Immunopathogenesis of non-healing American cutaneous leishmaniasis and progressive visceral leishmaniasis.
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TLDR
Recent evidence from human and animal studies is summarized 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 Leishesmania amazonensis and Leishmaniasis donovani.Abstract:
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.read more
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New World and Old World Leishmania Infections: A Practical Review
TL;DR: The current state of epidemiology, pathogenesis, clinical presentation, diagnosis, and treatment options for leishmaniasis are discussed, with a special focus on cutaneous manifestations and their treatment.
Journal ArticleDOI
The Equivocal Role of Th17 Cells and Neutrophils on Immunopathogenesis of Leishmaniasis.
Suênia da Cunha Gonçalves-de-Albuquerque,Rômulo Pessoa-e-Silva,Lays Adrianne Mendonça Trajano-Silva,Tayná Correia de Goes,Rayana Carla Silva de Morais,Cíntia Nascimento da Costa Oliveira,Virgínia Maria Barros de Lorena,Milena de Paiva-Cavalcanti +7 more
TL;DR: The roles of Th17–neutrophil interaction as a crucial component of anti-Leishmania immunity, and the clinical evolution of cutaneous or visceral leishmaniasis are described.
Journal ArticleDOI
Deception and manipulation: the arms of leishmania, a successful parasite
Pedro Cecílio,Begoña Pérez-Cabezas,Nuno Santarém,Joana Maciel,Vasco Rodrigues,Anabela Cordeiro da Silva +5 more
TL;DR: Here, it is revised how the parasite manipulates cell death and immune responses to survive and thrive in the shadow of the immune system.
Journal ArticleDOI
Interferon Gamma in Leishmaniasis
Peter E. Kima,Lynn Soong +1 more
TL;DR: Current understanding of some of the host responses during Leishmania infections that are regulated by IFN-γ is summarized and studies that explore the nature of parasite-derived molecular mediators that might affect the host response to IFn-γ are discussed.
Journal ArticleDOI
Recent progress in host immunity to avian coccidiosis: IL-17 family cytokines as sentinels of the intestinal mucosa.
TL;DR: This review highlights recent progress in IL-17 research in the context of host immunity to avian coccidiosis by highlighting the uniqueness of the innate immune response to Eimeria infection and the discovery of previously uncharacterized host genes and proteins whose expression levels were modulated following parasite infection.
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