CD8+ T cells in situ in different clinical forms of human cutaneous leishmaniasis

Marina Loyola Dantas,Sara Timoteo Passos,Sergio Arruda,Adriano Queiroz,Juliana Cabral De Oliveira,Lucas Carvalho,Edgar Carvalho,Paulo Machado

doi:10.1590/0037-8682-0174-2013

Abstract

Leishmania braziliensis infection induces a large spectrum of lesions that clinically manifest as nodules or papules that progress to ulcers. Although it is already known that T helper cells predominate in the lesions, cytotoxic T cells have also been reported to be present, and their role in leishmaniasis immunopathogenesis is not well known. This study investigated the amounts of CD8+ and granzyme B+ cells in different clinical forms of human cutaneous leishmaniasis (CL). Forty tissue fragments from early (E-CL) and late CL (L-CL) lesions and from disseminated leishmaniasis (DL) - papules and ulcers - were characterized. The inflamed area per fragment was calculated, and the CD8 and granzyme B expression levels in the infiltrates were quantified by counting positive cells in 15 fields. The localization of CD8 and granzyme B was graded subjectively. Inflammation was higher in L-CL and DL ulcers. CD8 expression was increased in late ulcerated lesions compared to recent lesions. The increase in CD8+ cells also correlated with the duration of the lesion. Papules had a higher frequency of granzyme B+ cells than E-CL lesions, although the frequency was similar to those for late and DL ulcers. CD8+ cells were mostly found in the papillary dermis. CD8+ T and granzyme B+ cells are present in the inflammatory infiltrates of CL and DL and may participate in the immunopathogenesis of Leishmania infection.

Highlights

Leishmania braziliensis infection induces a large spectrum of lesions that clinically manifest as nodules or papules that progress to ulcers
We investigated the proportions of Cluster of differentiation 8 (CD8)+ T cells and granzyme B+ cells in primary and secondary lesions from disseminated leishmaniasis (DL) and in early and late cutaneous leishmaniasis (CL) lesions to better understand the roles of these cells in the pathogenesis of the disease
Cases with durations of more than 20 days were classified as late cutaneous lesions (L-CL), and cases with durations of 20 days or less were grouped as early cutaneous lesions (E-CL)

Summary

Introduction

Leishmania braziliensis infection induces a large spectrum of lesions that clinically manifest as nodules or papules that progress to ulcers. Papules had a higher frequency of granzyme B+ cells than E-CL lesions, the frequency was similar to those for late and DL ulcers. Conclusions: CD8+ T and granzyme B+ cells are present in the inflammatory infiltrates of CL and DL and may participate in the immunopathogenesis of Leishmania infection. Cutaneous leishmaniasis lesions start as small papules in the presence or absence of lymphadenopathy, and they progress into one or more skin ulcers. This localized skin ulceration is characterized by a chronic inflammatory response involving lymphocytes, plasma cells and macrophages, with and an eventual granulomatous reaction and necrosis[1,2]. The presence of cluster of differentiation 4 (CD4)+ T cells within the inflammatory infiltrate in leishmaniasis lesions has already been shown, cytotoxic T cells in the lesions of CL patients[6] have been reported

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Results

Conclusion