Recognition of Antigenic Clusters of Candida albicans by T Lymphocytes from Human Immunodeficiency Virus-Infected Persons

Kunkl, Annalisa; Mortara, Lorenzo; Valle, Maurizio; Fenoglio, Daniela; Terranova, Paola; Megiovanni, Anna Maria; Alessandrini, A.; Pira, Giuseppina Li; Mazzarello, Giovanni; Bono, Valerio Del; Canessa, Andrea; Bassetti, Dante; Manca, Fabrizio

doi:10.1086/515620

Cited by 29 publications

(20 citation statements)

References 29 publications

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“…Sensitive in vitro and in vivo assays include antigen-specific proliferation, 67 precursor frequency evaluation by limiting dilution, 97 intracytoplasmic cytokine staining, 102 tetramers 103 and delayed T cell hypersensitivity (DTH) to relevant antigenic extracts. However informative these biological parameters may be, no one is singularly a better predictor of therapy-linked immune recovery than clinical effectiveness.…”

Section: Discussionmentioning

confidence: 99%

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Genetically modified immunocompetent cells in HIV infection

Palù

Pira²,

Gennari

et al. 2001

Gene Ther

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Even in the era of highly active antiretroviral therapy (HAART), gene therapy (GT) can remain a promising approach for suppressing HIV infection, especially if complemented with other forms of pharmacological and immunological intervention. A large number of vectors and targets have been studied. Here we discuss the potential of genetically treated, antigen-specific immunocompetent cells for adoptive autologous immunotherapy of HIV infection. Cellu-

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Section: Discussionmentioning

confidence: 99%

“…66,67 If the specific precursors are infected, exposure to single antiviral drugs, 68 or to cocktails that mimic HAART, may prevent viral replication and infection spreading in culture.…”

Section: Figure 1 Consequences Of Selective Infection Of Activated CDmentioning

confidence: 99%

Genetically modified immunocompetent cells in HIV infection

Palù

Pira²,

Gennari

et al. 2001

Gene Ther

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“…The predisposition for OPC and esophageal candidiasis among HIV-infected patients, initially attributed to T-cell impairment, is enigmatic (72,74,240,446). Colonization of oral mucosal surfaces and symptomatic disease are closely correlated with the development and progression of the cellular immunodeficiency of HIV infection (230,311,414).…”

Section: Introductionmentioning

confidence: 99%

Immunopathogenesis of Oropharyngeal Candidiasis in Human Immunodeficiency Virus Infection

2004

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Oropharyngeal and esophageal candidiases remain significant causes of morbidity in human immunodeficiency virus (HIV)-infected patients, despite the dramatic ability of antiretroviral therapy to reconstitute immunity. Notable advances have been achieved in understanding, at the molecular level, the relationships between the progression of HIV infection, the acquisition, maintenance, and clonality of oral candidal populations, and the emergence of antifungal resistance. However, the critical immunological defects which are responsible for the onset and maintenance of mucosal candidiasis in patients with HIV infection have not been elucidated. The devastating impact of HIV infection on mucosal Langerhans' cell and CD4+ cell populations is most probably central to the pathogenesis of mucosal candidiasis in HIV-infected patients. However, these defects may be partly compensated by preserved host defense mechanisms (calprotectin, keratinocytes, CD8+ T cells, and phagocytes) which, individually or together, may limit Candida albicans proliferation to the superficial mucosa. The availability of CD4C/HIV transgenic mice expressing HIV-1 in immune cells has provided the opportunity to devise a novel model of mucosal candidiasis that closely mimics the clinical and pathological features of candidal infection in human HIV infection. These transgenic mice allow, for the first time, a precise cause-and-effect analysis of the immunopathogenesis of mucosal candidiasis in HIV infection under controlled conditions in a small laboratory animal

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“…The predisposition for OPC among HIV-infected patients, attributed to T cell impairment, is enigmatic [9][10][11][12][13][14]. Candida colonization of the keratinocyte surface takes place without invasion of the submucosa, and, therefore, the occurrence of this superficial fungal disease in a T cell-poor environment has not been adequately explained.…”

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confidence: 99%

Mucosal Candidiasis in Transgenic Mice Expressing Human Immunodeficiency Virus Type 1

et al. 2002

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The availability of CD4C/HIV(MutA) transgenic (Tg) mice expressing human immunodeficiency virus type 1 in immune cells and developing an AIDS-like disease has provided the opportunity to devise a model of mucosal candidiasis that closely mimics the clinical and pathologic features of candidal infection in human AIDS. After intraoral infection with Candida albicans, oral burdens were strikingly elevated in the Tg mice, compared with non-Tg littermates (P<.05), during primary infection, a 6-10-week carrier state, and a marked terminal outgrowth preceding death. The chronic carrier state was absent in the non-Tg mice because of clearing of C. albicans. Candida hyphae penetrated the epithelium of the oral cavity, esophagus, and cardial-atrium fold of the stomach, accompanied by a mononuclear cell infiltrate. Immunohistochemical analysis suggested that decreased frequencies of major histocompatibility complex class II-expressing cells, combined with reduced CD4+ cells, may underlie the susceptibility to mucosal candidiasis in these Tg mice.

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Recognition of Antigenic Clusters of Candida albicans by T Lymphocytes from Human Immunodeficiency Virus-Infected Persons

Cited by 29 publications

References 29 publications

Genetically modified immunocompetent cells in HIV infection

Genetically modified immunocompetent cells in HIV infection

Immunopathogenesis of Oropharyngeal Candidiasis in Human Immunodeficiency Virus Infection

Mucosal Candidiasis in Transgenic Mice Expressing Human Immunodeficiency Virus Type 1

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