Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2017 Nov;112(11):733-740.
doi: 10.1590/0074-02760170109.

Cytotoxic activity in cutaneous leishmaniasis

Taís M Campos  1   2 , Rúbia Costa  1   2 , Sara Passos  1   3 , Lucas P Carvalho  1   2   4   5
Affiliations
Review

Cytotoxic activity in cutaneous leishmaniasis

Taís M Campos et al. Mem Inst Oswaldo Cruz. 2017 Nov.

Abstract

Cutaneous leishmaniasis (CL) is a chronic disease caused by species of the protozoan Leishmania and characterised by the presence of ulcerated skin lesions. Both parasite and host factors affect the clinical presentation of the disease. The development of skin ulcers in CL is associated with an inflammatory response mediated by cells that control parasite growth but also contribute to pathogenesis. CD8+ T cells contribute to deleterious inflammatory responses in patients with CL through cytotoxic mechanisms. In addition, natural killer cells also limit Leishmania infections by production of interferon-γ and cytotoxicity. In this review, we focus on studies of cytotoxicity in CL and its contribution to the pathogenesis of this disease.

PubMed Disclaimer

Figures

None
Tissue damage and inflammation mediated by cytotoxic cells in human cutaneous leishmaniasis. With degranulation of natural killer (NK) and CD8+ T cells, granzyme B (GzmB) and perforin are released and apoptosis of infected macrophages is induced. Additionally, granzyme B may indirectly induce inflammation through the activation of pro-inflammatory cytokines and degradation of extracellular matrix (ECM) substrates, contributing to tissue damage. *This image has not been previously published.
See this image and copyright information in PMC

References

    1. Afonina IS, Tynan GA, Logue SE, Cullen SP, Bots M, Luthi AU, et al. Granzyme B-dependent proteolysis acts as a switch to enhance the proinflammatory activity of IL-1alpha. Mol Cell. 2011;44(2):265–278. - PMC - PubMed
    1. Antonelli LR, Dutra WO, Almeida RP, Bacellar O, Carvalho EM, Gollob KJ. Activated inflammatory T cells correlate with lesion size in human cutaneous leishmaniasis. Immunol Lett. 2005;101(2):226–230. - PubMed
    1. Arias MA, de Bagues MPJ, Aguilo N, Menao S, Hervas-Stubbs S, de Martino A, et al. Elucidating sources and roles of granzymes A and B during bacterial infection and sepsis. Cell Rep. 2014;8(2):420–429. - PubMed
    1. Bacellar O, Lessa H, Schriefer A, Machado P, de Jesus AR, Dutra WO, et al. Up-regulation of Th1-type responses in mucosal leishmaniasis patients. Infect Immun. 2002;70(12):6734–6740. - PMC - PubMed
    1. Bajenoff M, Breart B, Huang AY, Qi H, Cazareth J, Braud VM, et al. Natural killer cell behavior in lymph nodes revealed by static and real-time imaging. J Exp Med. 2006;203(3):619–631. - PMC - PubMed

MeSH terms