Journal articles: 'IMMUNODEFICIENZE'

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Giancane, Gabriella, Elisabetta Cortis, AnnaMaria Zicari, Paola Pansa, and Marzia Duse. "Dalle immunodeficienze alle malattie reumatologiche." Area Pediatrica 13, no. 3 (June 2012): 72–76. http://dx.doi.org/10.1016/j.arped.2011.09.001.

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Giancane, Gabriella, Elisabetta Cortis, Ilaria Ernesti, Annalisa Di Coste, and Marzia Duse. "Dalle immunodeficienze alle malattie reumatologiche." Area Pediatrica 13, no. 4 (October 2012): 111–16. http://dx.doi.org/10.1016/j.arped.2012.10.005.

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Azzari, Chiara. "Lo screening neonatale delle immunodeficienze severe combinate." Area Pediatrica 13, no. 1 (February 2012): 20–24. http://dx.doi.org/10.1016/j.arped.2012.03.007.

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AL Farsi, Tariq, Sanjeewani Weerakoon, Jalila Mohsin, Hussein Al Mashayakhi, Khawater Ahmed, Amal Al Maani, Khuloud Aboqusida, and Nashat Al Sukaiti. "Disseminated Cryptosporidiosis in an Infant with Non-HIV Pediatric Immunodeficiency: First Case Report from Oman." Oman Medical Journal 36, no. 6 (November 30, 2021): e326-e326. http://dx.doi.org/10.5001/omj.2021.44.

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Cryptosporidium is a rare but important pathogen, especially in children with immunodeficiency. Intestinal cryptosporidiosis is well described in immunocompetent and immunocompromised children, but respiratory and disseminated cryptosporidiosis in immunodeficient children is not often reported. We describe an Omani infant with disseminated cryptosporidiosis and failing pharmacological therapy in the context of severe combined immunodeficiency. Chronic diarrhea can be an initial symptom of immunodeficiency in the pediatric population. Awareness of cryptosporidiosis is critical to early detection and management for such patients. As antiparasitic agents are often ineffective, amelioration of immunosuppression in immunodeficient children should be a priority.

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Campisi, Paolo, Linda Vong, Jonathan M. Sgro, Nikolaus Wolter, Bo Ngan, and Jacob Friedberg. "Transcervical thymic biopsy in the immunodeficient child." LymphoSign Journal 6, no. 4 (December 1, 2019): 141–47. http://dx.doi.org/10.14785/lymphosign-2019-0014.

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Objective: The objectives of this study are to present a case series of immunodeficient children who underwent a transcervical thymic biopsy and to describe the transcervical approach to the thymus gland. Design: Case series. Setting: Pediatric otolaryngology practice in an academic setting. Patients: Consecutive sample of immunodeficient children (≤18 years old) who underwent thymic biopsies from 1996 to 2019 for the purpose of confirming or excluding profound T cell immunodeficiency. Intervention: Diagnostic transcervical thymic biopsy. Results: A total of 14 patients with atypical combined immunodeficiency underwent the procedure during the study period, with minimal post-operative complication. The thymus was found to be abnormal histologically in 9 children and normal in another 5 patients. In all cases, thymus morphology helped define the extent of the immunodeficiency, resulting in either supporting a decision to perform a bone marrow transplant (8 patients) or avoid this high risk procedure (3 patients). Conclusion: Thymus biopsy is helpful in the characterization of childhood immunodeficiency and provides critical information that affects the medical management. The transcervical approach to the thymus is feasible in children and can be accomplished with minimal morbidity. Statement of novelty: Biopsies of the thymus have assisted in the characterization of new entities of primary immunodeficiency.

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Ito, Yusuke, Kensuke Takaoka, Kazuhiro Toyama, Yoshitaka Wakabayashi, Aya Shinozaki-Ushiku, Aiko Okazaki, Kinuyo Chikamatsu, Satoshi Mitarai, Tetsuo Ushiku, and Mineo Kurokawa. "The First Case of Concomitant Mycobacterium genavense lymphadenitis and EBV-positive lymphoproliferative disorder." Mediterranean Journal of Hematology and Infectious Diseases 12, no. 1 (June 28, 2020): e2020035. http://dx.doi.org/10.4084/mjhid.2020.035.

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This is the first case of concurrent Mycobacterium genavense lymphadenitis and Epstein-Barr virus (EBV)-positive lymphoproliferative disorder (LPD) in the same lymph node with no immunocompromised history. M. genavense infection is a rare opportunistic infection mainly for human immunodeficiency virus (HIV)-infected patients. Although no immunodeficiency was detected in our patient, our case indicates that the immunodeficiency in the background of EBV latency type III and the immunosuppression by malignant lymphoma itself might induce the M. genavense lymphadenitis. This case highly alerts clinicians the immunosuppressive state of EBV-positive LPD with latency type III even if any serological immunodeficient factors are not detected.

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Burns, S. "Podiatric manifestations of AIDS." Journal of the American Podiatric Medical Association 80, no. 1 (January 1, 1990): 15–20. http://dx.doi.org/10.7547/87507315-80-1-15.

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Dermatologic, vascular, neurologic, and musculoskeletal complications are common among persons with acquired immunodeficiency syndrome (AIDS). These manifestations frequently involve the lower extremities and may be the initial presenting symptoms of human immunodeficiency virus (HIV) infection. It is important that practitioners of podiatric medicine be aware of these syndromes to facilitate early diagnosis of AIDS and to provide the best possible care for immunodeficient patients. The author provides a review of the manifestations of AIDS frequently encountered in podiatric practice, along with guidelines for treatment.

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Chalifoux, Laura V., Angela Carville, Douglas Pauley, Brendon Thompson, Andrew A. Lackner, and Keith G. Mansfield. "Enterocytozoon bieneusi as a Cause of Proliferative Serositis in Simian Immunodeficiency Virus–Infected Immunodeficient Macaques (Macaca mulatta)." Archives of Pathology & Laboratory Medicine 124, no. 10 (October 1, 2000): 1480–84. http://dx.doi.org/10.5858/2000-124-1480-ebaaco.

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Abstract Context.—Enterocytozoon bieneusi is the most frequent microsporidian parasite of human patients with acquired immunodeficiency syndrome and is a significant cause of diarrhea and wasting. Recently, this organism has also been recognized as a spontaneous infection of several species of captive macaques. As in humans, E bieneusi frequently causes enteropathy and cholangiohepatitis in immunodeficient simian immunodeficiency virus (SIV)–infected macaques. Objective.—To examine E bieneusi as an etiologic agent of nonsuppurative proliferative serositis in immunodeficient rhesus macaques (Macaca mulatta). Design.—Retrospective analysis of necropsy material obtained from immunodeficient SIV-infected rhesus macaques. Results.—Examination of SIV-infected rhesus macaques (n = 225) revealed E bieneusi proliferative serositis in 7 of 16 cases of peritonitis of unknown origin. The organism could be identified by in situ hybridization and polymerase chain reaction in sections of pleura and peritoneum obtained at necropsy. Serositis was always accompanied by moderate-to-severe infection of the alimentary tract, and morphologic evidence suggested dissemination through efferent lymphatics. Colabeling experiments revealed most infected cells to be cytokeratin positive and less frequently positive for the macrophage marker CD68. Sequencing of a 607–base pair segment of the small subunit ribosomal gene revealed 100% identity to sequences obtained from rhesus macaques (Genbank accession AF023245) and human patients (Genbank accession AF024657 and L16868). Conclusions.—These findings indicate that E bieneusi disseminates in immunodeficient macaques and may be a cause of peritonitis in the immunocompromised host.

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Hofmann, Adam, Gerasimos Zaharatos, and Mark Miller. "Case Report and Review of the Literature:Toxoplasma gondiiEncephalitis in a 40-Year-Old Woman with Common Variable Immunodeficiency and a New Diagnosis of Large Granular Lymphocytic Leukemia." Canadian Journal of Infectious Diseases and Medical Microbiology 19, no. 4 (2008): 309–10. http://dx.doi.org/10.1155/2008/614279.

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Toxoplasma gondiihas been well-documented to cause central nervous system infections in immunodeficient patients. The present study describes a case of central nervous system toxoplasmosis in a patient with common variable immunodeficiency and newly diagnosed large granular lymphocytic leukemia, with a review of the literature for this association.

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Ferreira Santos, Carla, Marlene Delgado, Ana Bárbara Simões, Joana Nunes, Isabel Pereira, and Orlando Gaspar. "Encefalite a Citomegalovírus em Doente com Vírus da Imunodeficiência Humana Negativa." Acta Médica Portuguesa 26, no. 5 (October 31, 2013): 608. http://dx.doi.org/10.20344/amp.4949.

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Secondary immunodeficiences are associated with an increased incidence of infection and malignancy, as well with development ofautoimmune disease. Immune system function is altered by many conditions, such as aging, malnutrition and mycobacterial infections. However, the treatment of the primary condition often results in the improvement of the immune compromise. The authors present a case of cytomegalovirus encephalitis and hepatitis, due to viral reactivation associated with development of secondary immunodeficience in an HIV-negative patient.

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Yokote, Hiroyuki, Yasuhiko Shinmura, Tomomi Kanehara, Shinichi Maruno, Masahiko Kuranaga, Hajime Matsui, and So Hashizume. "Safety of Attenuated Smallpox Vaccine LC16m8 in Immunodeficient Mice." Clinical and Vaccine Immunology 21, no. 9 (July 2, 2014): 1261–66. http://dx.doi.org/10.1128/cvi.00199-14.

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ABSTRACTFreeze-dried live attenuated smallpox vaccine LC16m8 prepared in cell culture has been the sole smallpox vaccine licensed in Japan since 1975 and was recently recommended as a WHO stockpile vaccine. We evaluated the safety of recently remanufactured lots of LC16m8 using a series of immunodeficient mouse models. These models included suckling mice, severe combined immunodeficiency disease (SCID) mice, and wild-type mice treated with cyclosporine. LC16m8 showed extremely low virulence in each of the three mouse models compared with that of its parental strains, Lister and LC16mO. These results provide further evidence that LC16m8 is one of the safest replication-competent smallpox vaccines in the world and may be considered for use in immunodeficient patients.

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Kim, B. S., and K. M. Hui. "Induction of infectious immunodeficiency in BALB/c mice by serial transfer of lymphocytes immune to alloantigens." Journal of Immunology 135, no. 1 (July 1, 1985): 255–60. http://dx.doi.org/10.4049/jimmunol.135.1.255.

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Abstract Serial transfer of spleen cells immune to allogeneic or semi-allogeneic cells induced transferable splenomegaly and general immune deficiencies, including the lack of proliferative responses to T and B cell mitogens and antibody responses to specific antigens. Parallel experiments with spleen cells from mice that had been administered rectally with allogeneic spleen or sperm cells also resulted in a similar immunodeficiency. The immune deficiencies were transferable into normal mice by injection of spleen cells, cellfree extracts, or culture supernatants of spleen cells from immunodeficient mice. The particle responsible for transmission of immunodeficiency appears to be a high m.w. (greater than 2 X 10(6], 1.14 g/ml density agent. These results suggest strongly that serial transfer of lymphocytes immune to alloantigens triggers the release of a transmissible virus-like agent, which results in an immunodeficiency similar to acquired immune deficiency syndrome (AIDS) of humans. Therefore, this system may provide a valuable animal model system for studying AIDS.

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Jalil, Maaz, Julianne Pietras, Syed N. Ahmed, Phuong Daniels, and Robert Hostoffer. "COVID-19 Infection in Patients with Humoral Immunodeficiency: A Case Series and Literature Review." Allergy & Rhinology 13 (January 2022): 215265752210960. http://dx.doi.org/10.1177/21526575221096044.

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Background The coronavirus 2019 disease (COVID-19) has infected many individuals worldwide and continues to pose a significant threat to those with weakened immune systems. The data evaluating the clinical outcomes of patients with humoral immunodeficiencies that contract COVID-19 is limited and conflicting. Objective To describe the clinical outcomes of COVID-19 infections in patients with primary humoral immunodeficiency and compare results to current literature. Methods We conducted a retrospective cohort review on 15 patients with a humoral immunodeficiency defined as Common Variable Immunodeficiency, Specific Antibody Deficiency, or unspecified hypogammaglobulinemia, who contracted COVID-19. Severity scores were determined to evaluate the clinical outcomes of these patients. Results Of our 15-patient cohort, 33% of individuals with a humoral immunodeficiency infected with COVID-19 had moderate to severe disease, requiring hospitalization or resulting in death. COVID-19 mortality rate was found to be 7%. All 5 of our patients with severe COVID-19 infection had at least 1 comorbidity or risk factor. Conclusion Within our cohort of humoral immunodeficient patients infected with COVID-19, we found a higher rate of moderate to severe COVID-19 infection and worse clinical outcomes, particularly in patients with comorbidities or risk factors.

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Jalil, Maaz, Julianne Pietras, Syed N. Ahmed, Phuong Daniels, and Robert Hostoffer. "COVID-19 Infection in Patients with Humoral Immunodeficiency: A Case Series and Literature Review." Allergy & Rhinology 13 (January 2022): 215265752210960. http://dx.doi.org/10.1177/21526575221096044.

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Background The coronavirus 2019 disease (COVID-19) has infected many individuals worldwide and continues to pose a significant threat to those with weakened immune systems. The data evaluating the clinical outcomes of patients with humoral immunodeficiencies that contract COVID-19 is limited and conflicting. Objective To describe the clinical outcomes of COVID-19 infections in patients with primary humoral immunodeficiency and compare results to current literature. Methods We conducted a retrospective cohort review on 15 patients with a humoral immunodeficiency defined as Common Variable Immunodeficiency, Specific Antibody Deficiency, or unspecified hypogammaglobulinemia, who contracted COVID-19. Severity scores were determined to evaluate the clinical outcomes of these patients. Results Of our 15-patient cohort, 33% of individuals with a humoral immunodeficiency infected with COVID-19 had moderate to severe disease, requiring hospitalization or resulting in death. COVID-19 mortality rate was found to be 7%. All 5 of our patients with severe COVID-19 infection had at least 1 comorbidity or risk factor. Conclusion Within our cohort of humoral immunodeficient patients infected with COVID-19, we found a higher rate of moderate to severe COVID-19 infection and worse clinical outcomes, particularly in patients with comorbidities or risk factors.

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Miyasaka, Yoshiki, Jinxi Wang, Kosuke Hattori, Yuko Yamauchi, Miho Hoshi, Kazuto Yoshimi, Saeko Ishida, and Tomoji Mashimo. "A high-quality severe combined immunodeficiency (SCID) rat bioresource." PLOS ONE 17, no. 8 (August 12, 2022): e0272950. http://dx.doi.org/10.1371/journal.pone.0272950.

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Immunodeficient animals are valuable models for the engraftment of exogenous tissues; they are widely used in many fields, including the creation of humanized animal models, as well as regenerative medicine and oncology. Compared with mice, laboratory rats have a larger body size and can more easily undergo transplantation of various tissues and organs. Considering the absence of high-quality resources of immunodeficient rats, we used the CRISPR/Cas9 genome editing system to knock out the interleukin-2 receptor gamma chain gene (Il2rg) in F344/Jcl rats—alone or together with recombination activating gene 2 (Rag2)—to create a high-quality bioresource that researchers can freely use: severe combined immunodeficiency (SCID) rats. We selected one founder rat with frame-shift mutations in both Il2rg (5-bp del) and Rag2 ([1-bp del+2-bp ins]/[7-bp del+2-bp ins]), then conducted mating to establish a line of immunodeficient rats. The immunodeficiency phenotype was preliminarily confirmed by the presence of severe thymic hypoplasia in Il2rg-single knockout (sKO) and Il2rg/Rag2-double knockout (dKO) rats. Assessment of blood cell counts in peripheral blood showed that the white blood cell count was significantly decreased in sKO and dKO rats, while the red blood cell count was unaffected. The decrease in white blood cell count was mainly caused by a decrease in lymphocytes. Furthermore, analyses of lymphocyte populations via flow cytometry showed that the numbers of B cells (CD3- CD45+) and natural killer cells (CD3- CD161+) were markedly reduced in both knockout rats. In contrast, T cells were markedly reduced but showed slightly different results between sKO and dKO rats. Notably, our immunodeficient rats do not exhibit growth retardation or gametogenesis defects. This high-quality SCID rat resource is now managed by the National BioResource Project in Japan. Our SCID rat model has been used in various research fields, demonstrating its importance as a bioresource.

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Farah, C. S., S. Elahi, K. Drysdale, G. Pang, T. Gotjamanos, G. J. Seymour, R. L. Clancy, and R. B. Ashman. "Primary Role for CD4+ T Lymphocytes in Recovery from Oropharyngeal Candidiasis." Infection and Immunity 70, no. 2 (February 2002): 724–31. http://dx.doi.org/10.1128/iai.70.2.724-731.2002.

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ABSTRACT Oropharyngeal candidiasis is associated with defects in cell-mediated immunity and is commonly seen in human immunodeficiency virus positive individuals and AIDS patients. A model for oral candidiasis in T-cell-deficient BALB/c and CBA/CaH nu/nu mice was established. After inoculation with 108 Candida albicans yeasts, these mice displayed increased levels of oral colonization compared to euthymic control mice and developed a chronic oropharyngeal infection. Histopathological examination of nu/nu oral tissues revealed extensive hyphae penetrating the epithelium, with polymorphonuclear leukocyte microabscess formation. Adoptive transfer of either naive or immune lymphocytes into immunodeficient mice resulted in the recovery of these animals from the oral infection. Reconstitution of immunodeficient mice with naive CD4+ but not CD8+ T cells significantly decreased oral colonization compared to controls. Interleukin-12 and gamma interferon were detected in the draining lymph nodes of immunodeficient mice following reconstitution with naive lymphocytes. This study demonstrates the direct requirement for T lymphocytes in recovery from oral candidiasis and suggests that this is associated with the production of cytokines by CD4+ T helper cells.

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Zolotnickaya, V. P., A. A. Speranskaya, V. I. Amosov, and A. O. Agafonov. "DIFFICULTY OF PNEUMONIA IMAGING IN A PATIENT WITH CHRONIC LYMPHATIC LEUKEMIA." Diagnostic radiology and radiotherapy, no. 2 (July 18, 2018): 72–78. http://dx.doi.org/10.22328/2079-5343-2018-9-2-72-78.

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In patients with chronic lymphocytic leukemia, pneumonia and tuberculosis are the dominant complications that play a major role in the outcome of the disease and lead to a fatal outcome. The purpose of the study: to carry out an analysis of computer tomographic complications semiotics in comparison with clinical and pathomorphological data. Results: A patient with chronic immunodeficiency diagnosed with 2-sided pneumonia, H1N1 influenza was verified. At the time, tuberculosis was not verified and pathogenetic treatment was not initiated, which led to a fatal outcome. Conclusion: the complexity of clinical and radiation pattern against the background of immunodeficiency state (CLL) cause difficulties in diagnosing. It is necessary to remember the possibility of rapid development of caseous pneumonia against the background of a combined pathology in immunodeficient conditions requiring phthisiatric consultation for the timely administration of anti-tuberculosis therapy.

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AMBROISE-THOMAS, P. "Parasitic diseases and immunodeficiencies." Parasitology 122, S1 (March 2001): S65—S71. http://dx.doi.org/10.1017/s0031182000017339.

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In the last two decades, major immunodeficiency syndromes have strongly influenced medical parasitology. Some animal parasitoses, once unknown in human medicine, have become zoonotic and sometimes anthroponotic. In other cases, the clinical evolution of human parasitoses has been severely aggravated and/or modified in immunodeficient patients especially in toxoplasmosis, cryptosporidiosis, leishmaniasis, strongyloidiasis and scabies. The parasites implicated are varied (protozoa, helminths and even Acaridae) but have in common the capacity to reproduce in or on the human host. These immunodeficiency syndromes are often related to AIDS but other major immunodepressions, such as post-therapeutically in organ transplantation, may also be responsible and raise difficult problems for prevention. The immunological mechanisms involved are not always well understood. In addition, genetic predisposition factors, gradually becoming better-understood in parasites and man, complete and complicate our understanding of the immunological mechanisms.

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Arulprakash, Narenraj, Lavanya Narayanan, and Senthil Narayanan. "A Young Patient with Stroke and Primary Tuberculosis." Journal of Neurosciences in Rural Practice 09, no. 04 (October 2018): 613–15. http://dx.doi.org/10.4103/jnrp.jnrp_59_18.

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ABSTRACTA 21-year-old woman presented with left hemiparesis, fever, dyspnea, tachycardia, and pericardial rub on examination. She was provisionally diagnosed with infective endocarditis and received the final diagnosis of the primary pulmonary tuberculosis (PTB) and extra PTB (EPTB) with pericardial effusion and thoracic lymphadenitis. Left hemiparesis due to a pontine infarct was attributed to TB with neurovasculitis. The diagnosis was supported by findings on imaging studies such as echocardiography, computed tomography of the thorax, and magnetic resonance imaging of the brain. She improved with anti-TB treatment. It is interesting to note that she was not immunodeficient, with the usual suspects such as acquired immunodeficiency syndrome, diabetes mellitus, and renal failure ruled out. We conclude that PTB and EPTB must be considered in any febrile illness, even in patients who are not immunodeficient, considering its atypical presentation and prevalence in India.

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Silva Júnior, Sergio Vital da, Wilton José de Carvalho Silva, Natalia Silva Lourenço, Jordana Almeida Nogueira, Ana Cristina de Oliveira e Silva, and Maria Eliane Moreira Freire. "Quality of life of people living with the human immunodeficiency virus and acquired immunodeficiency syndrome." Rev Rene 20 (May 9, 2019): e39638. http://dx.doi.org/10.15253/2175-6783.20192039638.

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Dekate, Jyoti, and Runjan Chetty. "Epstein-Barr Virus–Associated Smooth Muscle Tumor." Archives of Pathology & Laboratory Medicine 140, no. 7 (July 1, 2016): 718–22. http://dx.doi.org/10.5858/arpa.2015-0120-rs.

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Immunodeficient individuals are prone to develop a number of opportunistic infections and unique neoplasms. Epstein-Barr virus–associated smooth muscle tumor is an uncommon neoplasm associated with immunodeficiency. It has been described in patients infected with human immunodeficiency virus, in the posttransplant setting, and in those with congenital immunodeficiency. Different anatomic sites can be involved by Epstein-Barr virus–associated smooth muscle tumor, and even multiple locations can contain these unique lesions within the same patient. The presence of variable numbers of intratumoral lymphocytes and primitive round cell areas are the unique defining features for this tumor. Histopathologic features may vary considerably in terms of cellular atypia, mitotic activity, and necrosis, with no correlation to the clinical behavior. Demonstration of Epstein-Barr virus infection by in situ hybridization within tumor cell remains critical for the diagnosis. The mechanism for Epstein-Barr virus infection of progenitor cells and neoplastic transformation has been an area of interest and conjecture. Different treatment strategies are proposed according to underlying disease status. This paper reviews the clinicopathologic features of this uncommon neoplasm with detailed discussion of the role of Epstein-Barr virus in the pathogenesis.

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Coelho, K. I. R., S. A. Maeda, and M. E. A. Marques. "Intestinal cryptosporidiosis. association with Pneumocystis carinii, cytomegalovirus and Candida sp. Infections." Revista do Instituto de Medicina Tropical de São Paulo 29, no. 5 (October 1987): 323–26. http://dx.doi.org/10.1590/s0036-46651987000500010.

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This is a case report of intestinal cryptosporidiosis diagnosed in histological specimen collected from autopsy. The patient was a child of 5 months admitted to the hospital with severe acute diarrhea associated with Pneumocystis carinii pneumonia, cytomegalic sialadenitis, oral and dermal candidiasis. The presence of multiple opportunistic infections in this case indicated immunodeficiency state. Cryptosporidium sp is a possible etiology of acute diarrhea in both immunodeficient and immunocompetent patients and has to be searched for at autopsy when diagnosis was not possible "in vivo".

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Kumar, Shimareet, Mariarita Santi, Gilbert Vezina, Tena Rosser, Roma S. Chandra, and Robert Keating. "Epstein-Barr Virus-Associated Smooth Muscle Tumor of the Basal Ganglia in an HIV+ Child: Case Report and Review of the Literature." Pediatric and Developmental Pathology 7, no. 2 (March 2004): 198–203. http://dx.doi.org/10.1007/s10024-003-7079-2.

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We describe the clinicopathologic features of an Epstein-Barr virus (EBV)-associated smooth muscle tumor arising in the basal ganglia of a 10-year-old human immunodeficiency virus (HIV)-positive child. Only a few cases of intracranial smooth muscle tumors are reported in the literature and virtually all of these have been extra-axial, involving the dura or sinuses in HIV+ adults. Our case underscores the need to include an EBV-associated smooth muscle tumor in the differential diagnosis when evaluating intracranial mass lesions in immunodeficient children.

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Wesołowski, Roland, Marta Pawłowska, Małgorzata Smoguła, and Karolina Szewczyk-Golec. "Advances and Challenges in Diagnostics of Toxoplasmosis in HIV-Infected Patients." Pathogens 12, no. 1 (January 9, 2023): 110. http://dx.doi.org/10.3390/pathogens12010110.

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Toxoplasma gondii is a worldwide distributed protozoan parasite. This apicomplexan parasite infects one-third of the population worldwide, causing toxoplasmosis, considered one of the neglected parasitic infections. In healthy humans, most infections are asymptomatic. However, in immunocompromised patients, the course of the disease can be life-threatening. Human immunodeficiency virus (HIV)-infected patients have a very high burden of Toxoplasma gondii co-infection. Thus, it is essential to use modern, sensitive, and specific methods to properly monitor the course of toxoplasmosis in immunodeficient patients.

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Florea, Anca V., Diana N. Ionescu, and Mona F. Melhem. "Parvovirus B19 Infection in the Immunocompromised Host." Archives of Pathology & Laboratory Medicine 131, no. 5 (May 1, 2007): 799–804. http://dx.doi.org/10.5858/2007-131-799-pbiiti.

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Abstract Human parvovirus B19 is a single-stranded DNA virus with a predilection for infecting rapidly dividing cell lines, such as bone marrow erythroid progenitor cells. People with defective cell-mediated immunity (eg, severe combined immunodeficiency syndrome; acquired immunodeficiency syndrome; and patients receiving immunosuppressive therapy, ie, post organ transplant) can develop pure red cell aplasia, in which suppression of erythroid precursors is permanent. Identification of parvovirus inclusions in marrow biopsies and subsequent confirmation of infection by in situ hybridization is important in the assessment of anemia in immunodeficient patients. Our objective is to provide a general overview of the parvovirus B19 infection and its characteristics in immunocompromised patients and to summarize updated information regarding the clinicopathologic features, pathobiology, and laboratory diagnosis of this subject. The pathologist should be aware of the wide spectrum of manifestations of parvovirus B19 infection depending on the patient's hematologic and immunologic status.

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Sleasman, J. W. "The Association Between Immunodeficiency and the Development of Autoimmune Disease." Advances in Dental Research 10, no. 1 (April 1996): 57–61. http://dx.doi.org/10.1177/08959374960100011101.

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There is a paradoxical relationship between immunodeficiency diseases and autoimmunity. While not all individuals with immunodeficiency develop autoimmunity, nor are all individuals with autoimmunity immunodeficient, defects within certain components of the immune system carry a high risk for the development of autoimmune disease. Inherited deficiencies of the complement system have a high incidence of systemic lupus erythematosus (SLE), glomerulonephritis, and vasculitis. Carrier mothers of children with chronic granulomatous disease, an X-linked defect of phagocytosis, often develop discoid lupus. Several antibody deficiencies are associated with autoimmune disease. Autoimmune cytopenias are commonly observed in individuals with selective IgA deficiency and common variable immune deficiency. Polyarticular arthritis can be seen in children with X-linked agammaglobulinemia. Combined cellular and antibody deficiencies, such as Wiskott-Aldrich syndrome, carry an increased risk for juvenile rheumatoid arthritis and autoimmune hemolytic anemia. Several hypothetical mechanisms have been proposed to explain the associations between autoimmunity and immunodeficiency. Immunologic defects may result in a failure to exclude microbial antigens, resulting in chronic immunologic activation and autoimmune symptoms. There may be shared genetic factors, such as common HLA alleles, which predispose an individual to both autoimmunity and immunodeficiency. Defects within one component of the immune system may alter the way a pathogen induces an immune response and lead to an inflammatory response directed at self-antigens. An understanding of the immunologic defects that contribute to the development of autoimmunity will provide an insight into the pathogenesis of the autoimmune process.

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Feichtinger, H., S. L. Li, E. Kaaya, P. Putkonen, K. Grünewald, K. Weyrer, D. Böttiger, I. Ernberg, A. Linde, and G. Biberfeld. "A monkey model for Epstein Barr virus-associated lymphomagenesis in human acquired immunodeficiency syndrome." Journal of Experimental Medicine 176, no. 1 (July 1, 1992): 281–86. http://dx.doi.org/10.1084/jem.176.1.281.

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High-grade malignant nonHodgkin's lymphomas--five lymphoblastic, three pleomorphic, and two immunoblastic--developed in 10/25 cynomolgus monkeys (Macaca fascicularis) followed for up to 746 d after infection with simian immunodeficiency virus, strain SIVsm. These lymphomas were shown to be associated with an Epstein-Barr (EB)-like cynomolgus B-lymphotropic herpesvirus (CBLV) by electron microscopy, by Southern blot hybridization with probes against human EBV, and by the expression of antigens corresponding to EBV-associated nuclear antigens (EBNAs) involved in human B cells transformation. Southern blot demonstration of immunoglobulin gene rearrangements and homogeneous EBV episomes indicated that all the lymphomas were CBLV-associated monoclonal B cell proliferations. Our findings suggest that these tumors correspond to the EBV-associated malignant lymphomas in acquired immunodeficiency syndrome with respect to clinical, morphological, phenotypic, and genotypic characteristics. The particular susceptibility of SIVsm immunodeficient cynomolgus monkeys for CBLV-associated lymphomagenesis appears therefore a useful model for EBV-associated lymphomas in humans.

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Tonomura, Noriko, Katsuyoshi Habiro, Akira Shimizu, Megan Sykes, and Yong-Guang Yang. "Antigen-specific human T-cell responses and T cell–dependent production of human antibodies in a humanized mouse model." Blood 111, no. 8 (April 15, 2008): 4293–96. http://dx.doi.org/10.1182/blood-2007-11-121319.

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Abstract Humanized mice with a functional human immune system would be very useful for in vivo studies of human immunobiology. We have previously shown that cotransplantation of human fetal thymus/liver tissues and CD34+ fetal liver cells into immunodeficient nonobese diabetic severe combined immunodeficiency (NOD/SCID) mice leads to the development of multiple lineages of human lymphohematopoietic cells and formation of secondary lymphoid organs with normal architecture. Here, we evaluated the ability of these humanized mice to develop antigen-specific, T cell–dependent antibody responses after in vivo immunization with T-dependent antigen, 2,4-dinitrophenyl hapten-keyhole limpet hemocyanin (DNP23-KLH). Human T cells from DNP23-KLH–immunized mice showed strong proliferation in response to KLH in vitro. Furthermore, T cell–dependent production of DNP-specific human antibodies (mainly IgG1 and IgG2) was detected in all immunized mice. These results confirm that a functional human immune system can be established in immunodeficient mice through cotransplantation of human fetal thymus/liver tissues and CD34+ hematopoietic stem/progenitor cells.

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Santangelo, Michele L., Carmen Criscitiello, Andrea Renda, Stefano Federico, Giuseppe Curigliano, Concetta Dodaro, Alessandro Scotti, et al. "Immunosuppression and Multiple Primary Malignancies in Kidney-Transplanted Patients: A Single-Institute Study." BioMed Research International 2015 (2015): 1–8. http://dx.doi.org/10.1155/2015/183523.

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Immunodeficiency is associated with higher cancer incidence. However, it is unknown whether there is a link between immunodeficiency and development of multiple primary malignancies. In the present study we analyse this link focusing on kidney-transplanted patients, as they are at higher risk of developing cancer due to the chronic assumption of immunosuppressants. We followed up 1200 patients who underwent kidney transplantation between 1980 and 2012. A total of 77/1200 kidney-transplanted patients developed cancer and 24 of them developed multiple cancers. Most multiple cancers were synchronous with a nonsignificant association between cancer and rejection episodes. In the general cancer population, one-ninth of patients are at higher risk of developing a second tumor over a lifetime; hence it would be reasonable to conclude that, from a merely theoretical and statistical viewpoint, long-term transplanted patients potentially have a higher risk of developing MPMs. However, data did not confirm this assumption, probably because these patients die before a second primary malignancy appears. Despite many observations on the increased incidence of different tumor types in immunodeficient patients and despite immunosuppression certainly being a predisposing factor for the multicancer syndrome, data so far are not robust enough to justify a correlation between immunodeficiency and multiple primary malignancies in transplanted patients.

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Matsushita, Shuzo. "Human immunodeficiency virus (HIV) infection/acquired immunodeficiency syndrome (AIDS) and intensive care unit." Journal of the Japanese Society of Intensive Care Medicine 14, no. 3 (2007): 260–62. http://dx.doi.org/10.3918/jsicm.14.260.

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Ogrodowczyk, Marta, Natalia Olszak, Karolina Pietraszewska, and Bożena Polańska. "Иммунные расстройства у детей с чертами дисморфии." Paediatrics & Family Medicine 2, no. 2 (June 30, 2015): 135–46. http://dx.doi.org/10.15557/pfm.2015.0013.

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Eddy Warman, Nur ‘Aini, and Nurul Yaqeen Mohd Esa. "A Rare and Challenging Case of Pulmonary Mycobacterium genavense in an Immunocompetent Adult." Journal of Clinical and Health Sciences 3, no. 1 (June 30, 2018): 47. http://dx.doi.org/10.24191/jchs.v3i1.6158.

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Mycobacterium genavense, a non-tuberculous mycobacterium (NTM), usually affects patients severely immunodeficient from human immunodeficiency virus (HIV) infection or any other immunocompromised states. We reported a case in a 70-year-old female with well-controlled diabetes and history of proximal cystic bronchiectasis. She presented with 2 months history of cough, haemoptysis, and night sweats of which serial sputa were positive for acid-fast bacilli and the culture repeatedly grew M. genavense. Treatment with rifampicin, ofloxacin, and clarithromycin was complicated with drug-induced liver injury and intractable gastrointestinal side effects. We also presented a brief review of relevant literature.

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Hartsfield, C. L., D. Lipke, Y. L. Lai, D. A. Cohen, and M. N. Gillespie. "Pulmonary mechanical and immunologic dysfunction in a murine model of AIDS." American Journal of Physiology-Lung Cellular and Molecular Physiology 272, no. 4 (April 1, 1997): L699—L706. http://dx.doi.org/10.1152/ajplung.1997.272.4.l699.

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Human immunodeficiency virus-infected patients occasionally exhibit alveolar septal wall thickening and decreases in gas diffusion capacity, but the mechanism underlying these abnormalities is unknown. The present study evaluated septal wall thickness and gas exchange properties in a murine model of the acquired immunodeficiency syndrome and determined whether there were alterations in lung lymphocyte deposition and activation that could contribute to changes in respiratory structure and function. Although alveolar septal wall thickness did not differ from control at 1, 2, and 4 wk postimmunosuppressive virus infection, at 8 wk after infection, septal wall thickness was substantially increased. Immunohistochemical evaluation at this time revealed marked increases in the septal wall deposition of fibronectin and collagen type IV. Pulmonary function tests on anesthetized mice with virus-induced septal wall thickening demonstrated that, although total lung capacity, compliance, and functional residual capacity were unaltered, diffusion capacity for carbon monoxide was significantly impaired. A diffuse nonspecific interstitial pneumonitis was present in lungs of immunodeficient mice, and flow cytometry indicated that both lymphocytes and macrophages were activated. Reverse transcriptase-polymerase chain reaction analysis of lung lymphocytes demonstrated enhanced mRNA expression for several cytokines known to affect lung structure. These results show that impaired gas exchange occurs in a murine model of acquired immunodeficiency syndrome and suggest that such alterations may be mediated by elaboration of cytokines from activated lung lymphocytes and macrophages.

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Morio, T., M. Nagasawa, S. Nonoyama, H. Okawa, and J. Yata. "Phenotypic profile and functions of T cell receptor-gamma delta-bearing cells from patients with primary immunodeficiency syndrome." Journal of Immunology 144, no. 4 (February 15, 1990): 1270–75. http://dx.doi.org/10.4049/jimmunol.144.4.1270.

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Abstract TCR-gamma delta-bearing T cells have been reported to be increased in several immunodeficient patients. However, their functional role and phenotypic characterization have not yet been well documented. In this study we examined the surface phenotypes and functional properties of TCR-gamma delta+ cells from several patients with primary immunodeficiency syndrome. It was demonstrated that TCR-gamma delta+ cells detected by TCR-delta 1 mAb were increased in some of the patients, particularly in patients with Wiskott-Aldrich syndrome and severe combined immune deficiency. The TCR-gamma delta+ cells showed such a unique profile that more than 60% of the cells expressed delta-TCS1, which is normally present in a lesser amount, and that most of the cells lacked CD5 T lineage marker. TCR-gamma delta+ cells from the patients with primary immunodeficiency syndrome served as NK cells as observed in normal individuals, while displaying weak LAK and allogeneic cell-specific killer activities. The TCR-gamma delta+ cells were classified into several subpopulations according to their antigenic phenotype, then their NK activity of normal individuals and patients, lymphokine-activated killer and allo-specific killer activities of normal individuals were compared among the subpopulations. Delta-TCS1+ cells mediated almost the same killer activities as total TCR-gamma delta+ cells, whereas CD8+ TCR-gamma delta+ cells displayed stronger cytotoxic activities in both normal subjects and the patients with primary immunodeficiency syndrome.

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Roths, J. B., A. L. Smith, and C. L. Sidman. "Lethal exacerbation of Pneumocystis carinii pneumonia in severe combined immunodeficiency mice after infection by pneumonia virus of mice." Journal of Experimental Medicine 177, no. 4 (April 1, 1993): 1193–98. http://dx.doi.org/10.1084/jem.177.4.1193.

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Mice homozygous for the mutant allele scid (severe combined immunodeficiency) have been described as excellent models for Pneumocystis carinii (Pc) pneumonia (PCP), a major health problem in patients with acquired immune deficiency syndrome (AIDS) and other immunodeficiency states. Other microorganisms have been shown to infect AIDS patients simultaneously with Pc, but whether one opportunist is able to directly influence the pathogenicity of another has not been determined previously. We have deliberately coinfected scid mice (with extent Pc infection) with a variety of primarily pneumotropic viruses and bacteria and have identified pneumonia virus of mice as causing a dramatic increase in the density of Pc organisms and the morbidity due to PCP in immunodeficient scid mice. This finding has clinical significance in the management of PCP, in that the identification and treatment of coinfecting pneumotropic pathogens may be as important as treatment targeted at Pc. A search for other synergistic (or antagonistic) microorganisms and determination of their mechanism(s) of action in altering the progression of PCP is indicated.

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Kechichian, Talar B., John Shea, and Maurizio Del Poeta. "Depletion of Alveolar Macrophages Decreases the Dissemination of a Glucosylceramide-Deficient Mutant of Cryptococcus neoformans in Immunodeficient Mice." Infection and Immunity 75, no. 10 (July 30, 2007): 4792–98. http://dx.doi.org/10.1128/iai.00587-07.

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ABSTRACT In previous studies we showed that a Cryptococcus neoformans mutant lacking glucosylceramide (Δgcs1) is avirulent and unable to reach the brain when it is administered intranasally into an immunocompetent mouse and is contained in a lung granuloma. To determine whether granuloma formation is key for containment of C. neoformans Δgcs1, we studied the role of C. neoformans glucosylceramide in a T- and NK-cell-immunodeficient mouse model (Tgε26) in which alveolar macrophages (AMs) are not activated and granuloma formation is not expected. The results show that Tgε26 mice infected with Δgcs1 do not produce a lung granuloma and that the Δgcs1 mutant proliferates in the lungs and does disseminate to the brain, although its virulence phenotype is dramatically reduced. Since Δgcs1 can grow only in acidic niches, such as the phagolysosome of AMs, and not in neutral or alkaline environments, such as the extracellular spaces, we hypothesize that in immunodeficient mice Δgcs1 proliferates inside AMs. Indeed, we found that depletion of AMs significantly improved Tgε26 mouse survival and decreased the dissemination of Δgcs1 cells to the central nervous system. Thus, these results suggest that the growth of Δgcs1 in immunodeficient mice is maintained within AMs. This study highlights the hypothesis that AMs may exacerbate C. neoformans infection in conditions in which there is severe host immunodeficiency.

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Hsieh, Chu-Han, Peng-Chieh Chen, and Chi-Chang Shieh. "Novel SLC5A6 Mutations Lead to B Lymphocyte Maturation Defects with Metabolic Abnormality Rescuable by Biotin Replenishment." Journal of Immunology 208, no. 1_Supplement (May 1, 2022): 168.03. http://dx.doi.org/10.4049/jimmunol.208.supp.168.03.

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Abstract Primary immunodeficiencies (PIDs) comprise inherited genetic mutations with a wide spectrum of clinical immune manifestations. We enrolled a seven-years-old female patient whose clinical laboratory tests showed very low levels of all five isotypes of immunoglobulins but with normal numbers of T cells and B cells. By using whole exome sequencing (WES) on the patient and family members, we identified a novel compound heterozygous gene mutations (termed SLC5A6 mutations) in the patient and her deceased elder sister. We successfully established a CRISPR-Cas9 mouse model bearing the same mutation gene from our patient and provide a further chance to investigate detailed mechanism underlie primary immunodeficiency. We found that biotin deficiency because of SLC5A6 mutations lead to defective B cell maturation and antibody insufficiency. We also found that aberrant cellular metabolism profile due to biotin deficiency restrain the efficiency of plasma cell formation and functions. Furthermore, biotin replenishment can not only rescue cellular TCA cycle but also ameliorate immunodeficient phenotypes including antibody insufficiency in patient and in our mouse model. Our results demonstrated the pivotal role of metabolic reprogramming in B cell terminal differentiation and indicated that SLC5A6 is a causative gene for immunodeficiency.

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Andoh, Masako, Takashi Naganawa, Akitoyo Hotta, Tsuyoshi Yamaguchi, Hideto Fukushi, Toshiaki Masegi, and Katsuya Hirai. "SCID Mouse Model for Lethal Q Fever." Infection and Immunity 71, no. 8 (August 2003): 4717–23. http://dx.doi.org/10.1128/iai.71.8.4717-4723.2003.

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ABSTRACT Q fever, a worldwide zoonosis caused by Coxiella burnetii, has many manifestations in humans. Endocarditis is the most serious complication of Q fever. Animal models are limited to acute pulmonary or hepatic disease and reproductive disorders. An appropriate experimental animal model for Q fever endocarditis does not yet exist. In this study, severe combined immunodeficient (SCID) mice infected with C. burnetii showed persistent clinical symptoms and died, whereas immunocompetent mice similarly infected became asymptomatic and survived. The SCID mice examined in this study had severe chronic lesions in their primary organs: the heart, lung, spleen, liver, and kidney. The heart lesions of the SCID mice were similar to those in humans with chronic Q fever endocarditis: they had focal calcification and expanded macrophages containing C. burnetii. The 50% lethal dose of C. burnetii in SCID mice was at least 108 times less than that in immunocompetent mice. The SCID mouse is highly susceptible to C. burnetii, and the immunodeficiency of the host enhances the severity of Q fever. This animal model could provide a new tool for the study of chronic Q fever and Q fever in immunodeficient hosts.

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Hitoshi, Y., Y. Okada, E. Sonoda, A. Tominaga, M. Makino, K. Suzuki, J. Kinoshita, K. Komuro, T. Mizuochi, and K. Takatsu. "Delayed progression of a murine retrovirus-induced acquired immunodeficiency syndrome in X-linked immunodeficient mice." Journal of Experimental Medicine 177, no. 3 (March 1, 1993): 621–26. http://dx.doi.org/10.1084/jem.177.3.621.

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The murine acquired immunodeficiency syndrome (MAIDS) caused by defective LP-BM5 murine leukemia virus (MuLV) is a disease that shows severe immunodeficiency with abnormal lymphoproliferation, and hypergammaglobulinemia in susceptible C57BL/6 (B6) mice. To examine the cellular mechanisms of development of MAIDS, we injected LP-BM5 MuLV intraperitoneally into B6 mice bearing the X chromosome-linked immunodeficiency (xid). xid mice lack functionally mature B cells including Ly-1 B cells (also known as B-1 cells). All B6 mice died by 20 wk after LP-BM5 MuLV inoculation. In marked contrast, xid mice have continued to survive without any sign of MAIDS-related symptoms till at least 20 wk after the inoculation. The delayed progression of MAIDS in xid mice appears to depend on xid mutation, according to our experiments using both sexes of (B6.xid x B6)F1 and (B6 x B6.xid)F1 mice. Furthermore, Ly-1 B cells, enriched by a FACS, were shown to integrate the defective genome and appeared to be a major virus-infected B cell population. Our data corroborate that Ly-1 B cells play an important role in the induction and progression of MAIDS.

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Shams, Saeed, Niloofar Rezaie, Anna Beltrame, Lucia Moro, Chiara Piubelli, Fahimeh Bagheri Amiri, and Saber Esmaeili. "Tropheryma whipplei intestinal colonization in immunocompromised children in Iran: a preliminary study." Future Microbiology 16, no. 15 (October 2021): 1161–66. http://dx.doi.org/10.2217/fmb-2021-0091.

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Aim & method: Tropheryma whipplei causes Whipple’s disease. Children are reservoirs of this bacterium. The aim of this study was to investigate the presence of T. whipplei in children with immunodeficiency in central Iran from July 2018 to February 2019. Stool samples were tested by SYBR Green and Taq-Man real-time PCR assays. For confirmation, the isolated DNA was sequenced. Results: One hundred and thirty children were enrolled. Acute lymphocytic leukemia was the most reported immunodeficient disease (77%), followed by non-Hodgkin lymphoma and retinoblastoma. Thirteen (10%) children had T. whipplei DNA in the stool; 11.4% of the children under 5 years old were positive. Conclusion: This is the first study showing the circulation of T. whipplei in Iran.

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Pai, Sung-Yun, Kathryn Lurain, and Robert Yarchoan. "How immunodeficiency can lead to malignancy." Hematology 2021, no. 1 (December 10, 2021): 287–95. http://dx.doi.org/10.1182/hematology.2021000261.

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Abstract Immunodeficiency, whether acquired in the case of human immunodeficiency virus (HIV) infection or congenital due to inborn errors of immunity (IEIs), presents clinically with not only infection and immune dysregulation but also increased risk of malignancy. The range of malignancies seen is relatively limited and attributable to the particular cellular and molecular defects in each disease. CD4+ T-cell lymphopenia in people living with HIV infection (PLWH) and certain IEIs drive the predisposition to aggressive B-cell non-Hodgkin lymphomas, including certain rare subtypes rarely seen in immunocompetent individuals. PLWH and IEI that lead to profound T-cell lymphopenia or dysfunction also are at risk of cancers related to oncogenic viruses such as Kaposi sarcoma herpesvirus, Epstein-Barr virus, human papillomavirus (HPV), and Merkel cell polyomavirus. IEIs that affect natural killer cell development and/or function heavily predispose to HPV-associated epithelial cancers. Defects in DNA repair pathways compromise T- and B-lymphocyte development during immune receptor rearrangement in addition to affecting hematopoietic and epithelial DNA damage responses, resulting in both hematologic and nonhematologic cancers. Treatment of cancers in immunodeficient individuals should be curative in intent and pursued in close consultation with disease experts in immunology and infectious disease.

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Hunter, Paul R., and Gordon Nichols. "Epidemiology and Clinical Features of Cryptosporidium Infection in Immunocompromised Patients." Clinical Microbiology Reviews 15, no. 1 (January 2002): 145–54. http://dx.doi.org/10.1128/cmr.15.1.145-154.2002.

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SUMMARY Cryptosporidium spp. are a major cause of diarrheal disease in both immunocompetent and immunodeficient individuals. They also cause waterborne disease in both the United States and United Kingdom. Studies on the mechanisms of immunity to cryptosporidiosis indicate the importance of the T-cell response. The spectrum and severity of disease in immunocompromised individuals with cryptosporidiosis reflect this importance since the most severe disease is seen in individuals with defects in the T-cell response. The most commonly studied group is that of patients with AIDS. These patients suffer from more severe and prolonged gastrointestinal disease that can be fatal; in addition, body systems other than the gastrointestinal tract may be affected. The widespread use of antiretroviral therapy does appear to be having a beneficial effect on recovery from cryptosporidiosis and on the frequency of infection in human immunodeficiency virus-positive patients. Other diseases that are associated with increased risk of severe cryptosporidiosis, such as primary immunodeficiencies, most notably severe combined immunodeficiency syndrome, are also predominantly associated with T-cell defects. Of the remaining groups, children with acute leukemia seem to be most at risk from cryptosporidiosis. There is less evidence of severe complications in patients with other malignant diseases or in those receiving immunosuppressive chemotherapy.

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Lev, Atar, Amos J. Simon, Luba Trakhtenbrot, Itamar Goldstein, Meital Nagar, Polina Stepensky, Gideon Rechavi, Ninette Amariglio, and Raz Somech. "Characterizing T Cells in SCID Patients Presenting with Reactive or Residual T Lymphocytes." Clinical and Developmental Immunology 2012 (2012): 1–9. http://dx.doi.org/10.1155/2012/261470.

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Introduction. Patients with severe combined immunodeficiency (SCID) may present with residual circulating T cells. While all cells are functionally deficient, resulting in high susceptibility to infections, only some of these cells are causing autoimmune symptoms.Methods. Here we compared T-cell functions including the number of circulating CD3+T cells,in vitroresponses to mitogens, T-cell receptor (TCR) repertoire, TCR excision circles (TREC) levels, and regulatory T cells (Tregs) enumeration in several immunodeficinecy subtypes, clinically presenting with nonreactive residual cells (MHC-II deficiency) or reactive cells. The latter includes patients with autoreactive clonal expanded T cell and patients with alloreactive transplacentally maternal T cells.Results. MHC-II deficient patients had slightly reduced T-cell function, normal TRECs, TCR repertoires, and normal Tregs enumeration. In contrast, patients with reactive T cells exhibited poor T-cell differentiation and activity. While the autoreactive cells displayed significantly reduced Tregs numbers, the alloreactive transplacentally acquired maternal lymphocytes had high functional Tregs.Conclusion. SCID patients presenting with circulating T cells show different patterns of T-cell activity and regulatory T cells enumeration that dictates the immunodeficient and autoimmune manifestations. We suggest that a high-tolerance capacity of the alloreactive transplacentally acquired maternal lymphocytes represents a toleration advantage, yet still associated with severe immunodeficiency.

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Klein, C., M. Cavazzana-Calvo, F. Le Deist, N. Jabado, M. Benkerrou, S. Blanche, B. Lisowska-Grospierre, C. Griscelli, and A. Fischer. "Bone marrow transplantation in major histocompatibility complex class II deficiency: a single-center study of 19 patients." Blood 85, no. 2 (January 15, 1995): 580–87. http://dx.doi.org/10.1182/blood.v85.2.580.580.

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Abstract Major histocompatibility complex (MHC) class II deficiency (bare lymphocyte syndrome) is a rare inborn error of the immune system characterized by impaired antigen presentation and combined immunodeficiency. It causes severe and unremitting infections leading to progressive liver and lung dysfunctions and death during childhood. As in other combined immunodeficiency disorders, bone marrow transplantation (BMT) is considered the treatment of choice for MHC class II deficiency. We analyzed the files of 19 patients who have undergone BMT in our center. Of the 7 patients who underwent HLA- identical BMT, 3 died in the immediate posttransplant period of severe viral infections, whereas the remaining 4 were cured, with recovery of normal immune functions. Of the 12 patients who underwent HLA-haplo- identical BMT, 3 were cured, 1 was improved by partial engraftment, 7 died of infectious complications due to graft failure or rejection, and 1 is still immunodeficient because of engraftment failure. A favorable outcome in the HLA-non-identical BMT group was associated with an age of less than 2 years at the time of transplantation. All the patients with stable long-term engraftment had persistently low CD4 counts after transplantation (105 to 650/microL at last follow up), but no clear susceptibility to opportunistic infections despite persisting MHC class II deficiency on thymic epithelium and other nonhematopoietic cells. We conclude that HLA-identical and -haploidentical BMT can cure MHC class II deficiency, although the success rate of haploidentical BMT is lower than that in other combined immunodeficiency syndromes. HLA- haploidentical BMT should preferably be performed in the first 2 years of life, before the acquisition of chronic virus carriage and sequelae of infections.

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Klein, C., M. Cavazzana-Calvo, F. Le Deist, N. Jabado, M. Benkerrou, S. Blanche, B. Lisowska-Grospierre, C. Griscelli, and A. Fischer. "Bone marrow transplantation in major histocompatibility complex class II deficiency: a single-center study of 19 patients." Blood 85, no. 2 (January 15, 1995): 580–87. http://dx.doi.org/10.1182/blood.v85.2.580.bloodjournal852580.

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Major histocompatibility complex (MHC) class II deficiency (bare lymphocyte syndrome) is a rare inborn error of the immune system characterized by impaired antigen presentation and combined immunodeficiency. It causes severe and unremitting infections leading to progressive liver and lung dysfunctions and death during childhood. As in other combined immunodeficiency disorders, bone marrow transplantation (BMT) is considered the treatment of choice for MHC class II deficiency. We analyzed the files of 19 patients who have undergone BMT in our center. Of the 7 patients who underwent HLA- identical BMT, 3 died in the immediate posttransplant period of severe viral infections, whereas the remaining 4 were cured, with recovery of normal immune functions. Of the 12 patients who underwent HLA-haplo- identical BMT, 3 were cured, 1 was improved by partial engraftment, 7 died of infectious complications due to graft failure or rejection, and 1 is still immunodeficient because of engraftment failure. A favorable outcome in the HLA-non-identical BMT group was associated with an age of less than 2 years at the time of transplantation. All the patients with stable long-term engraftment had persistently low CD4 counts after transplantation (105 to 650/microL at last follow up), but no clear susceptibility to opportunistic infections despite persisting MHC class II deficiency on thymic epithelium and other nonhematopoietic cells. We conclude that HLA-identical and -haploidentical BMT can cure MHC class II deficiency, although the success rate of haploidentical BMT is lower than that in other combined immunodeficiency syndromes. HLA- haploidentical BMT should preferably be performed in the first 2 years of life, before the acquisition of chronic virus carriage and sequelae of infections.

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Doyle, Patricia S., Yuan M. Zhou, Juan C. Engel, and James H. McKerrow. "A Cysteine Protease Inhibitor Cures Chagas' Disease in an Immunodeficient-Mouse Model of Infection." Antimicrobial Agents and Chemotherapy 51, no. 11 (August 13, 2007): 3932–39. http://dx.doi.org/10.1128/aac.00436-07.

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ABSTRACT Chagas' disease, caused by the parasite Trypanosoma cruzi, remains the leading cause of cardiopathy in Latin America with about 12 million people infected. Classic clinical manifestations derive from infection of muscle cells leading to progressive cardiomyopathy, while some patients develop megacolon or megaesophagus. A very aggressive clinical course including fulminant meningoencephalitis has been reported in patients who contract Chagas' disease in the background of immunodeficiency. This includes patients with human immunodeficiency virus infection as well as patients receiving immunosuppressive therapy for organ transplant. Currently, only two drugs are approved for the treatment of Chagas' disease, nifurtimox and benznidazole. Both have significant limitations due to common and serious side effects as well as limited availability. A promising group of new drug leads for Chagas' disease is cysteine protease inhibitors targeting cruzain, the major protease of T. cruzi. The inhibitor N-methyl-Pip-F-homoF-vinyl sulfonyl phenyl (N-methyl-Pip-F-hF-VSφ) is in late-stage preclinical development. Therefore, the question arose as to whether protease inhibitors targeting cruzain would have efficacy in Chagas' disease occurring in the background of immunodeficiency. To address this question, we studied the course of infection in recombinase-deficient (Rag1−/−) and normal mice infected with T. cruzi. Infections localized to heart and skeletal muscle in untreated normal animals, while untreated Rag1−/− mice showed severe infection in all organs and predominantly in liver and spleen. Treatment with the dipeptide N-methyl-Pip-F-hF-VSφ rescued immunodeficient animals from lethal Chagas' infection. The majority (60 to 100%) of inhibitor-treated Rag1−/− mice had increased survival, negative PCR, and normal tissues by histopathological examination.

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Jalil, Maaz, Marija Rowane, Jayanth Rajan, and Robert Hostoffer. "Successful Anti-SARS-CoV-2 Spike Protein Antibody Response to Vaccination in MAGT1 Deficiency." Allergy & Rhinology 12 (January 2021): 215265672110562. http://dx.doi.org/10.1177/21526567211056239.

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Background Novel messenger RNA vaccines against severe acute respiratory syndrome coronavirus (SARS-CoV-2) have been vital in resolving the coronavirus disease-2019 (COVID-19) pandemic. Detection of neutralizing antibodies (NAbs) against the SARS-CoV-2 spike protein (S) confirms immunogenicity with high sensitivity and specificity. Few recent studies with primary and secondary immunodeficient cohorts present adequate or reduced antibody response. We describe the first reported successful response to anti-SARS-CoV-2 S antibody post-vaccination in magnesium transporter 1 (MAGT1) gene deficiency, more commonly recognized as x-linked immunodeficiency with magnesium defect, Epstein-Barr Virus infection, and neoplasia (XMEN). Case Presentation We present a 30-year-old male with selective anti-polysaccharide antibody deficiency, peripheral blood CD5 + /CD19 + B-cell predominance (97%), MAGT1 mutation, and reduced CD16 + CD56 + natural killer- and/or CD8 + T-cell receptor, Group 2, Member D expression. His initial immunological evaluation revealed all seronegative post-vaccination antibody titers but clinically adequate response to protein antigens tetanus and diphtheria anti-toxoids. COVID-19 vaccination and associated serology antibody testing was recommended at this office visit. Anti-SARS-CoV-2 immunoglobulin (Ig)M and IgG antibodies before and after the first BNT162b2 mRNA COVID-19 vaccine doses, as well as nucleocapsid antibody, were negative. S protein total antibody was reactive after the second dose. Discussion Robust immunological sequelae post-COVID-19 vaccination in the general population are well-documented in the recent literature. Few studies have evaluated COVID-19 vaccination antibody response in immunodeficient patients. The majority positive anti-S antibody detection in most primary immunodeficient (PID) patients among the few studies in the literature, such as the present case, support the safety and efficacy of mRNA COVID-19 vaccination in immunodeficient patients, although larger scale studies are needed. Conclusion We demonstrate successful vaccination in the PID MAGT1 deficiency in this first reported case of reactive anti-S antibody post-COVID-19 vaccination.

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Bateman, Caroline M., Alison Kesson, Madeleine Powys, Melanie Wong, and Emily Blyth. "Cytomegalovirus Infections in Children with Primary and Secondary Immune Deficiencies." Viruses 13, no. 10 (October 5, 2021): 2001. http://dx.doi.org/10.3390/v13102001.

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Cytomegalovirus (CMV) is a human herpes virus that causes significant morbidity and mortality in immunosuppressed children. CMV primary infection causes a clinically mild disease in healthy children, usually in early childhood; the virus then utilises several mechanisms to establish host latency, which allows for periodic reactivation, particularly when the host is immunocompromised. It is this reactivation that is responsible for the significant morbidity and mortality in immunocompromised children. We review CMV infection in the primary immunodeficient host, including early identification of these infants by newborn screening to allow for CMV infection prevention strategies. Furthermore, clinical CMV is discussed in the context of children treated with secondary immunodeficiency, particularly paediatric cancer patients and children undergoing haematopoietic stem cell transplant (HSCT). Treatments for CMV are highlighted and include CMV immunotherapy.

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Hege, Kristen M., Keegan S. Cooke, Mitchell H. Finer, Krisztina M. Zsebo, and Margo R. Roberts. "Systemic T Cell–independent Tumor Immunity after Transplantation of Universal Receptor–modified Bone Marrow into SCID Mice." Journal of Experimental Medicine 184, no. 6 (December 1, 1996): 2261–70. http://dx.doi.org/10.1084/jem.184.6.2261.

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Gene modification of hematopoietic stem cells (HSC) with antigen-specific, chimeric, or “universal” immune receptors (URs) is a novel but untested form of targeted immunotherapy. A human immunodeficiency virus (HIV) envelope–specific UR consisting of the extracellular domain of human CD4 linked to the ζ chain of the T cell receptor (CD4ζ) was introduced ex vivo into murine HSC by retroviral transduction. After transplantation into immunodeficient SCID mice, sustained high level expression of CD4ζ was observed in circulating myeloid and natural killer cells. CD4ζ-transplanted mice were protected from challenge with a lethal dose of a disseminated human leukemia expressing HIV envelope. These results demonstrate the ability of chimeric receptors bearing ζ-signaling domains to activate non–T cell effector populations in vivo and thereby mediate systemic immunity.

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Rème, Thierry, Elisabeth Gueydon, Chantal Jacquet, Bernard Klein, and Jean Brochier. "Growth and immortalization of human myeloma cells in immunodeficient severe combined immunodeficiency mice: a preclinical model." British Journal of Haematology 114, no. 2 (August 2001): 406–13. http://dx.doi.org/10.1046/j.1365-2141.2001.02947.x.

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Journal articles on the topic 'IMMUNODEFICIENZE'

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