Leite-Silva Jéssica, Oliveira-Ribeiro Carla, Morgado Fernanda Nazaré, Pimentel Maria Inês Fernandes, Lyra Marcelo Rosandiski, Fagundes Aline, Miranda Luciana Freitas Campos, Valete-Rosalino Claudia Maria, Schubach Armando Oliveira, Conceição-Silva Fátima
Laboratory of Immunoparasitology, Oswaldo Cruz Institute (IOC), Fundação Oswaldo Cruz (Fiocruz), Rio de Janeiro 21041-250, RJ, Brazil.
Service of Oncological Dermatology-National Institute of Cancer (INCA), Rio de Janeiro 20570-120, RJ, Brazil.
Microorganisms. 2023 Jun 22;11(7):1631. doi: 10.3390/microorganisms11071631.
Localized cutaneous leishmaniasis caused by can either respond well or poorly to the treatment or heal spontaneously; It seems to be dependent on the parasite and/or host factors, but the mechanisms are not fully understood. We evaluated the in situ immune response in eighty-two active lesions from fifty-eight patients prior to treatment classified as early spontaneous regression (SRL-n = 14); treatment responders (GRL-n = 20); and non-responders (before first treatment/relapse, PRL1/PRL2-n = 24 each). Immunohistochemistry was used to identify cell/functional markers which were correlated with the clinical characteristics. PRL showed significant differences in lesion number/size, clinical evolution, and positive parasitological examinations when compared with the other groups. SRL presented a more efficient immune response than GRL and PRL, with higher IFN-γ/NOS2 and a lower percentage of macrophages, neutrophils, NK, B cells, and Ki-67+ cells. Compared to SRL, PRL had fewer CD4+ Tcells and more CD163+ macrophages. PRL1 had more CD68+ macrophages and Ki-67+ cells but less IFN-γ than GRL. PRL present a less efficient immune profile, which could explain the poor treatment response, while SRL had a more balanced immune response profile for lesion healing. Altogether, these evaluations suggest a differentiated profile of the organization of the inflammatory process for lesions of different tegumentary leishmaniasis evolution.
由[具体病原体未给出]引起的局限性皮肤利什曼病对治疗的反应可能良好或不佳,也可能自发愈合;这似乎取决于寄生虫和/或宿主因素,但其机制尚未完全明确。我们评估了58例患者在治疗前82个活动性病变中的原位免疫反应,这些患者被分类为早期自发消退(SRL,n = 14);治疗反应者(GRL,n = 20);以及无反应者(首次治疗前/复发,PRL1/PRL2,每组n = 24)。免疫组织化学用于识别与临床特征相关的细胞/功能标志物。与其他组相比,PRL在病变数量/大小、临床进展和寄生虫学检查阳性方面表现出显著差异。SRL呈现出比GRL和PRL更有效的免疫反应,具有更高的IFN-γ/NOS2以及更低比例的巨噬细胞、中性粒细胞、NK细胞、B细胞和Ki-67+细胞。与SRL相比,PRL的CD4+ T细胞较少,CD163+巨噬细胞较多。PRL1的CD68+巨噬细胞和Ki-67+细胞较多,但IFN-γ比GRL少。PRL呈现出效率较低的免疫特征,这可以解释其治疗反应不佳,而SRL具有更平衡的免疫反应特征以促进病变愈合。总之,这些评估表明不同皮肤利什曼病演变的病变在炎症过程组织方面存在差异特征。