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Autoimmunity and Immune Pathological Aspects of Virus Disease
Published in Irun R. Cohen, Perspectives on Autoimmunity, 2020
H. Wege, R. Dörries, P. Massa, R. Watanabe
Measles leads within an incubation period of 10 to 14 days to signs of a respiratory disease, and patients develop typical exanthema of the skin. The virus spreads to intestinal and renal tracts as well as to the lymph organs. Multinucleated giant cells and breakage of chromosomes are observed, and a transient suppression of lymphocyte responses to mitogen is measurable. This suppression does not hinder the development of a strong virus-specific lymphoproliferative response.44 A high percentage of patients display signs of subclinical CNS involvement. During viremia, virus can enter the brain; later, infected lymphocytes or macrophages disseminate virus. Most patients recover from acute disease without sequelae, protected by a strong cellular immune response. A persistent infection of lymphoid tissue is suspected to be the basis of lifelong immunity.
Historical Perspectives on Psychoneuroimmunology
Published in Herman Friedman, Thomas W. Klein, Andrea L. Friedman, Psychoneuroimmunology, Stress, and Infection, 2020
It was during his first year of a medical fellowship with Elliot Middleton, Jr. that Hadden learned of Szentivanyi’s formulation and set out to determine if lymphocytes had adrenergic receptors that could regulate immune function in a meaningful way. Hadden and his associates showed that, in the presence of hydrocortisone, alpha-adrenergic stimulation augmented and beta adrenergic stimulation inhibited the lymphoproliferative response to the mitogen, PHA.34 This was the first observation linking lymphocytes to the sympathetic nervous system, opening a wide door to the study of neural influences on immunity.
Death Receptor-Mediated Apoptosis and Lymphocyte Homeostasis
Published in Richard K. Burt, Alberto M. Marmont, Stem Cell Therapy for Autoimmune Disease, 2019
Lixin Zheng, Richard M. Siegel, Jagan R. Muppidi, Felicita Hornung, Michael J. Lenardo
It has been found that genetic deficiencies in apoptosis pathways can lead to developmental abnormalities and disease.12 One of the major breakthroughs in determining the physiological relevance of lymphocyte apoptosis and autoimmune disorders came from the identification of genetic mutations of CD95 (Fas) in Ipr mice and CD95 ligand (FasL) in gld mice.121,122 The Ipr stands for “lymphoproliferative response” and the gld for “generalized lymphoproliferative disease”. In Ipr mice, a transposable element insertion in the 2nd intron of CD95 gene disrupts transcription of the gene while in gld mice, a point mutation in the CD95L gene produces a mutant protein that fails to bind CD95. In both cases, peripheral lymphocytes escape from CD95-mediated cell death. Over their lifetime, these mice develop progressive lymphoadenopathy, splenomegaly, and autoimmune disease.123 These data indicate that death receptor-mediated apoptosis is important for shaping the immune system by limiting lymphocyte accumulation.
The Postnatal Leptin Surge Supports Immune Cell Function in Rats
Published in Immunological Investigations, 2022
Caroline Hunsche, Oskarina Hernandez, Virginia Mela, M. Paz Viveros, Mónica De la Fuente
Increasing evidence suggests that leptin has a regulatory role within the cytokine network (Gainsford et al. 1996; Lam and Lu 2007; Lord 2006; Martín-Romero et al. 2000; Santos-Alvarez et al. 1999). Therefore, in agreement with the impairments found in innate and adaptive immune functions, the neonatal leptin antagonist treatment also resulted in a lower release of several cytokines in ConA and LPS-stimulated spleen leukocytes of peripubertal rats. IL-2, an essential regulatory cytokine, which acts mainly on lymphoid populations, including T, B, and NK cells (Liao et al. 2011), was diminished in treated females. In this sense, leptin has been shown to influence the proliferation and secretion of IL-2 by immune cells, through the activation of the mitogen-activated protein kinase (MAPK) and phosphatidylinositol-3-kinase (PI3-K) pathways (Liao et al. 2011; Lord et al. 1998). Since IL-2 is related to lymphocyte proliferation, lower concentrations of this cytokine in treated females could explain the reduced lymphoproliferative response in those cells.
Life Events, Emotions, and Immune Function: Evidence from Whitehall II Cohort Study
Published in Behavioral Medicine, 2020
Nadya Dich, Maarten Pieter Rozing, Mika Kivimäki, Stacey N. Doan
The hypothesis that negative emotions may moderate the effects of stressful life events on health has up to date not been extensively explored, however. We are aware of only four studies that investigated potential interactions between stressful events and negative emotions on immune function, which have yielded mixed findings. González-Quijano and colleagues19 found that trait anxiety interacted with stressful life events in predicting immunity, operationalized as lymphoproliferative response to mitogens, in a sample of 85 male college students. Non-anxious individuals who recently experienced stressful life events had poorer immune function compared to non-anxious individual who did not experience any stressful events. In anxious individuals, immune function was lowered independent of life events.
Lymphoprolipherative skin reactions induced by anti-TNFα: an open question
Published in Journal of Dermatological Treatment, 2020
Vasiliki Nikolaou, Maria Gerochristou, Leonidas Marinos, Afroditi Economidi, Dimitra Voudouri, Dimitris Rigopoulos, Alexander J Stratigos
Since anti-TNFα agents were successfully introduced in the treatment of inflammatory diseases, such as rheumatoid arthritis or Crohn’s disease, various concerns have been reported regarding their potential immunosuppressive effects. In 2015, we published a series of eight patients diagnosed with cutaneous lymphomas after anti-TNFα treatment (for psoriasis in six of them). In that cohort, Mycosis Fungoides (MF) developed, and persisted in spite of cessation of therapy. MF was treated with either methotrexate and/or PUVA and immunotherapy cessation with various response (1). We, along with other authors, hypothesized that the anti-TNFα immunosuppression demasked the coexisting MF and accelerated the disease evolution (2,3). Moreover, a possible relation between psoriasis and MF has been recently described by us and by others (4,5). In this study, we present five additional cases with no history of skin disease in which a lymphoproliferative response was detected after introduction of anti-TNFα agent. In three cases, disease regressed after no other treatment than drug discontinuation, suggesting an unobserved provocative effect.