Lesional T‐cell subset in post‐kala‐azar dermal leishmaniasis

Abstract

Background The pathogenesis of post-kala-azar dermal leishmaniasis (PKDL) is ill understood. This study was carried out to find the percentage of T-helper and T-suppressor cells in lesional tissue and their probable role in the pathogenesis of PKDL.Methods An immunoperoxidase monoclonal antibody technique was used to characterize and quantify the subsets of T lymphocytes in the infiltrate in 25 patients with PKDL. ResultsThe ratio of T-helper to T-suppressor cells was 0.87 in hypopigmented macules and 0.85 in nodule and /or plaque lesions of PKDL. ConclusionsIn this study, there was a definite preponderance of T-suppressor cells over T-helper cells in both types of skin lesions of PKDL. Further studies should be undertaken on larger numbers of patients to compare T-cell subsets both in skin lesions and the circulation, in order to determine the pathogenesis of PKDL.

Post‐kala‐azar dermal leishmaniasis – an overview

“…In Indian PKDL, one of the first studies on the lesional profile 33 highlighted the preponderance of CD8 + over CD4 + T cells within both dermal lesions and draining lymph nodes; this was more prominent in patients presenting with advanced nodular lesions. A similar predominance of CD8 + over CD4 + lymphocytes in both hypopigmented, macular and nodular/ plaque lesional tissue was reported from Indian patients with PKDL 34 …”

“…A similar predominance of CD8 + over CD4 + lymphocytes in both hypopigmented, macular and nodular/ plaque lesional tissue was reported from Indian patients with PKDL. 34 On a molecular level, studies on the cytokine expression profiles within the localized milieu have established IFN-c, IL-6, TNF-a, IFN-cR1 (receptor for IFN-c) along with IL-10 as being the primary immunodeterminants of disease pathology in Indian PKDL. 35 In the same study, the authors suggest that the raised mRNA levels of IL-10 and TGF-b indicates a role for these cytokines in disease pathogenesis, via derailment of Th1 responses.…”

Tissue damage and immunity in cutaneous leishmaniasis

“…Post kala‐azar dermal leishmaniasis ( PKDL ), the cutaneous sequel of visceral leishmaniasis, is a nonulcerative disease, which display marked dermal lymphocyte infiltration dominated by T cells ( CD 3 + lymphocytes). In A frican PKDL , a predominance of CD 4 over CD 8 cells has been shown , while in I ndian PKDL , CD 8 cells are predominant over CD 4 . Macrophages are detected in variable numbers and are rarely parasitized.…”

Post kala-azar dermal leishmaniasis: A threat to elimination program

“…However, Sudanese PKDL subjects showed a shorter lag period, which may be due to their active immune memory responses that might mimic post-VL, whereas, in South Asia, PKDL subjects show an extended lag period, which may be due to their immune anergy in eliciting an antigen-specific immunological response [ 65 ]. It has also been postulated that the self-healing ability of Sudanese PKDL is due to the presence of augmented levels of effector memory T cells in the skin, which has been found alleviated in the case of the non–self-healing nature of Indian PKDL [ 61 , 67 , 68 ]. This hypothesis may become feasible if comparative studies on memory responses have to be done between self-healing Sudanese PKDL and non–self-resolving Indian PKDL.…”