Trends in immune activation, maturation, and co-stimulatory markers in a group of children with stable HIV infection before and after HAART: Preliminary analysis of the PACTG 377 protocol
H ROSENBLATTLin‐Ye SongK. O. StanleyAndrew WizniaGeorge M. JohnsonPaul KrogstadAnita BallowSharon Nachman
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Helminth parasites are able to induce immune regulation in their host. Suppression of the host immune system is beneficial for both the parasite, by inhibiting anti-parasite immunity, and for the host, by preventing tissue damage due to excessive inflammation. There are indications that in countries where parasites have been eliminated the immune regulatory network is impaired, leading to inflammatory diseases such as allergies and asthma.
An important player in immune regulation is the regulatory T cell (Treg). We have shown that the number and/or function of Tregs were indeed enhanced in several helminth and also malaria infections in humans. Tregs were not only involved in suppression of anti-parasite responses, but also of responses to other infections or vaccines.
We further investigated the effect of helminth elimination in a randomized placebo-controlled trial. Treatment of helminths led to a strong increase in –mainly pro-inflammatory– immune responses, which confirms the importance of immune regulation during infection. Furthermore, the prevalence of malaria was transiently increased and allergy was slightly on the rise in treated school children. These results further endorse the possible beneficial effects of helminthic therapy, which is currently being tested in a number of clinical trials.
Hygiene hypothesis
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Parasitic
helminths modulate host immune responses. While the induction of type 2 immune
responses is a widely recognized feature of helminth infections, a network of
regulatory immune responses is often dominant during the chronic phase of
infection. Suppression of the host immune system during helminth infections
inhibits anti-parasite immunity, prevents tissue damage due to excessive
inflammation and conveys spill-over suppression to inflammatory conditions such
as allergy and asthma. The first part of this thesis focuses on the role of
regulatory B cells, a prominent member of the immune regulatory network, in
protection from allergic asthma by chronic Schistosoma (S.) mansoni infections.
It furthermore identifies signals required for schistosome-induced regulatory B
cell development. The second part of this thesis describes the protective
effect of S. mansoni eggs, and a specific egg-derived glycoprotein, against
allergic asthma in the absence of chronic infection. A better understanding how
helminthes including S. mansoni modulate host immune responses, and the
implications this has for inflammatory diseases such as allergic asthma, may
provide valuable leads for the development of novel pharmaceutical agents for
the treatment of allergic disorders.
Regulatory T cell
Allergic Inflammation
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Bronchiectasis (BC) is a chronic pulmonary disease with tremendous morbidity and significant mortality. As pathogen infection has been advocated as a triggering insult in the development of BC, a central role for the immune response in this process seems obvious. Inflammatory cells are present in both the airways as well as the lung parenchyma, and multiple mediators of immune cells including proteases and cytokines or their humoral products are increased locally or in the periphery. Interestingly, a defect in the immune system or suppression of immune response during conditions such as immunodeficiency may well predispose one to the devastating effects of BC. Thus, the outcome of an active immune response as detrimental or protective in the pathogenesis of BC may be dependent on the state of the patient's immunity, the severity of infection, and the magnitude of immune response. Here we reassess the function of the innate and acquired immunity in BC, the major sites of immune response, and the nature of the bioactive mediators. Furthermore, the potential link(s) between an ongoing immune response and structural alterations accompanying the disease and the success of therapies that can modulate the nature and extent of immune response in BC are elaborated upon.
Pathogenesis
Cellular immunity
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Our understanding of how the host immune response influences the risk of developing disease has changed dramatically over the past decade. Previously, the spectrum of disease associated with lymphatic filariasis was largely attributed to the nature of the host immune response. Now, we appreciate that the duration and intensity of infection and possibly the direct influence of parasite‐derived molecules also determine the risk of disease. Individuals chronically infected with lymphatic filariasis generally have an impaired lymphocyte proliferation response to filarial antigens and favour Th2‐type cytokine responses. This ability to down‐modulate the host immune response may help protect the host from disease. Defects in antigen‐presenting cell (APC) function appear to participate in this acquired immune hyporesponsiveness, although the mechanisms as to how this occurs are poorly understood. Here, we present evidence that repeated exposure to infective stage larvae and their secreted products may stimulate basophils and mast cells to related products that may impair APC function.
Lymphatic Filariasis
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The host immune response is critical in Pneumocystis pneumonia (PCP). Immunocompetent hosts can eliminate the fungus without symptoms, while immunodeficient hosts develop PCP with an unsuitable excessive inflammatory response leading to lung damage. From studies based on rodent models or clinical studies, this review aimed to better understand the pathophysiology of Pneumocystis infection by analysing the role of immune cells, mostly lymphocytes, according to the immune status of the infected host. Hence, this review first describes the immune physiological response in infected immunocompetent hosts that are able to eliminate the fungus. The objective of the second part is to identify the immune elements required for the control of the fungus, focusing on specific immune deficiencies. Finally, the third part concentrates on the effect of the different immune elements in immunocompromised subjects during PCP, to better understand which cells are detrimental, and which, on the contrary, are beneficial once the disease has started. This work highlights that the immune response associated with a favourable outcome of the infection may differ according to the immune status of the host. In the case of immunocompetency, a close communication between B cells and TCD4 within tertiary lymphocyte structures appears critical to activate M2 macrophages without much inflammation. Conversely, in the case of immunodeficiency, a pro-inflammatory response including Th1 CD4, cytotoxic CD8, NK cells, and IFNγ release seems beneficial for M1 macrophage activation, despite the impact of inflammation on lung tissue.
Pneumocystis pneumonia
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A series of clinical problems caused by mucosal immune damage in children′s immune diseases need to be paid more attention. The pathogenesis is complex and the clinical manifestations are various, which may lead to misdiagnosis and missed the right treatment. The clinical phenotypes of allergic, autoimmune and inflammatory diseases, and primary immunodeficiency diseases often overlap.The immunological characteristics of mucosal immune system, the characteristics of several related clinical immune diseases, the characteristics of serum immunoglobulin(Ig) E and IgG, the difference roles between specific IgE and IgG in allergic and autoimmune diseases, the role of mucosal immune system and probiotics, mucosal immune system and vaccine, the role of mucosal immune system in the diagnosis and treatment in the related immune diseases were reviewed in this article. The treatment of IgG4-related diseases and other aspects are elaborated to show the research progress of blood IgE and mucosal immune damage in immune diseases.
Key words:
Blood immunoglobulin E; Immune disease; Mucosal immunity
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To characterize the development and evolution of cellular immune responsiveness in individuals infected with the parasite Schistosoma mansoni, we studied fifteen patients with acute, subacute and chronic schistosomiasis. Lymphocytes from the three acutely infected patients responded vigorously to schistosome antigens in an in vitro blastogenic assay. By contrast, cells from nine chronically infected individuals were essentially unreactive to these same antigens. Patients infected for an intermediate period of time (9 months) generated responses between those of acute and chronic patients. The diminished responsiveness of chronically infected individuals was specific for schistosome antigens and did not extend to humoral immune responses. Following treatment of the infection with niridazole, these patients temporarily regained responsiveness to schistosome antigens. From these data we speculate that during the course of this parasitic helminth infection there develops a progressive and specific modulation of antigen recognition and proliferation by lymphocytes to schistosome antigens, and that such diminished immune reactivity may be important in maintaining the unique biological relationship which exists between a host and its parasites.
Schistosoma
Niridazole
Cellular immunity
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A 33year-old man was admitted to the medical ward at Queen Elizabeth Central Hospital for evaluation of a pleural effusion that had progressed despite anti-bacterial and tuberculosis treatment. Eight months earlier he was diagnosed with sputum smear alcohol and acid-fast bacilli [AAFB] negative pulmonary tuberculosis. At that time his symptoms were fever, night sweats, cough and shortness of breath. The results of his initial chest X-ray are not known. He received standard tuberculosis treatment (rifampicin, isoniazid, pyrazinamide and ethambutol for 2 months followed by rifampicin and isoniazid for four months). He stated that his symptoms improved during the first two months of tuberculosis treatment,but he then developed a pleural effusion that was tapped three times over the course of the four months prior to admission. Straw colored fluid was obtained twice but results of microbiological and biochemical analysis of the pleural fluid samples were not available.The last time a dry pleural tap was recorded. Courses of amoxicillin and chloramphenicol were given without improvement. Five days before admission he developed progressive complaints of productive cough with brownish sputum and shortness of breath on exertion. He had no constitutional symptoms. He was a lifetime non-smoker and had no exposure to asbestos or significant amounts of particulate matter. He was HIV positive with World Health Organization (WHO)
Pyrazinamide
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H. pylori elicits specific humoral and cellular immune responses in the mucosal immune system. However, the type and extent of T lymphocyte response in the systemic immune system is not clear for H. pylori positive patients. In this study, peripheral blood T lymphocyte phenotypes and serum Th1/Th2 based cytokines of 32 H. pylori positive patients were analyzed and compared to those of healthy controls. While alphabeta TCR(+) lymphocytes and their phenotype analysis were not significantly different to those of healthy controls, the percentage of pan gammadelta TCR(+) lymphocytes was up to 2.4 times greater in the H. pylori positive group then in healthy controls. Furthermore, significant increases in IL-10 concentrations in serum samples of H. pylori patients indicated that their immune systems had switched toward a Th2 type immune response. The correlation between phenotype and type of T cell response in the peripheral blood during H. pylori infection is discussed.
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