Immunophenotyping of circulating T cells in a mucosal leishmaniasis patient coinfected with HIV

Castellano, Lúcio Roberto Cançado; Llaguno, Mauricio; Silva, Marcos; Machado, Juliana Reis; Correia, Dalmo; Silva‐Vergara, Mario León; Rodrigues, Virmondés

doi:10.1590/s0037-86822011000400025

Cited by 7 publications

(8 citation statements)

References 8 publications

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“…Parasites avoided the upregulation of transcription and surface expression of CD40 and CD86 co-stimulatory molecules on BMDC, through activation of the PI3k/Akt pathway and the impairment of NF-κB transcription factor ( 243 ). This DCs activation/maturation arrest was also described for L. amazonensis infection on mice and human cells ( 150 , 217 , 231 , 244 ). Leishmania has also been associated with T cell exhaustion ( 245 ).…”

Section: Impairing Cellular Functionsupporting

confidence: 72%

“…Although there are not many studies showing Leishmania modulation of this cytokine, some clues exist about how this can happen. Castellano et al showed that L. amazonensis antigens possibly induce a decrease in the percentage of CD3 + CD4 + IL-17 + human cells, at least in cases of HIV/ Leishmania co-infection ( 217 ). Interestingly, patients with signs of active disease present lower levels of Th17 cytokines ( 218 , 219 ).…”

Section: Modulating the Immune Response Through Alteration Of Cytokinmentioning

confidence: 99%

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Deception and Manipulation: The Arms of Leishmania, a Successful Parasite

Cecílio

Pérez-Cabezas²,

Santarém

et al. 2014

Front. Immunol.

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Leishmania spp. are intracellular parasitic protozoa responsible for a group of neglected tropical diseases, endemic in 98 countries around the world, called leishmaniasis. These parasites have a complex digenetic life cycle requiring a susceptible vertebrate host and a permissive insect vector, which allow their transmission. The clinical manifestations associated with leishmaniasis depend on complex interactions between the parasite and the host immune system. Consequently, leishmaniasis can be manifested as a self-healing cutaneous affliction or a visceral pathology, being the last one fatal in 85–90% of untreated cases. As a result of a long host–parasite co-evolutionary process, Leishmania spp. developed different immunomodulatory strategies that are essential for the establishment of infection. Only through deception and manipulation of the immune system, Leishmania spp. can complete its life cycle and survive. The understanding of the mechanisms associated with immune evasion and disease progression is essential for the development of novel therapies and vaccine approaches. Here, we revise how the parasite manipulates cell death and immune responses to survive and thrive in the shadow of the immune system.

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Section: Impairing Cellular Functionsupporting

confidence: 72%

Section: Modulating the Immune Response Through Alteration Of Cytokinmentioning

confidence: 99%

Deception and Manipulation: The Arms of Leishmania, a Successful Parasite

Cecílio

Pérez-Cabezas²,

Santarém

et al. 2014

Front. Immunol.

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“…More recently, Castellano et al [29] found that following stimulation with L. braziliensis antigens, there was a decreased frequency of IL-17 + CD3 + CD4 + cells in circulating T cells from an HIV-positive ML patient; however, the biological significance of this alteration remained unclear. Collectively, these clinical studies indicated that the regulated production of IL-17 contributes to infection control, while excessive IL-17 can promote neutrophil influx and tissue damage, thereby increasing the risk of ML.…”

Section: Non-healing Human Diseases Associated With L Braziliensis Imentioning

confidence: 99%

Immunopathogenesis of non-healing American cutaneous leishmaniasis and progressive visceral leishmaniasis

2012

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The outcomes of Leishmania infection are determined by host immune and nutrition status, parasite species, and co-infection with other pathogens. While subclinical infection and self-healing cutaneous leishmaniasis (CL) are common, uncontrolled parasite replication can lead to non-healing local lesions or visceral leishmaniasis (VL). It is known that infection control requires Th1-differentiation cytokines (IL-12, IL-18, and IL-27) and Th1 cell and macrophage activation. However, there is no generalized consensus for the mechanisms of host susceptibility. The recent studies on regulatory T cells and IL-17-producing cells help explain the effector T cell responses that occur independently of the known Th1/Th2 cell signaling pathways. This review focuses on the immunopathogenesis of non-healing American CL and progressive VL. We summarize recent evidence from human and animal studies that reveals the mechanisms of dysregulated, hyper-responses to Leishmania braziliensis, as well as the presence of disease-promoting or the absence of protective responses to Leishmania amazonensis and Leishmania donovani. We highlight immune-mediated parasite growth and immunopathogenesis, with an emphasis on the putative roles of IL-17 and its related cytokines as well as arginase. A better understanding of the quality and regulation of innate immunity and T cell responses triggered by Leishmania will aid in the rational control of pathology and the infection.

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“…This increases the susceptibility of the host to infection and is responsible for the development of anergic forms of ATL. 29 This situation is a problem for the public health sector, since it is linked to greater diagnostic challenges, poorer prognosis and higher recurrence rates.…”

Section: Clinical Diagnosismentioning

confidence: 99%

Complementary exams in the diagnosis of american tegumentary leishmaniasis

Gomes

Paula

Morais

et al. 2014

An. Bras. Dermatol.

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The diagnosis of American Tegumentary Leishmaniasis is a difficult but essential task when considering the high toxicity profile of the drugs available. Since the discovery of its etiologic agent, numerous diagnostic tests have been developed. None of the tests available today can be considered as the gold standard, since they do not add enough accuracy for the disease detection. Good epidemiological and clinical knowledge of the disease are fundamental precepts of the dermatology practice and precede the rational use of existing diagnostic tests. In this article we aim, through extensive literature review, to recall fundamental concepts of any diagnostic test. Subsequently, based on this information, we will weave important comments about the characteristics of existing diagnostic tests, including immunological tests such as Montenegro's skin test, serology and detection of parasites by direct examination, culture or histopathology. Finally we will discuss the new technologies and options for the diagnosis of Cutaneous Leishmaniasis. The molecular biology technique is considered a promising tool, promoting the rapid identification of the species involved. We also aim to educate dermatologists about a disease with high morbidity and assist in its difficult recognition.

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Immunophenotyping of circulating T cells in a mucosal leishmaniasis patient coinfected with HIV

Cited by 7 publications

References 8 publications

Deception and Manipulation: The Arms of Leishmania, a Successful Parasite

Deception and Manipulation: The Arms of Leishmania, a Successful Parasite

Immunopathogenesis of non-healing American cutaneous leishmaniasis and progressive visceral leishmaniasis

Complementary exams in the diagnosis of american tegumentary leishmaniasis

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