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      Immune Regulation during Chronic Visceral Leishmaniasis

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          Abstract

          Visceral leishmaniasis is a chronic parasitic disease associated with severe immune dysfunction. Treatment options are limited to relatively toxic drugs, and there is no vaccine for humans available. Hence, there is an urgent need to better understand immune responses following infection with Leishmania species by studying animal models of disease and clinical samples from patients. Here, we review recent discoveries in these areas and highlight shortcomings in our knowledge that need to be addressed if better treatment options are to be developed and effective vaccines designed.

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          The relationship between leishmaniasis and AIDS: the second 10 years.

          Jorge Alvar, Pilar Aparicio, Abraham Aseffa … (2008)
          To date, most Leishmania and human immunodeficiency virus (HIV) coinfection cases reported to WHO come from Southern Europe. Up to the year 2001, nearly 2,000 cases of coinfection were identified, of which 90% were from Spain, Italy, France, and Portugal. However, these figures are misleading because they do not account for the large proportion of cases in many African and Asian countries that are missed due to a lack of diagnostic facilities and poor reporting systems. Most cases of coinfection in the Americas are reported in Brazil, where the incidence of leishmaniasis has spread in recent years due to overlap with major areas of HIV transmission. In some areas of Africa, the number of coinfection cases has increased dramatically due to social phenomena such as mass migration and wars. In northwest Ethiopia, up to 30% of all visceral leishmaniasis patients are also infected with HIV. In Asia, coinfections are increasingly being reported in India, which also has the highest global burden of leishmaniasis and a high rate of resistance to antimonial drugs. Based on the previous experience of 20 years of coinfection in Europe, this review focuses on the management of Leishmania-HIV-coinfected patients in low-income countries where leishmaniasis is endemic.
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            A dominant function for interleukin 27 in generating interleukin 10-producing anti-inflammatory T cells.

            Amit Awasthi, Yijun Carrier, Jean Peron … (2007)
            Regulatory T cells (T(reg) cells) expressing the transcription factor Foxp3 are key in maintaining the balance of immune homeostasis. However, distinct induced T regulatory type 1 (Tr1) cells that lack Foxp3 expression also regulate T cell function, mainly by producing the immunosuppressive cytokine interleukin 10 (IL-10). However, the factors required for the induction of IL-10-producing suppressive T cells are not fully understood. Here we demonstrate that dendritic cells modified by T(reg) cells induced the generation of IL-10-producing Tr1 cells. The differentiation of naive CD4+ T cells into IL-10-producing cells was mediated by IL-27 produced by the T(reg) cell-modified dendritic cells, and transforming growth factor-beta amplified the generation of induced IL-10+ Tr1 cells by IL-27. Thus, IL-27 and transforming growth factor-beta promote the generation of IL-10-producing Tr1 cells.
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              Post-kala-azar dermal leishmaniasis.

              E Zijlstra, A. M. Musa, E A G Khalil … (2003)
              Post-kala-azar dermal leishmaniasis (PKDL) is a complication of visceral leishmaniasis (VL); it is characterised by a macular, maculopapular, and nodular rash in a patient who has recovered from VL and who is otherwise well. The rash usually starts around the mouth from where it spreads to other parts of the body depending on severity. It is mainly seen in Sudan and India where it follows treated VL in 50% and 5-10% of cases, respectively. Thus, it is largely restricted to areas where Leishmania donovani is the causative parasite. The interval at which PKDL follows VL is 0-6 months in Sudan and 2-3 years in India. PKDL probably has an important role in interepidemic periods of VL, acting as a reservoir for parasites. There is increasing evidence that the pathogenesis is largely immunologically mediated; high concentrations of interleukin 10 in the peripheral blood of VL patients predict the development of PKDL. During VL, interferon gamma is not produced by peripheral blood mononuclear cells (PBMC). After treatment of VL, PBMC start producing interferon gamma, which coincides with the appearance of PKDL lesions due to interferon-gamma-producing cells causing skin inflammation as a reaction to persisting parasites in the skin. Diagnosis is mainly clinical, but parasites can be seen by microscopy in smears with limited sensitivity. PCR and monoclonal antibodies may detect parasites in more than 80% of cases. Serological tests and the leishmanin skin test are of limited value. Treatment is always needed in Indian PKDL; in Sudan most cases will self cure but severe and chronic cases are treated. Sodium stibogluconate is given at 20 mg/kg for 2 months in Sudan and for 4 months in India. Liposomal amphotericine B seems effective; newer compounds such as miltefosine that can be administered orally or topically are of major potential interest. Although research has brought many new insights in pathogenesis and management of PKDL, several issues in particular in relation to control remain unsolved and deserve urgent attention.
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                Author and article information

                Contributors
                Peter C. Melby: Role: Editor
                Journal
                Journal ID (nlm-ta): PLoS Negl Trop Dis
                Journal ID (iso-abbrev): PLoS Negl Trop Dis
                Journal ID (publisher-id): plos
                Journal ID (pmc): plosntds
                Title: PLoS Neglected Tropical Diseases
                Publisher: Public Library of Science (San Francisco, USA )
                ISSN (Print): 1935-2727
                ISSN (Electronic): 1935-2735
                Publication date Collection: July 2014
                Publication date (Electronic): 10 July 2014
                Volume: 8
                Issue: 7
                Electronic Location Identifier: e2914
                Affiliations
                [1 ]QIMR Berghofer, Brisbane, Australia
                [2 ]Queensland University of Technology, Brisbane, Australia
                University of Texas Medical Branch, United States of America
                Author notes

                The authors have declared that no competing interests exist.

                Article
                Publisher ID: PNTD-D-13-01558
                DOI: 10.1371/journal.pntd.0002914
                PMC ID: 4091888
                PubMed ID: 25010815
                SO-VID: a4a8407e-1453-4300-a430-7973c7f630fc
                Copyright statement: Copyright @ 2014
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

                History
                Page count
                Pages: 11
                Funding
                Research in the author's laboratory is funded by grants from the Australian National Health and Medical Research Council ( http://www.nhmrc.gov.au) and the Australian government's Department of Industry, Innovation, Science Research and Tertiary Education ( http://www.innovation.gov.au/aisrf). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
                Categories
                Subject: Review
                Subject: Biology and Life Sciences
                Subject: Immunology
                Subject: Immunity
                Subject: Microbiology
                Subject: Parasitology
                Subject: Medicine and Health Sciences
                Subject: Pathology and Laboratory Medicine
                Subject: Pathogenesis

                ScienceOpen disciplines: Infectious disease & Microbiology
                Data availability:
                ScienceOpen disciplines: Infectious disease & Microbiology

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