurrent malignancy (p < 0.01). IMPP patients had higher serum creatine kinase values (p < 0.05), more frequent serum Jo-1 (p < 0.03) or SSA/SSA52 autoantibodies (p < 0.05), and less frequent antinuclear antibodies (p < 0.01). IMPP patients with serum Jo-1/antisynthetase antibodies were more likely to have ILD (p < 0.05) and inflammatory arthritis (p < 0.05) than IMPP patients without these antibodies.ConclusionsIMPP myopathology is associated with an increased risk of ILD, Raynaud phenomenon, mechanic's hands, and inflammatory arthritis when compared with another immune myopathy (DM-VP). IMPP patients require regular screening for ILD, particularly those with antisynthetase antibodies. The absence of myositis-specific autoantibodies in a large percentage of IMPP patients emphasizes the important role for myopathology in identifying patients at higher risk of severe comorbid conditions such as ILD.
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5

Hayes, M. M., P. Jacobs, L. Wood, and D. M. Dent. "Splenic pathology in immune thrombocytopenia." Journal of Clinical Pathology 38, no. 9 (September 1, 1985): 985–88. http://dx.doi.org/10.1136/jcp.38.9.985.

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6

Dienes, Hans-Peter, and Uta Drebber. "Pathology of Immune-Mediated Liver Injury." Digestive Diseases 28, no. 1 (2010): 57–62. http://dx.doi.org/10.1159/000282065.

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7

Racusen, Lorraine C. "Pathology and the Allo-Immune Response." American Journal of Transplantation 3, no. 12 (November 21, 2003): 1461–62. http://dx.doi.org/10.1046/j.1600-6135.2003.00288.x.

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8

Shmagel, K. V., and V. A. Chereshnev. "Molecular bases of immune complex pathology." Biochemistry (Moscow) 74, no. 5 (May 2009): 469–79. http://dx.doi.org/10.1134/s0006297909050010.

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9

Tlish, M. M., E. B. Popovskayа, N. L. Sycheva, N. V. Sorokina, and F. A. Psavok. "ASSOCIATED PATHOLOGY: CLINICAL ОBSERVATION." Vestnik dermatologii i venerologii 93, no. 4 (August 9, 2017): 66–73. http://dx.doi.org/10.25208/0042-4609-2017-93-4-66-73.

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The article analyzes the literature on polymorbidity of immune dermatoses. They confirm the possibility of combining with each other immune diseases, due to the presence of immune and metabolic abnormalities that are characteristic for the majority of chronic dermatoses and may indicate the possibility of combining several nosology. We present 2 clinical cases polymorbidity. In the first case — a combination demonstrated in one patient planus, idiopathic atrophoderma Pasini — Pierini and multi-colored lichen. In the second case detected combination of 4 kinds of dermatological diseases — horny eczema, psoriasis vulgaris, scleroderma, and rosacea. Patients underwent complex clinical examination and histomorphological examination of skin biopsies. The presented clinical cases demonstrate the possibility of a combination of several skin diseases in one patient with common etiopathogenic mechanisms
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10

Tousankina, I. A. "SOME ISSUES OF DIAGNOSTICS IN IMMUNE PATHOLOGY." Medical Immunology (Russia) 12, no. 6 (July 21, 2014): 485. http://dx.doi.org/10.15789/1563-0625-2010-6-485-496.

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11

Pleskanovskaya, A. S., A. M. Orazalieva, and D. B. Lamanova. "SOME IMMUNE-MORPHOLOGICAL CHARACTERISTICS OF THYROID PATHOLOGY." International Journal of Applied and Fundamental Research (Международный журнал прикладных и фундаментальных исследований), no. 9 2022 (2022): 19–23. http://dx.doi.org/10.17513/mjpfi.13434.

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12

Auriault, C., V. Pancré, I. Wolowczuk, C. Asseman, I. Ferru, and C. Verwaerde. "Cellular immune response and pathology in schistosomiasis." Parasite 3, no. 3 (September 1996): 199–208. http://dx.doi.org/10.1051/parasite/1996033199.

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13

Semerjyan, Anna Babken, Mariam Armenak Sargsyan, Hranush Harutyun Arzumanyan, Lina Hayrapet Hakobyan, Liana Onik Abroyan, Zara Babken Semerjyan, Aida Sergey Avetisyan, et al. "Immune cell pathology in rabbit hemorrhagic disease." August-2019 12, no. 8 (August 2019): 1332–40. http://dx.doi.org/10.14202/vetworld.2019.1332-1340.

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Aim: The aim of this research was to study the effect of rabbit hemorrhagic disease virus (RHDV) on the host immune response by examining the cellular composition/pathology of lymphoid organs and serum levels of tumor necrosis factor-alpha (TNF-α) and interferon-gamma (IFN-γ). Materials and Methods: Nine adult rabbits were inoculated with 1 ml of 10% infected liver homogenate, and three rabbits served as controls. The rabbit hemorrhagic disease (RHD)-induced animals were studied on 3 consecutive days post-infection. Diagnosis of RHD was made through routine hemagglutination tests and the polymerase chain reaction. Blood smears and tissue samples from bone marrow (BM), spleen, lymph nodes, and liver were analyzed for cell composition and cytopathology. Serum levels of TNF-α and IFN-γ were measured by enzyme-linked immunosorbent assay. Results: RHD showed a decreased absolute cell count of blood as well as lymph nodes, spleen, and BM cell populations with marked left shift. This was seen as a progressive rise in immature and blast cells. Quantitative cellular changes were accompanied by an increase in specific inflammatory cytokines. Immunocytopathological alterations were evidenced by: Vacuolized, hyperactivated tissue macrophages, finding of Dohle bodies in neutrophils, and activated lymphocytes with increased nuclear-cytoplasmic ratio. Cytoplasmic eosinophilic viral inclusions found in tissue (liver, spleen, and BM) macrophages were shown for the 1st time in RHD. Megakaryocytic emperipolesis was a common feature of RHD. Conclusion: These studies suggest that RHDV induces pathology in leukocytes due to hyperactivation with left shift (toward immature stages of the different cell lineages). Macrophages are increased in number and show an expressed cytopathic effect often accompanied by viral eosinophilic cytoplasmic inclusions. They also developed a secretory activation (increased levels of pro-inflammatory cytokines). Keywords: cytopathology, emperipolesis, eosinophilic viral inclusions, immune response, macrophages, rabbit hemorrhagic disease virus.
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14

Rosenberg, Amy S., Montserrat Puig, Kanneboyina Nagaraju, Eric P. Hoffman, S. Armando Villalta, V. Ashutosh Rao, Lalage M. Wakefield, and Janet Woodcock. "Immune-mediated pathology in Duchenne muscular dystrophy." Science Translational Medicine 7, no. 299 (August 5, 2015): 299rv4. http://dx.doi.org/10.1126/scitranslmed.aaa7322.

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15

Varadhachary, Arun S., Conrad C. Weihl, and Alan Pestronk. "Mitochondrial pathology in immune and inflammatory myopathies." Current Opinion in Rheumatology 22, no. 6 (November 2010): 651–57. http://dx.doi.org/10.1097/bor.0b013e32833f108a.

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16

Amadi, Emmanuel Chike, Emmanuel Eze, and Vincent Chigor. "Effect of malaria pathology on CD4 and immune cells." Journal of Immunology 202, no. 1_Supplement (May 1, 2019): 122.9. http://dx.doi.org/10.4049/jimmunol.202.supp.122.9.

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Abstract Knowledge of immunity in malariology can help in understanding the pathology, treatment and vaccine production. The effect of malaria disorder on CD4 and immune cells counts was carried out at a Teaching Hospital in Enugu, Eastern Nigeria between October-December 2018. Patients on doctor’s provisional diagnosis of malaria were examined for Plasmodium infections and the degree of parasitaemia (0, +, ++, and +++). Positive samples and negative ones (0) were thereafter examined for their CD4 (Flow cytometry) and immune cells (Automated blood cell counter) counts. 45 patients were studied. All the Plasmodium-negative specimens were within reference ranges of CD4 cell count (464–1308); with mean value of 835. The (+) parasitaemia showed lower ranges of CD4 count (502–1282); mean = 678; with immune falls in one (427). The 12 (++) parasitaemia showed crash in 9 CD4 cells counts; range: 301–415; mean = 399. All the 7 (+++) parasitaemia showed crashes in CD4 cell counts, range: 160–357; mean = 225. The CD4 cells falls and crashes were detected only in Plasmodium falciparum parasitaemia infections. Depending on the CD4 cells count, also a reflex of parasitaemia, variances occur in the various immune cells’ percent and numeric. TWBC count fell in only 3 patients (1.99, 3.42 & 3.64) × 109 cells/L, corresponding to (+++), (++) & (+) parasitaemia, respectively. Low CD4 counts does not always produce low lymphocyte numeric, probably because other CD or killer cells compensates it. In conclusion, Plasmodium falciparum infection causes immuno-suppression in patients. Corollary, it means that malaria infection in the immunodeficients and AIDS patients will accelerate the complications as well as death, unlike prevailing reports.
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17

Benoit, Patrick, and Claude Boucheix. "Manipulation of the immune response by monoclonal antibodies in auto-immune pathology." Current Eye Research 9, sup1 (January 1990): 201–5. http://dx.doi.org/10.3109/02713689008999442.

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18

Ibraheim, Hajir, Esperanza Perucha, and Nick Powell. "Pathology of immune-mediated tissue lesions following treatment with immune checkpoint inhibitors." Rheumatology 58, Supplement_7 (December 1, 2019): vii17—vii28. http://dx.doi.org/10.1093/rheumatology/kez465.

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Abstract Immune check point inhibitor (CPI) therapy has revolutionized treatment paradigms for several cancers, but at the cost of triggering a diverse spectrum of immune-mediated injury to non-cancer tissues. The complex biology of these toxicities remains incompletely understood, partly because tissue acquisition from affected areas can be challenging to retrieve, thus hindering development of targeted therapy. Here, we review the literature describing pathology of immune-mediated tissue lesions including gastrointestinal, skin, rheumatic, pulmonary, cardiac, renal and hepatic lesions and highlight key immunological insights.
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19

Moroz, B. V., V. N. Nikiforov, and I. P. Tryakina. "Toxoplasmosis in clinical pathology." Kazan medical journal 70, no. 3 (June 15, 1989): 179–81. http://dx.doi.org/10.17816/kazmj99848.

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The significance of toxoplasmosis in clinical pathology has not yet been fully clarified. On the one hand, T. gondii is an opportunistic microorganism with low pathogenicity and evolutionarily adapted to long-term asymptomatic existence in the immune organism of its host, in particular humans; on the other hand, this parasite can activate up to life-threatening for the host if the latter has weakened or damaged immune defense mechanisms. In this context, it should be borne in mind the probability of increasing sporadic morbidity of toxoplasmosis against the background of widespread asymptomatic carriage (endemicity) due to the increasing use of corticosteroids, cytostatics, radiotherapy, leading to immunosuppression.
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20

Han, Rafael T., Rachel D. Kim, Anna V. Molofsky, and Shane A. Liddelow. "Astrocyte-immune cell interactions in physiology and pathology." Immunity 54, no. 2 (February 2021): 211–24. http://dx.doi.org/10.1016/j.immuni.2021.01.013.

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21

Jamal, Muhammad, Hina Iqbal Bangash, Maria Habiba, Yufei Lei, Tian Xie, Jiaxing Sun, Zimeng Wei, Zixi Hong, Liang Shao, and Qiuping Zhang. "Immune dysregulation and system pathology in COVID-19." Virulence 12, no. 1 (January 1, 2021): 918–36. http://dx.doi.org/10.1080/21505594.2021.1898790.

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22

Hughes, Krystal. "Molecular Pathology of Immune Checkpoint Inhibitor-Induced Myocarditis." Journal of Analytical Oncology 9 (December 20, 2020): 25–32. http://dx.doi.org/10.30683/1927-7229.2020.09.04.

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23

C. Wickramarachchi, Dilki, Argyrios N. Theofilopoulos, and Dwight H. Kono. "Immune pathology associated with altered actin cytoskeleton regulation." Autoimmunity 43, no. 1 (December 10, 2009): 64–75. http://dx.doi.org/10.3109/08916930903374634.

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24

Aller, M. A., J. L. Arias, L. Lorente, M. P. Nava, H. J. Durán, and J. Arias. "Neuro-immune-endocrine functional system and vascular pathology." Medical Hypotheses 57, no. 5 (November 2001): 561–69. http://dx.doi.org/10.1054/mehy.2001.1408.

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25

Giulian, Dana. "Microglia and the Immune Pathology of Alzheimer Disease." American Journal of Human Genetics 65, no. 1 (July 1999): 13–18. http://dx.doi.org/10.1086/302477.

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26

Mason, Don, and Fiona Powrie. "Control of immune pathology by regulatory T cells." Current Opinion in Immunology 10, no. 6 (December 1998): 649–55. http://dx.doi.org/10.1016/s0952-7915(98)80084-8.

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27

Cook, Matthew C., Carola G. Vinuesa, and Christopher C. Goodnow. "ENU-mutagenesis: insight into immune function and pathology." Current Opinion in Immunology 18, no. 5 (October 2006): 627–33. http://dx.doi.org/10.1016/j.coi.2006.07.011.

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28

Baulch, Janet E., Munjal M. Acharya, Sudhanshu Agrawal, Lauren A. Apodaca, Clarice Monteiro, and Anshu Agrawal. "Immune and Inflammatory Determinants Underlying Alzheimer’s Disease Pathology." Journal of Neuroimmune Pharmacology 15, no. 4 (February 24, 2020): 852–62. http://dx.doi.org/10.1007/s11481-020-09908-9.

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29

Boylston, A. W., H. T. Cook, N. D. Francis, and R. D. Goldin. "Biopsy pathology of acquired immune deficiency syndrome (AIDS)." Journal of Clinical Pathology 40, no. 1 (January 1, 1987): 1–8. http://dx.doi.org/10.1136/jcp.40.1.1.

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30

Glasgow, Ben J., Kenneth D. Steinsapir, Karl Anders, and Lester J. Layfield. "Adrenal Pathology in the Acquired Immune Deficiency Syndrome." American Journal of Clinical Pathology 84, no. 5 (November 1, 1985): 594–97. http://dx.doi.org/10.1093/ajcp/84.5.594.

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31

Ilkovitch, Dan. "Role of immune-regulatory cells in skin pathology." Journal of Leukocyte Biology 89, no. 1 (July 13, 2010): 41–49. http://dx.doi.org/10.1189/jlb.0410229.

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32

SYDORCHUK, L., R. SYDORCHUK, and I. SYDORCHUK. "Vascular pathology and immune disorders in hypertensive patients." American Journal of Hypertension 18, no. 5 (May 2005): A49. http://dx.doi.org/10.1016/j.amjhyper.2005.03.133.

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33

Bulmer, Judith N. "4 Immune aspects of pathology of the placental bed contributing to pregnancy pathology." Baillière's Clinical Obstetrics and Gynaecology 6, no. 3 (September 1992): 461–88. http://dx.doi.org/10.1016/s0950-3552(05)80006-9.

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34

K.C., Shiva Raj. "Pathology of Inflammatory Bowel Disease." Journal of Pathology of Nepal 5, no. 9 (March 27, 2015): 756–65. http://dx.doi.org/10.3126/jpn.v5i9.13787.

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Inflammatory bowel disease is a group of inflammatory disorders of unknown etiology. Various genetic factors, mucosal immune response, inappropriate activation of immune system driven by the presence of various luminal flora and epithelial defects have been postulated. Crohn disease and Ulcerative colitis are the two most common inflammatory bowel diseases. Since, specific clinical laboratory features are lacking which may help in establishing a diagnosis histopathological diagnosis remains the gold standard. This review highlights the known hypothesis regarding the etiopathogenesis of these two diseases and also describes pertinent histological features.Journal of Pathology of Nepal (2015) Vol. 5, 756-765
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35

Ritter, Jana M., Roosecelis B. Martines, and Sherif R. Zaki. "Zika Virus: Pathology From the Pandemic." Archives of Pathology & Laboratory Medicine 141, no. 1 (October 5, 2016): 49–59. http://dx.doi.org/10.5858/arpa.2016-0397-sa.

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Context.—As the number of Zika virus (ZIKV) infections continues to grow, so, too, does the spectrum of recognized clinical disease, in both adult and congenital infections. Defining the tissue pathology associated with the various disease manifestations provides insight into pathogenesis and diagnosis, and potentially future prevention and treatment, of ZIKV infections. Objective.—To summarize the syndromes and pathology associated with ZIKV infection, the implications of pathologic findings in the pathogenesis of ZIKV disease, and the use of pathology specimens for diagnosis of ZIKV infection. Data Sources.—The major sources of information for this review were published articles obtained from PubMed and pathologic findings from cases submitted to the Infectious Diseases Pathology Branch at the Centers for Disease Control and Prevention. Conclusions.—Pathologic findings associated with ZIKV infection are characteristic but not specific. In congenital Zika syndrome, tissue pathology is due to direct viral infection of neural structures, whereas in Guillain-Barré syndrome, pathology is likely due to a postviral, aberrant host-directed immune response. Both fetal and placental pathology specimens are useful for ZIKV diagnosis by molecular and immunohistochemical assays; however, the implications of ZIKV detection in placentas from second- and third-trimester normal live births are unclear, as the potential postnatal effects of late gestational exposure remain to be seen.
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36

Vincent, Crystal M., and Marc S. Dionne. "Disparate regulation of IMD signaling drives sex differences in infection pathology in Drosophila melanogaster." Proceedings of the National Academy of Sciences 118, no. 32 (August 2, 2021): e2026554118. http://dx.doi.org/10.1073/pnas.2026554118.

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Male and female animals exhibit differences in infection outcomes. One possible source of sexually dimorphic immunity is the sex-specific costs of immune activity or pathology, but little is known about the independent effects of immune- versus microbe-induced pathology and whether these may differ for the sexes. Here, by measuring metabolic and physiological outputs in Drosophila melanogaster with wild-type and mutant immune responses, we test whether the sexes are differentially impacted by these various sources of pathology and identify a critical regulator of this difference. We find that the sexes exhibit differential immune activity but similar bacteria-derived metabolic pathology. We show that female-specific immune-inducible expression of PGRP-LB, a negative regulator of the immune deficiency (IMD) pathway, enables females to reduce immune activity in response to reductions in bacterial numbers. In the absence of PGRP-LB, females are more resistant to infection, confirming the functional importance of this regulation and suggesting that female-biased immune restriction comes at a cost.
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37

Lee, Jong-Mok. "Immune-Mediated Necrotizing Myopathy: A Review for Clinicians." Journal of Electrodiagnosis and Neuromuscular Diseases 24, no. 3 (December 31, 2022): 57–61. http://dx.doi.org/10.18214/jend.2022.00087.

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Immune-mediated necrotizing myopathy (IMNM) is a group of inflammatory myopathies showing necrotic and regenerating fibers without noteworthy inflammatory cell infiltration on pathology. The pathologic findings are different from those of dermatomyositis or sporadic inclusion body myositis. Furthermore, the discovery of myositis-specific antibodies in patients with IMNM, such as anti-signal recognition particle or anti-3-hydroxy-3-methylglutaryl-CoA reductase antibodies, has enabled us to expand our knowledge of IMNM. However, the phenotype and pathological findings of IMNM are unremarkable; therefore, it is difficult to diagnose, and IMNM has been relatively unrecognized. In this review, we introduce the clinical features, diagnosis, pathomechanism, and treatment of IMNM for clinicians.
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38

Forsberg, L., C. H. Florén, E. Hederström, and H. Prytz. "Ultrasound Examination in Diffuse Liver Disease." Acta Radiologica 28, no. 3 (May 1987): 281–84. http://dx.doi.org/10.1177/028418518702800310.

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Seventy-three patients with pathologic liver function tests were examined using ultrasound one day prior to liver biopsy. The ultrasound findings were compared with the histologic findings. In 23 patients enlarged lymph nodes were found in the hepato-duodenal ligament and 21 of these had active immune-mediated liver disease. Of the remaining 2 patients one had ulcerative colitis (and fatty liver) and one chronic cholecystitis (and ***haemosiderosis). Of the 33 patients with biopsy-proven active ***immune-mediated liver disease 21 had pathologic lymph nodes in the hepato-duodenal ligament at ultrasound. It was not possible to identify the ligament in 8 patients and in the remaining 4 no pathologic lymph nodes could be found. Twenty-one of these patients had normal liver echoes on ultrasound, 5 exhibited increased echogenicity and 5 had heterogeneous echogenicity. In a further 2 patients both increased echogenicity and heterogeneous parenchyma were found. Ultrasound examination of the liver parenchyma alone would thus lead to 21 of the 33 patients being classified as normal and a further 5 being classified as having fatty changes of the liver. Only 7 would be regarded as having significant liver pathology. However, if demonstration at ultrasound of pathologic lymph nodes in the hepato-duodenal ligament is regarded as being consistent with significant hepatic pathology a further 15 patients could be added to these 7 patients, giving a total of 22 out of 33 patients (67%) identified as having significant liver pathology using ultrasound alone. The reliability of ultrasound in the diagnosis of immune-mediated liver disease can thus be improved considerably by actively searching for lymph nodes in the hepato-duodenal ligament.
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Hennings, Leah, Cecile Artaud, Fariba Jousheghany, Behjatolah Monzavi-Karbassi, Anastas Pashov, and Thomas Kieber-Emmons. "Carbohydrate Mimetic Peptides Augment Carbohydrate-Reactive Immune Responses in the Absence of Immune Pathology." Cancers 3, no. 4 (November 11, 2011): 4151–69. http://dx.doi.org/10.3390/cancers3044151.

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40

Milner, Joshua D. "Broad spectrum of immune and non-immune pathology in inherited defects of STAT signalling." Pathology 48 (February 2016): S44—S45. http://dx.doi.org/10.1016/j.pathol.2015.12.110.

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41

Todd, I., and C. Davenport. "Immune Reactions." Molecular Pathology 49, no. 2 (April 1, 1996): M124. http://dx.doi.org/10.1136/mp.49.2.m124-b.

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42

Bourke, Jack. "Immune related adverse events to immune checkpoint inhibitors." Pathology 49 (February 2017): S46. http://dx.doi.org/10.1016/j.pathol.2016.12.113.

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43

Azoicai, Alice Nicoleta. "Immune deficiency and infection in pediatric chronic respiratory pathology." Revista Medico-Chirurgicala 126, no. 1 (March 30, 2022): 18–24. http://dx.doi.org/10.22551/msj.2022.01.03.

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44

Kalali, Behnam, Raquel Mejías-Luque, Anahita Javaheri, and Markus Gerhard. "H. pyloriVirulence Factors: Influence on Immune System and Pathology." Mediators of Inflammation 2014 (2014): 1–9. http://dx.doi.org/10.1155/2014/426309.

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Helicobacter pyloriis the most widespread chronic bacterial agent in humans and is well recognized for its association with ulcer disease and gastric cancer, with both representing major global health and socioeconomic issues. Given the high level of adaptation and the coevolution of this bacterium with its human host, a thorough and multidirectional view of the specific microbiological characteristics of this infection as well as the host physiology is needed in order to develop novel means of prevention of therapy. This review aims to pinpoint some of these potentially important angles, which have to be considered mutually when studyingH. pylori’s pathogenicity. The host’s biological changes due to the virulence factors are a valuable pillar ofH. pyloriresearch as are the mechanisms by which bacteria provoke these changes. In this context, necessary adhesion molecules and significant virulence factors ofH. pyloriare discussed. Moreover, metabolism of the bacteria, one of the most important aspects for a better understanding of bacterial physiology and consequently possible therapeutic and prophylactic strategies, is addressed. On the other hand, we discuss the recent experimental proofs of the “hygiene hypothesis” in correlation withHelicobacter’s infection, which adds another aspect of complexity to this infection.
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45

BURT, ALASTAIR D. "Spectrum of liver pathology in immune mediated liver diseases." Journal of Gastroenterology and Hepatology 19, s7 (December 2004): S353—S355. http://dx.doi.org/10.1111/j.1440-1746.2004.03647.x.

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46

Jutel, M., M. Akdis, and C. A. Akdis. "Histamine, histamine receptors and their role in immune pathology." Clinical & Experimental Allergy 39, no. 12 (December 2009): 1786–800. http://dx.doi.org/10.1111/j.1365-2222.2009.03374.x.

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47

Guo, Yansu, Yaling Liu, Lei Xu, Shuyu Wu, Cheng Yang, Dongxia Wu, Hongran Wu, and Chunyan Li. "Astrocytic pathology in the immune‐mediated motor neuron injury." Amyotrophic Lateral Sclerosis 8, no. 4 (January 2007): 230–34. http://dx.doi.org/10.1080/17482960701278612.

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48

Delisle, M. B., H. Bouissou, and A. Saidi. "What's New in Cerebral Pathology in Acquired Immune Deficiencies?" Pathology - Research and Practice 181, no. 1 (March 1986): 85–92. http://dx.doi.org/10.1016/s0344-0338(86)80192-3.

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Jacobs, J. J. L. "Neutralizing antibodies mediate virus-immune pathology of COVID-19." Medical Hypotheses 143 (October 2020): 109884. http://dx.doi.org/10.1016/j.mehy.2020.109884.

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Golenbock, Douglas T. "S1-02-03: Innate immune pathology in Alzheimer's disease." Alzheimer's & Dementia 5, no. 4S_Part_2 (July 2009): P71. http://dx.doi.org/10.1016/j.jalz.2009.05.162.

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