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Blastomycosis
Published in Rebecca A. Cox, Immunology of the Fungal Diseases, 2020
In humans with blastomycosis, the percentage of those manifesting cutaneous reactivity to blastomycin has ranged from 0 to 50%.59, 60 The observed anergy may be caused by the poor antigenicity of blastomycin. In this regard, retesting of infected patients after they have recovered from blastomycosis would be of value but has not been performed. Alternatively, anergy may be caused by profound impairment of cell-mediated immunity (see Section V. C).
The Lymphatic/Immune System and Its Disorders
Published in Walter F. Stanaszek, Mary J. Stanaszek, Robert J. Holt, Steven Strauss, Understanding Medical Terms, 2020
Walter F. Stanaszek, Mary J. Stanaszek, Robert J. Holt, Steven Strauss
Loss of immune function can also be detected with these same skin tests. The severely immunocompromised person may develop anergy, lack of response to antigens, even if the antibodies are present, because of suppressed cell-mediated response. Skin testing to detect anergy is used in evaluating immunosuppression in transplant recipients, AIDS patients, and others.
T Cells:Regulation and Cellular Immunity
Published in Constantin A. Bona, Francisco A. Bonilla, Textbook of Immunology, 2019
Constantin A. Bona, Francisco A. Bonilla
The “two signal theory” of lymphocyte activation proposed by Bretscher and Cohn some twenty years ago states that immune cells are activated by an antigen-specific signal (“signal 1”) derived via interaction with the immune receptor (Ig or TCR) and a non-specific signal (“signal 2”) mediated either by a cellular contact or soluble factor (cytokine). The theory further states that signal 1 alone is “paralytic,” i.e., in the absence of simultaneous signal 2, the cell will be rendered incapable of responding to future activating signals. This results from a long-lasting, or perhaps even permanent, alteration in the signalling machinery. This condition of unresponsiveness is called anergy. A large body of experimental evidence supports this model, and it is generally consistent with the schemata of activation presented in Chapter 5 for B cells and above for T cells. For T cells in particular, it is hypothesized that a special type of “defective” antigen-presenting cell may exist for the induction of anergy. This cell would present self peptides, but lacking appropriate co-stimulatory signals, could only deliver signal 1, thus rendering interacting T cells anergic. The two signal model of lymphocyte activation also applies to γδ T cells.
Polyphenol containing Sargassum horneri attenuated Th2 differentiation in splenocytes of ovalbumin-sensitised mice: involvement of the transcription factors GATA3/STAT5/NLRP3 in Th2 polarization
Published in Pharmaceutical Biology, 2021
Kalahe Hewage Iresha Nadeeka Madushani Herath, Jinhee Cho, Hyo Jin Kim, Duong Thi Thuy Dinh, Hyun-Soo Kim, Ginnae Ahn, You-Jin Jeon, Youngheun Jee
STAT5 activation also drives the expression of NLR family pyrin domain containing 3 (NLRP3), a component of the inflammasome, and home to the nucleus promoting the transcription of genes encoding IL-4, IL-5, and IL-13 in T cells (Ting and Harton 2015). The transcriptional upregulation of STAT5, NLRP3, and GATA3 was revealed to be a key event in Th2 differentiation (Zhu 2015). Immunotherapy for certain conditions, such as atopy in children and perennial allergic rhinitis, typically works via the induction of tolerance or anergy to Th2 cells (Tanaka et al. 1998; Smart and Kemp 2002). In particular, natural sources to attenuate the function of pathogenic Th2 cells and their released cytokines have undoubtedly revolutionised the interest in immune therapy due to the cost effectiveness and absence of adverse effects (Li et al. 2000; Chitnis et al. 2004).
Challenges in Treating Intraocular Inflammation in HIV Patients
Published in Ocular Immunology and Inflammation, 2020
Ilaria Testi, Safia Ahmed, Camrun Shah, Rupesh Agrawal
Similarly, the value of the purified protein derivative (PPD) skin test in patients infected with HIV could be limited by the anergy of the host induced by the virus. It is well known that anergy correlates with CD4 + T-lymphocyte count and the lower the count, the higher the prevalence of anergy. Anergy in HIV-infected patients derives from the ability of HIV envelope glycoprotein moieties to bind to CD4 + T-lymphocyte molecules and chemokine receptors, interfering with antigen presenting cell function and leading to a malfunction of the positive and negative molecules involved in the signal transduction pathway.27 Janis et al. analyzed the PPD skin response of 310 hospitalized subjects.28 Sixty-two of 310 patients (20%) had a skin response of more than 10 mm of induration.28 Fifty-two patients were infected with HIV and none of them had a positive PPD skin test result.28 Anergy was detected in 63% of the HIV subjects compared to 28% of non-HIV patients.28 Since the PPD skin test is still widely used as an important test for diagnosing tuberculosis and HIV infection, it appears as an independent risk factor for the development of anergy. Hence, care should be taken when interpreting a negative PPD skin test in immunocompromised patients.
Transgenic rice seeds expressing altered peptide ligands against the M3 muscarinic acetylcholine receptor suppress experimental sialadenitis-like Sjögren’s syndrome
Published in Modern Rheumatology, 2020
Hanae Kudo, Hiroto Tsuboi, Hiromitsu Asashima, Hiroyuki Takahashi, Yuko Ono, Saori Abe, Fumika Honda, Yuya Kondo, Yuhya Wakasa, Fumio Takaiwa, Makoto Takano, Minoru Matsui, Isao Matsumoto, Takayuki Sumida
The third possible pathway is induction of anergy. We have previously shown that intravenous administration of N1-APL7 repressed MIS via upregulation of Egr2 expression in CLN CD4+ T cells and elevation of anergy-related molecules in CD4+ T cells [14]. By contrast, we detected lower expression of Egr2 in the MLNs of the N1-APL7-rice-treated group than in those of the N1 group. Anderson et al. [33] revealed that Egr2 is induced after TCR stimulation by the antigen peptide in vivo. N1-APL7 has a substitution of amino acid residues at TCR contact sites; therefore, the mechanism of TCR stimulation could be altered to reduce TCR stimulation following less Egr2 expression. We speculate that the discrepancy in the results was caused by the difference in the administration route of APL. Oral administration of APL transgenic rice seems to affect the intestinal immune response, and N1-APL7 might upregulate Treg cells.