Lymphoproliferative Responses to Human Immunodeficiency Virus Antigen in Asymptomatic Intravenous Drug Abusers and in Patients with Lymphadenopathy or AIDS

Reddy, Mohan M.; Englard, Arthur; Brown, David J.; Buimovici-Klien, E.; Grieco, Michael H.

doi:10.1093/infdis/156.2.374

Cited by 27 publications

(7 citation statements)

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“…The mechanism(s) regulating T cell hypo-responsiveness to viral antigen stimulation have not been fully explained. Several mechanisms have been proposed including: cytokine dysregulation (decreased IL-2, increased IL-10 and IFN-γ production), activation-induced cell death (apoptosis) and clonal deletion or anergy (Clerici et al, 1989; Reddy et al, 1987; Wahren et al, 1987). The observation that CD4 + T cells produce IFN-γ, yet do not produce IL-2 or proliferate in response to HIV gag stimulation supports the theory of clonal anergy (Arrode et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

CD4+CD25+ regulatory T cells are infected and activated during acute FIV infection

Mexas

Fogle

Tompkins

et al. 2008

Veterinary Immunology and Immunopathology

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HIV-induced AIDS may be mediated by the activation of immunosuppressive CD4+CD25+ T regulatory cells (Treg cells). Treg cells have been shown to regulate CD4+ and CD8+ immune responses to HIV and FIV antigens in vitro. We tested the hypothesis that Treg cells become infected and activated during the acute infection with FIV leading to the suppression of CD4+ T helper cell responses. Cats were experimentally infected with FIV-NCSU1 and blood and lymph node cells were collected at weekly intervals following inoculation. Real-Time RT-PCR was used to determine plasma viremia and the relative expression of FIV, FoxP3, TGF-β, and GAPDH mRNA copies in CD4+CD25+ and CD4+CD25− T cell subsets. Flow cytometry was used to assess the absolute numbers of each cell type and the expression of surface TGF-β and intracellular FoxP3 in CD4+CD25+ and CD4+CD25− T cells at each time point. Treg suppression of IL-2 production in CD4+ T helper cells was assessed by ELISPOT assays. Our results showed that peak viremia occurred at 2 weeks post infection and correlated with maximal infectivity in CD4+CD25+ T cell populations. FIV-gag-mRNA levels were higher in CD4+CD25+ T cells than CD4+CD25− T cells throughout the acute phase of infection. Induction of FoxP3 and TGF-β indicated activation of Treg cells during the acute stage infection, which was confirmed by Treg cell suppression of IL-2 production by CD4+ Th cells in an ELISPOT assay. Our findings support the hypothesis that early activation of Treg immunosuppressor function may limit an effective anti-FIV response, contributing to the establishment of chronic infection and the immunodeficiency caused by this virus.

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Section: Introductionmentioning

confidence: 99%

CD4+CD25+ regulatory T cells are infected and activated during acute FIV infection

Mexas

Fogle

Tompkins

et al. 2008

Veterinary Immunology and Immunopathology

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“…These individuals tend to have few peripheral blood T-lymphocytes [67,83], inverted T-helper/T-suppressor cell ratios [57], and suppressed NK cell activity as well [77,83]. Suppressed mitogenic responses and production of IFN-7 have also been reported [83,87]. The duration of the addiction and the nutritional state of the addicts, however, are important factors in immune function for these individuals [83].…”

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confidence: 99%

Stress, immunity and mycotic diseases

Mishra¹,

Segal²,

Gunter³

et al. 1994

Med Mycol

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Stress, whether physical, emotional, or chemical, triggers a complex series of host responses encompassing elements of psychology, endocrinology, immunology, metabolism and infection. A wealth of scientific information has become available concerning neuroendocrine events during stress, the resultant alterations in immune functions and the interplay between the central nervous system, the endocrine system and the immune system. Stress is known to increase the secretion of corticotropin-releasing factor, adrenocorticotropic hormone, glucocorticoids, growth hormones and fl-endorphins, and is suspected of suppressing the production of thymosins, thyroid-stimulating hormone and sex hormones. Stress blunts cellular immunity, as characterized by reductions in lymphocyte mitogenic responses, natural killer cell activity and interferon-7 production. Chronic stress is an important contributor to the morbidity and mortality associated with neurotic illnesses, bereavement and drug addiction. It is becoming increasingly apparent that the course of disease can be influenced greatly by appropriate coping strategies as well as by improving nutritional status and hygienic factors.The roles that stress plays in the pathophysiology of cancer, diabetes mellitus, rheumatic fever and several viral and bacterial diseases have been discussed at length; however, the relationship between stress and mycotic diseases has received little attention. We seek to address this gap herein. After brief reviews of the psychophysiology of stress and its effects on immune functions, the relationship between hormones and mycotic diseases is explored in terms of direct interactions between hormones and fungal cells (e.g. Paracoccidioides brasiliensis and Trichophyton mentagrophytes). Next, the relevance of stress in candidiasis, an endogenous opportunistic mycosis, is examined in the light of stress induced immune impairment, and data from model studies using healthy volunteers are presented to demonstrate the effect of emotional and physical stress on yeast colonization of mucocutaneous tissue and antibody titres. The role of stress in the pathogenesis of aspergillosis, an exogenous opportunistic mycosis, is illustrated by experimental studies in mice, which further suggest that immune suppression due to stress can enhance susceptibility to Aspergillus fumigatus. Finally, the last section summarizes data on experimental systemic candidiasis of gastrointestinal origin in compromised hosts 379 Med Mycol Downloaded from informahealthcare.com by University of Sydney on 01/03/15 For personal use only.380 MISHRA ET AL. and draws attention to the possible role of stress induced alterations in gastrointestinal function and microflora in modifying the course of candidiasis in humans. Stress: an overviewWhat is stress? Despite several decades of study, the term 'stress' remains somewhat vague and difficult to define. According to Hans Selye [103], a pioneer in stress research, stress is 'the nonspecific response of the organism to any demand made upon it.' In t...

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“…The observation of a defect in HIVspecific lymphocyte proliferative responses prior to the loss of recall and allogeneic antigen responses has now been described in numerous subsequent studies [15,16,24]. Furthermore, the association of strong HIV-1-spe cific lymphoproliférative responses and delay in disease progression has been reported.…”

Section: Lymphocyte Proliferation To Hiv Antigensmentioning

confidence: 88%

HIV-1-Specific Functional Immune Measurements as Markers of Disease Progression

Moss¹,

Richieri²,

Ferre³

et al. 1997

J Biomed Sci

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The impairment of lymphocytes to proliferate to HIV antigen is a relatively early functional defect of cell-mediated immunity found in HIV-infected individuals. The finding of strong proliferative responses in nonprogressive HIV disease as well as its inverse association with viral load and clinical manifestation of AIDS supports the further use of this marker as a surrogate of disease progression. The observation that HIV-specific lymphocyte proliferation is associated with the production of CD8-derived HIV suppressive factors such as the β-chemokines further supports this conclusion. These functional immune measurements provide an additional marker to monitor disease progression in HIV-infected individuals, along with the current standards of CD4 counts and viral load.

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Lymphoproliferative Responses to Human Immunodeficiency Virus Antigen in Asymptomatic Intravenous Drug Abusers and in Patients with Lymphadenopathy or AIDS

Cited by 27 publications

References 0 publications

CD4+CD25+ regulatory T cells are infected and activated during acute FIV infection

CD4+CD25+ regulatory T cells are infected and activated during acute FIV infection

Stress, immunity and mycotic diseases

HIV-1-Specific Functional Immune Measurements as Markers of Disease Progression

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